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PubMed1977

Aldosterone and postprandial renal excretion of sodium and potassium in sheep.

When sheep rapidly eat a meal of dry feed a period of antinatriuresis and antidiuresis is rapidly initiated and lasts for 2-3 hrs. This is followed by a postprandial period of natriuresis and diuresis. This study tested the hypothesis that the postprandial natriuresis was due to a reduction in the secretion of aldosterone. In unanesthetized ewes of about 50 kg body wt, measurements were made of sodium and potassium excretion beginning in the terminal phase of the feed-induced antinatriuresis and continuing through the period of postprandial natriuresis. Aldosterone, given by constant infusion at a physiological dose (10 microgram/h), inhibited the natriuresis. Spironolactone, a competitive inhibitor of aldosterone given as a single intravenous injection of 5 mg/kg body wt, did not significantly increase the natriuresis. These results support the stated hypothesis. Neither aldosterone nor spironolactone had a significant effect on potassium excretion. This finding supports earlier view that aldosterone has only a small role in the homeostatic control of potassium excretion in sheep.

Aldosterone↗

PubMed1985

Sodium retention in nephrotic syndrome is due to an intrarenal defect: evidence from steroid-induced remission.

There is increasing evidence that the sodium retention of nephrotic syndrome is directly due to an intrarenal mechanism and not to a low blood volume stimulating the renin-angiotensin-aldosterone system. However the mechanism of the natriuresis that occurs during remission is not known. Patients with nephrotic syndrome were therefore studied during steroid-induced remission. At the onset of natriuresis, blood volume and plasma albumin were low and did not change. Plasma renin activity and plasma aldosterone were initially high and both fell during the natriuresis. At the end of the natriuresis when patients had lost their oedema, plasma renin activity and plasma aldosterone rose to high levels, plasma albumin and blood volume remained low, and yet the patients were no longer retaining sodium and were in sodium balance. These observations suggest that the natriuresis of remission is due to the correction of an intrarenal mechanism causing the sodium retention. This study raises two major unanswered questions. Firstly, when the presumed intrarenal mechanism is corrected, what tells the kidney to excrete large amounts of sodium when the blood volume remains low? Secondly, why do the patients come back into sodium balance when the blood volume is low, and plasma renin activity and plasma aldosterone are elevated?

Adolescent↗

PubMed1991

Atrial natriuretic factor and salt wasting after aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The causes of volume depletion and hyponatremia after subarachnoid hemorrhage are not fully understood but may be in part due to natriuresis or "cerebral salt wasting." Because previous studies using infrequent hormone sampling have given inconsistent results, we determined if elevations in atrial natriuretic factor concentrations preceded negative sodium and fluid balances. METHODS: We measured diurnal atrial natriuretic factor and vasopressin concentrations and sodium balance for 5 days in 14 consecutive patients after aneurysmal subarachnoid hemorrhage. RESULTS: Plasma concentrations of atrial natriuretic factor on admission were elevated in subarachnoid hemorrhage patients (mean +/- SD 106 +/- 59 pg/ml) compared with acutely ill controls (39 +/- 30 pg/ml). In eight patients, high peak concentrations of atrial natriuretic factor, greater than 300 pg/ml or a twofold increase above baseline, were followed by natriuresis and a negative sodium balance. Three patients, two of whom became hyponatremic, developed cerebral infarcts after natriuresis. Vasopressin concentrations were slightly elevated just after hemorrhage but subsequently declined to normal values. CONCLUSIONS: A markedly increased atrial natriuretic factor concentration precedes natriuresis in some patients and, with other abnormalities of water handling possibly including a relatively diminished vasopressin concentration, may cause volume depletion. Patients with natriuresis appear to be at increased risk for delayed cerebral infarction after subarachnoid hemorrhage.

Adult↗

PubMed1972

Renal sodium-potassium-activated adenosine triphosphatase and sodium reabsorption.

