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PubMed1998

Differential catecholamine responses to protein intake in healthy and hypertensive subjects.

Protein intake-induced natriuresis previously related to increased urinary dopamine excretion was reexamined in an extensive controlled study comparing healthy and hypertensive subjects. In healthy subjects, ingestion of 1 g/kg wt tuna induced natriuresis that was associated, between postprandial hours 1 and 2, with increased plasma tyrosine [191 +/- 13% (mean +/- SE); P < 0.01], 3, 4-dihydroxyphenylalanine (104 +/- 12%, P < 0.05 in plasma; 162 +/- 20%, P < 0.05 in urine), plasma free dopamine (156 +/- 32%; P < 0. 05), and dopamine sulfate (191 +/- 11%, P < 0.001 in plasma; 199 +/- 15%, P < 0.01 in urine) but affected urinary free dopamine excretion only at limits of significance. Hypertensive subjects had less (P < 0.02) natriuresis and, despite comparable plasma tyrosine and dopamine sulfate increases, no increase in plasma and urinary 3, 4-dihydroxyphenylalanine and plasma free dopamine. Their plasma and urinary free epinephrine responses were less (P < 0.05) than the borderline increases in control subjects. Compared with control subjects, they significantly increased plasma 3, 4-dihydroxyphenylalanine sulfate (P < 0.05), epinephrine sulfate (P < 0.05), and the dopamine sulfate-to-free dopamine ratio (P < 0.02). Postprotein natriuresis is thus associated with nutritional priming-induced plasma but not urinary free dopamine increase. Hypertensive subjects have attenuated natriuretic and plasma free dopamine responses and less free epinephrine increase. This may partly result from higher circulating 3,4-dihydroxyphenylalanine, dopamine, and epinephrine sulfoconjugates leaving fewer free amines for biological actions.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1995

Diuretic effect of acute hypoxia in humans: relationship to hypoxic ventilatory responsiveness and renal