The role of renal Na(+),K(+)-ATPase in sodium reabsorption was further examined in dogs in which digoxin, a specific inhibitor of the enzyme system, was infused into one renal artery in doses ranging from 0.4 to 0.9 mug/kg/min (low dose) and from 1.0 to 4.0 mug/kg/min (high dose). A significant natriuresis occurred with both dose ranges which was accompanied by inhibition of Na(+),K(+)-ATPase of cortex and medulla in the infused kidney. Despite over 90% enzyme inhibition in many experiments, at least 80% of the filtered sodium continued to be reabsorbed. The per cent change in enzyme activity correlated with the rate of digoxin administration and the total dose administered but not with changes in sodium excretion. Changes in medullary Na(+),K(+)-ATPase activity, however, bore a direct relationship to alterations in fractional solute free water reabsorption (T(c) (H2O)). Inhibition of cortical enzyme activity alone was not associated with natriuresis, suggesting that medullary enzyme activity must be depressed for increased sodium excretion to occur during digoxin infusion. In high-dose experiments, significant inhibition of cortical and medullary enzyme in the contralateral control kidney was also observed, but natriuresis did not occur. In these experiments the rate at which digoxin reached the control kidney rose progressively but never equaled the rates in the directly infused kidney with either dose. Nevertheless, it is clear that under certain circumstances enzyme inhibition of either cortex or medulla need not be accompanied by natriuresis. We conclude that the major role of renal Na(+),K(+)-ATPase is in sodium reabsorption in the medulla (ascending limb of Henle's loop) and that it has a relatively small role in proximal sodium reabsorption. The kidney can rely on other sodium reabsorptive mechanisms depending on the rate of enzyme inhibition, so that natriuresis may not occur at all if depression in activity occurs "slowly." The nature of these mechanisms is not clear.

Adenosine Triphosphatases↗

PubMed1972

A humoral component of the natriuretic mechanism in sustained blood volume expansion.

A natriuretic and diuretic response to whole blood infusion in the rat, exaggerated and sustained by intravenous reinfusion of excreted urine, was shown to be associated with increased glomerular filtration and reduced tubular reabsorption. Cross-circulation of animals so responding (donor rats) with isovolemic recipients led to a modest natriuretic and diuretic response in the latter, not accounted for by altered physical composition of the blood nor by observed changes in filtration rate or arterial blood pressure. The recipient natriuresis was unchanged when nephrectomized donors were used and it occurred in experiments in which donor urine was simultaneously replaced by intravenously infused Ringer-Locke solution; the natriuretic property of the cross-circulating blood could therefore not have been due to reinfusion of urinary constituents, nor to accumulation of metabolites, nor to a factor of renal origin. A recipient natriuresis was also observed when the expanded and urine reinfused donor had been acutely adrenalectomized, ruling out an altered secretion of adrenal cortical or medullary hormones as a principal cause of this natriuresis; the data, however, do not exclude participation of reduced aldosterone secretion in the normal effector mechanism. In control experiments in which whole blood was exchanged for donor blood, a small delayed natriuresis did occur in the recipient; this could be completely prevented by administration of aldosterone. In similar exchange experiments with adrenalectomized donors, a small natriuresis developed in the recipient before blood administration but declined afterwards. These minor natriuretic effects probably resulted from altered mineralocorticoid content of the cross-circulating blood due to factors other than blood volume change. The larger natriuretic response seen in all recipients when the donor was volume expanded must have been due largely to a humoral natriuretic factor of other than renal or adrenal origin.

Adrenal Glands↗

PubMed1976

The role of the medullary collecting ducts in postobstructive diuresis.

Medullary collecting duct function was studied by direct microcatheterization techniques in rats undergoing postobstructive diuresis. Significant net addition of water and sodium to the duct was demonstrated during postobstructive diuresis after relief of 24-h bilateral ureteral ligation. This striking abnormality in function was associated with reduced delivery of sodium and water to the collecting duct compared to sham-operated controls. To examine the role of circulating factors in this phenomenon, another group of rats was studied that underwent 24 h of total urine reinfusion into the femoral vein. Natriuresis and diuresis were similar to the postobstructive group, but absolute collecting duct reabsorption of sodium and water was normal. The natriuresis and diuresis in rats with urine reinfusion resulted from increased delivery of fluid and sodium to the medullary collecting duct. A third group of rats was studied with 24-h unilateral ureteral ligation as well as urine reinfusion from the contralateral normal kidney. Without urine reinfusion there was no diuresis-natriuresis but with urine reinfusion the diuresis and natriuresis after relief of unilateral obstruction was similar to that after relief of bilateral obstruction. Moreover, net addition of sodium and no significant water reabsorption were demonstrated in the medullary collecting duct of such animals. The results indicate that (a) the medullary collecting duct is the critical nephron segment affected by ureteral obstruction, since postobstructive diuresis occurred despite reduced delivery of fluid from the more proximal nephron; (b) the net addition of sodium to the medullary collecting duct observed during postobstructive diuresis is probably a direct effect of obstruction, since it was found during postobstructive diuresis after relief of bilateral or unilateral ureteral ligation, but not with urine reinfusion alone; and (c) blood-borne factors are important in the development of postobstructive natriuresis and diuresis, and probably act by increasing the fraction of filtered sodium and water delivered from the proximal and distal tubule to the collecting duct.

Absorption↗

PubMed1992

Effect of renal medullary circulation on arterial pressure.

PRESSURE-NATRIURESIS EFFECTS IN HYPERTENSION: Considerable advances have been made in our understanding of pressure-natriuresis and the effects of this mechanism in hypertension. We have shown that in the absence of changes in neural and endocrine factors, sodium and water excretion doubled when arterial pressure was increased by only 10 mmHg. These responses were greatly blunted or obscured by elevations in renal sympathetic tone, infusion of the vasoconstrictors angiotensin and vasopressin or by inhibition of paracrine factors such as eicosanoids and nitric oxide. EFFECT OF CHANGES ON MEDULLARY BLOOD FLOW: The pressure-natriuresis response is closely associated with changes in papillary blood flow as determined by laser-Doppler flowmetry. In volume-expanded rats, papillary blood flow is not well autoregulated, which results in elevations of vasa recta capillary pressure and renal interstitial fluid pressure. The increased interstitial fluid pressure is transmitted from the medulla to the cortex in the encapsulated organ and is associated with inhibition of sodium transport in the proximal tubule and/or the thin descending loop of Henle of deep nephrons. Selective reductions in medullary blood flow by infusion of the nitric oxide inhibitor N6-nitro-L-arginine methylester (L-NAME) into the renal medullary interstitial space resulted in decreased interstitial fluid pressure and reduced sodium excretion. The mechanisms by which small elevations in renal interstitial fluid pressure alter tubular sodium reabsorption remain to be determined. PRESSURE-NATRIURESIS EFFECTS IN HYPERTENSIVE RATS: Our studies have also shown that the pressure-natriuresis response is blunted in spontaneously hypertensive rats (SHR) compared to normotensive Wistar-Kyoto (WKY) rats. This abnormality is associated with shifts in the relationships among papillary flow, renal interstitial pressure and renal perfusion pressure towards higher pressures. The calcium antagonist nisoldipine corrected the defect in vasa recta hemodynamics in SHR and normalized relationships among sodium excretion, renal interstitial pressure and renal perfusion pressure. CONCLUSIONS: These studies indicate that sodium and water excretion is very sensitive to small changes in renal perfusion pressure due to associated changes in papillary blood flow, and that alterations in medullary hemodynamics can have an important effect on the relationship between arterial pressure and sodium and water excretion.

Animals↗

PubMedDate not supplied

[Atrial natriuretic peptide in children with nephrotic syndrome].

The mechanism causing sodium retention in nephrotic syndrome remains controversial. There is an increasing evidence that sodium retention is directly due to an intrarenal mechanism. Atrial natriuretic peptide (ANP), realized from the heart during hypervolaemia, increases glomerular filtration rate, renal sodium and water elimination in both experimental animals and healthy men. In attempt to clarify the possible role of ANP in the mechanism of sodium retention in nephrotic syndrome we carried out this study. The purpose was: a) to determine plasma concentrations of ANP and values of creatinine clearance (CCr), natriuresis and diuresis both in basal conditions and after remission of the ilness, and b) to analyze the influence of acute hypervolaemia on ANP, Ccr, diuresis and natriuresis. A group of 12 children (aged 2-13 years) was studied during relapse and remission of nephrotic syndrome. In addition, 8 patients were studied during acute hypervolaemia due to intravenous infusion of 12% albumine. Twelve healthy children served as control group. Our results showed that in nephrotic syndrome group ANP was higher than in control group. Creatinine clearance, diuresis and natriuresis were significantly lower during relapse than in remission. The increase in Ccr, diuresis and natriuresis were observed during infusion of albumine, but no correlation was found between increased ANP and other parameters. This study showed that during relapse of nephrotic syndrome plasma concentrations of ANP are moderately elevated, but Ccr, diuresis nad natriuresis are blunted. We speculate that natriuretic and diuretic effects of ANP are impaired in children with nephrotic syndrome.

Adolescent↗

PubMed1985

Reflex responses to reductions in functioning renal mass.

Both acute unilateral nephrectomy (AUN) and unilateral ureteral obstruction (UUO) result in an acute increase in cation excretion from the contralateral kidney. AUN results in reflex changes in systemic hemodynamics owing to an acute and transient increase in arterial pressure that activates carotid sinus baroreceptors and constitutes an afferent limb in the reflex; hemodynamic adjustments and increased cation excretion result. The reflex involves participation of the endogenous opioid system, with receptors located primarily in the central nervous system, and requires intact pituitary function because both hypophysectomy and pretreatment with large doses of dexamethasone prevent the postnephrectomy natriuresis. The natriuresis is closely correlated with an increase in the plasma concentration of the NH2-terminal fragment of the pituitary peptide precursor molecule proopiomelanocortin, which suggests that such a peptide could participate directly or indirectly in the postnephrectomy natriuresis. Surgical denervation of either the ipsilateral or the contralateral kidney markedly alters the response to AUN, which prevents the natriuresis and blunts the kaliuresis, and indicates a role for renal neural reflexes. Renorenal reflex pathways also mediate the response of the contralateral kidney to UUO, because denervation of either the ipsilateral (obstructed) or the contralateral kidney abolishes both the natriuresis and kaliuresis usually seen after UUO. This reflex also involves the endogenous opioid system, for it does not occur in rats receiving an i.v. infusion of the opiate receptor antagonist naloxone.

Adaptation, Physiological↗

PubMed1996

Atrial natriuretic peptide, sodium retention, and proteinuria in nephrotic syndrome.

BACKGROUND: Oedema formation in the nephrotic syndrome is primarily due to tubular sodium retention. The pathogenetic role of alpha atrial natriuretic peptide (ANP), a hormonal promoter of natriuresis is unknown. METHODS: In 31 patients (aged 35+/-11 years) with nephrotic syndrome and histopathological evidence of primary glomerulonephritis, we investigated plasma ANP concentration and its influence on renal haemodynamics, natriuresis, and proteinuria (total protein, albumin, IgG excretion). Patients with a compensated treated form of nephrotic syndrome due to primary glomerulonephritis were included in the study. Serum creatinine levels were <=1.4 mg/dl. Diuretic medication was discontinued at least 24 h before the investigation was started. Patients were randomly assigned to ANP infusion (0.005 microg/kg*min; group II, n=15) or received placebo (group III, n=16). Ten healthy subjects (group I) served as normal controls. RESULTS: In normal subjects (group I), ANP caused an increase in natriuresis from 14.5+/-4.2 mmol/h to 26.4+/-11.1 mmol/h (P<0.01). In patients with nephrotic syndrome (group II), baseline sodium excretion of 10.5+/-6.0 mmol/h was increased to 19.6+/-14.8 mmol/h with ANP infusion (P<0.01). No changes were seen in the placebo group III. The absolute increase in ANP induced natriuresis was not significantly different between group I and II. However, plasma ANP levels were significantly higher in patients with nephrotic syndrome (166+/-87 pg/ml vs. 74+/-21 pg/ml, P<0.05) and also reached higher levels after ANP infusion (P<0.01). Therefore, natriuresis was significantly reduced when circulating ANP levels were taken into account (P<0.05). ANP administration resulted in an increase of total protein excretion in patients with the nephrotic syndrome (group II, from 219+/-277 mg/h to 264+/-268 mg/h). Albumin elimination rose from 128+/-151 mg/h to 167+/-170 mg/h (P<0.05) and IgG excretion from 4.91+/-6.67 mg/h to 9.27+/-10.78 mg/h (P<0.05). Healthy subjects also showed a small but significant increase in albuminuria (48+/-38%, P<0.05). Low-dose ANP infusion did not, however, induce any significant alteration in GFR, ERPF and blood pressure. CONCLUSION: ANP plasma concentrations in the steady state are elevated in patients with the nephrotic syndrome. The natriuretic effect of ANP is reduced when referring to circulating ANP plasma levels. Elevated ANP levels enhance urinary protein excretion in the nephrotic syndrome. This is not due to modulation of GFR or FF, but is most probably attributable to increased glomerular permeability.

Adult↗

PubMed2001

Effect of angiotensin-converting enzyme inhibitor on renal function in ovarian hyperstimulation syndrome in the rabbit.

OBJECTIVE: To investigate renal function and whether captopril prevents alterations in the handling of sodium and water in the ovarian hyperstimulation syndrome (OHSS) in the rabbit. DESIGN: Experimental study SETTING: Physiology laboratory. ANIMAL(S): Six female New Zealand white rabbits were used as controls, and 13 were hyperstimulated with gonadotropins. INTERVENTION(S): Saline or captopril. MAIN OUTCOME MEASURE(S): Renal excretory and hemodynamic variables. RESULT(S): The 3% extracellular volume expansion in OHSS animals induced a significant elevation in mean arterial pressure by 27%, although increments in natriuresis and diuresis were similar to those observed in controls. The OHSS group had impaired pressure-natriuresis sensitivity compared with controls (0.36 +/- 0.07 microEq/min/g of Na excreted per mm Hg vs. 1.74 +/- 0.45 microEq/min/g of Na excreted per mm Hg; P<.05. Captopril significantly reduced mean arterial pressure (P<.05) and shifted the pressure-natriuresis response to the left by 0.85 +/- 0.17 microEq/min/g of Na excreted per mm Hg (P<.05). CONCLUSION(S): In OHSS in the rabbit model, pressure-natriuresis sensitivity is impaired. Angiotensin II may play a significant role in this phenomenon, since angiotensin-converting enzyme inhibition normalized the pressure-natriuresis relationship.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1997

The neuroendocrine control of atrial natriuretic peptide release.

In the initial experiments reviewed here, we show that atrial natriuretic peptide (ANP) plays an important inhibitory role in the control of sodium chloride and water intake since injections of ANP into the third ventricle (3V) caused a reduction in dehydration-induced drinking and also the drinking of salt in salt-depleted rats. Attention was then turned to the possible role of the brain ANP neurons in producing natriuresis which had earlier been shown to be caused by stimulations within the anterior ventral third ventricular region (AV3V). Stimulation in this region by carbachol produced natriuresis accompanied by a dramatic increase in plasma ANP concentrations and increased content of the peptide in medial basal hypothalamus (MBH), neurohypophysis (NH) and anterior pituitary gland (AP), without alterations in the content of ANP in lungs or atria. This suggested that the natriuresis resulting from the stimulation is brought about, at least in part, by the release of ANP from the brain. Conversely, there was a dramatic decline in plasma ANP at both 24 and 128 h after AV3V lesions had been placed. In view of the much larger quantities of the peptide stored in the atria, it is probable that the changes in the atrial release of the peptide were the main factors altering plasma ANP, but that there was concomitant alteration in the release of brain ANP as well. Blood volume expansion (BVE) by intraatrial injection of isotonic saline in the rat is a profound stimulus for ANP release. Lesions in the AV3V region, median eminence, or neurohypophysectomy blocked BVE-induced release of ANP indicating the crucial participation of the CNS in the response of ANP and natriuresis. Baroreceptor impulses from the carotid-aortic sinus regions and the kidney are important in the neuroendocrine control of ANP release since deafferentation of these regions lowered basal plasma ANP concentrations and prevented the increase after BVE. The evidence indicates that the ANP release, in response to BVE, is mediated by afferent baroreceptor impulses to the AV3V, which mediates the increased ANP release via activation of the hypothalamic ANP neuronal system. Our recent data support the hypothesis that BVE causes the release of ANP from ANPergic neurons in the hypothalamus that in turn stimulates release of oxytocin from the neurohypophysis. This oxytocin acts to release ANP from the right atrium that has negative chrono- and inotropic effects in the right atrium to reduce cardiac output, thereby reducing effective circulating blood volume. Then, the released ANP circulates to the kidneys and evokes natriuresis to return circulating blood volume to normal. This is further accomplished by reduction in intake of water and salt mediated also by brain ANP.

Animals↗

PubMed1990

Dopaminergic modulation of acute renal effects of nicardipine.

In order to investigate whether dopamine receptors are involved in the acute natriuretic effects of calcium channel blockade, experiments were carried out in humans with uncomplicated essential hypertension. In 8 hypertensives 5 mg intravenous nicardipine produced a large decrease in blood pressure and renal vascular resistance, a slight but significant increase in glomerular filtration rate (GFR) and marked natriuresis. When a second identical experiment was performed in the same subjects with the addition of 10 mg metoclopramide as dopamine blocker, changes in sodium excretion and vascular resistance were the same, but GFR did not increase during nicardipine. In a second set of experiments (n = 5) the same design was used, but nicardipine was infused at a dose of 0.01 mg/kg, ie, seven times less than in previous experiments. Under these conditions, blood pressure, renal vascular resistance and GFR did not change, but significant natriuresis occurred. Natriuresis was almost completely prevented by metoclopramide. In 5 additional hypertensives, metoclopramide alone was infused and 0.01 mg/kg nicardipine was added to the infusion. No change in any parameter was observed. Our findings suggest that the dopaminergic system participates in maintaining or increasing GFR during blood pressure reduction by calcium antagonists, although renal vasodilation and natriuresis are largely independent of dopamine receptor activity. In addition, when low doses of calcium antagonists produce natriuresis in the absence of renal or systemic hemodynamic changes (direct tubular effect), dopamine blockade is able to blunt this effect. This indicates a modulation by dopaminergic receptors of the direct tubular action of calcium antagonists.

Blood Pressure↗

PubMed2000

Is there a role for renin profiling in selecting chronic heart failure patients for ACE inhibitor treatment?

BACKGROUND: It remains uncertain whether angiotensin converting enzyme (ACE) inhibitors benefit all heart failure patients or just those with renin-angiotensin-aldosterone system (RAAS) activation. OBJECTIVE: To determine whether the response to an ACE inhibitor, assessed by urine sodium excretion, was different in patients with low renin versus those with high renin. DESIGN: Plasma renin activity (PRA) was measured in 38 patients with stable chronic heart failure (21 male, 17 female; mean (SD) age 71 (6) years, range 59-82 years) on chronic diuretic treatment alone. They were divided into three groups: low (PRA </= 1.5 ng/ml/h, n = 11); normal (1.5 < PRA < 5, n = 14); and high (PRA > 5, n = 13). The effect of ACE inhibition was then assessed on diuretic induced natriuresis with respect to renin status. RESULTS: There were no significant differences in age and sex distribution between the groups. Plasma angiotensin II and aldosterone increased serially from low to high renin groups, while 24 h urinary sodium concentrations fell from low to high renin groups (low PRA, 96.7 (39.5); normal PRA, 90.4 (26.7); high PRA, 66. 3 (18.9) mmol/l; p = 0.033), despite a higher diuretic dose in the high renin group. This blunted natriuretic effect of loop diuretics was caused by RAAS activation, which could partly be reversed by ACE inhibition. ACE inhibitors increased natriuresis by 22% in the high renin group (p = 0.029), but had no effect in the normal and low renin groups. Within the low renin group, five of the 11 patients had persistently low renin levels despite ACE inhibition. There was a non-significant reduction in natriuresis (-9.6%, p = 0.335) following ACE inhibition in this subgroup of patients. CONCLUSIONS: About one third of heart failure patients in our study had low renin status and a non-activated RAAS, despite diuretic treatment. ACE inhibitors did not alter natriuresis significantly in this subgroup of patients, and enhanced natriuresis only in patients with high renin. There is thus tentative support for renin profiling in targeting ACE inhibitors to the most deserving, by showing that short term sodium retention does not occur in low renin patients if ACE inhibitors are withdrawn.

Aged↗

PubMed1976

Cross-circulation study of natriuretic factors in postobstructive diuresis.

To study the role of circulating natriuretic factors in the postobstructive diuresis that occurs after relief of bilateral, but not unilateral ureteral ligation, cross-circulation was carried out between normal recipient rats and donor rats have either 24-h bilateral (BUL) or unilateral (UUL) ureteral ligation. With BUL donors, there was a rapid marked increase in sodium and water excretion in the recipient rats, sustained for 80-140 min, with a peak approximately 10 times control values. With UUL donors, no significant natriuretic response occurred. Changes in glomerular filtration rate, renal plasma flow, blood pressure, hematocrit, or circulating levels of aldosterone or Pitressin did not explain the diuresis-natriuresis produced by cross-circulation with BUL donors. Differences in the intrinsic renal damage produced by bilateral as compared to unilateral ureteral obstruction did not appear to account for this response, since UUL donors given an acute urea load and urine reinfusion caused a similar diuresis-natriuresis. Moreover, normal donor rats given a urea load also caused a diuresis-natriuresis nearly equal to that produced by BUL rats, and the relationship between increased urea excretion and sodium excretion or urine flow in the recipients was not different in the two groups. Total urine reinfusion for 3 h in donor rats produced a significant, although less marked, diuresis-natriuresis in recipient animals, with only a slight elevation of the blood urea nitrogen level, much less increase in urea excretion rate, and no significant relationship between urea excretion and sodium excretion or urine flow. The results indicate that potent natriuretic factors, which act by decreasing the tubular reabsorption of sodium and water, are present in the blood of rats with bilateral, but not unilateral, ureteral ligation. High blood and urine urea levels appear to be the factors responsible for the marked natriuresis-diuresis occurring in normal rats during cross-circulation with BUL donors, although suggestive evidence of other natriuretic factors in urine reinfused intravenously was also obtained. The data suggest that urea osmotic diuresis is an important mechanism for determining the striking difference between the postobstructive diuresis observed after relief of bilateral as compared to unilateral ureteral ligation.

Adenosine Triphosphatases↗

PubMed1980

The effect of insulin and of anti-insulin serum on handling of sodium by the isolated, perfused kidney of the streptozotocin-diabetic rat.

We studied the effects of insulin and of anti-insulin serum (AIS) on sodium excretion in isolated diabetic and normal, fed, rat kidneys perfused at a constant pressure of 100 mm Hg with Krebs-Ringer bicarbonate buffer containing 7.5% bovine serum albumin and 5 mM glucose and gassed with 95% O2 and 5% CO2. The addition of insulin produced antinatriuresis in kidneys from diabetic rats but not in those from normal rats. Moreover, before the addition of insulin, the baseline rate of sodium excretion was greater in the diabetic rat kidney than in the normal rat kidney, while no differences in glomerular filtration rate (GFR) were observed. The addition of AIS (enough to bind 1.4 mU of insulin per milliliter of perfusate) produced a brisk natriuresis in kidneys from normal rats, and this natriuresis could be reversed by the addition of saturating amounts of insulin. By contrast, the addition of normal guinea pig serum to the perfusate of normal kidneys or AIS to the perfusate of diabetic kidneys was unassociated with natriuresis. We conclude that (a) insulin promoted antinatriuresis in diabetic but not in normal rat kidneys, (b) AIS promoted natriuresis in normal kidneys, and (c) this natriuresis was a specific effect of AIS and was reversed by the addition of insulin. Our data support the view that insulin-induced antinatriuresis depends on endogenous levels of circulating insulin and on the availability of insulin-binding sites in the kidney.

Animals↗

PubMed1996

Modifications induced by -10 degrees Trendelenburg's posture in sodium tubular handling in patients with essential hypertension.

In essential hypertensive patients "exaggerated natriuresis" is a response to acute volume expansion. However, the underlying mechanisms for this remain to be determined. We studied 19 patients with essential hypertension (HP) and 9 normotensive subjects (NS). In all examined subjects the response to acute central volume expansion, without the plasma compositional change that Trendelenburg's position involves, was evaluated during 90 min (period T) after a similar period of deambulation (period D). Mean blood pressure (MBP), tubular sodium handling by the lithium clearance technique, plasma renin activity (PRA), plasma aldosterone (PA), plasma catecholamines and urine prostaglandine E2 and kallikrein were assessed after D and T. MBP was significantly higher in HP than in NS (p = 0.00001). HP showed "exaggerated natriuresis" after T (fractional excretion of sodium increased from 0.55 +/- 0.1% after D to 1.20 +/- 0.2% after T, p < 0.01). This was because of a decrease in their proximal fractional reabsorption of sodium (from 74.96 +/- 1.8% after D to 62.50 +/- 2.8% after T, p < 0.01). Plasma epinephrine and plasma dopamine after T were significantly lower than in standing position in HP (p < 0.01) but no in NS. The decrease in plasma renin activity after T in HP was 53%, and 32% in NS. There were not any significant differences between groups in the other neurohormonal systems studied. We conclude that the major determinant of "exaggerated natriuresis" in hypertensive patients is a higher stimulation of the cardiopulmonary receptors following Trendelenburg's position and consequently stronger reflex inhibition of sympathetic system activity and renin-angiotensin II activity. The "exaggerated natriuresis" after Trendelenburg's position in HP was an expression of abnormal pressure natriuresis.

Adult↗

PubMed1990

Effect of endopeptidase 24.11 inhibition in conscious cardiomyopathic hamsters.

An elevated plasma concentration of atrial natriuretic peptide (ANP) is characteristic of congestive heart failure (CHF) in both humans and animals. One strategy for facilitating the biological actions of this circulating hormone is to inhibit its metabolism. Neutral endopeptidase 24.11, an enzyme known to degrade ANP, has been implicated in the metabolic clearance of this hormone. Inhibition of endopeptidase 24.11 may produce increases in the local concentrations of ANP in organs rich in the enzyme, such as the kidney, thereby enhancing local actions, e.g. natriuresis. Exogenous administration of ANP to CHF patients produces limited natriuresis, perhaps because of the associated fall in arterial pressure. This approach of blocking endopeptidase 24.11 activity in CHF could offset the general effects of exogenous administration of ANP and result in enhanced natriuresis. We therefore undertook studies to determine if thiorphan, an endopeptidase 24.11 inhibitor, would increase circulating ANP levels and enhance natriuresis in conscious cardiomyopathic hamsters with CHF. Cardiomyopathic hamsters had significantly lower (P less than .05) basal mean arterial pressures in comparison to normal hamsters (90 +/- 2 vs. 135 +/- 3 mm Hg). Treatment with thiorphan (10 mg/kg i.v. bolus followed by 10 mg/kg/hr i.v. infusion) did not change arterial pressure in either group and produced a 3-fold increase in urinary sodium excretion in the cardiomyopathic group but not in the normal hamsters. This natriuretic response in the cardiomyopathic hamsters was associated with a doubling of the plasma concentration of ANP. These results indicate that inhibition of endopeptidase 24.11 increases natriuresis and circulating ANP concentrations in this model of CHF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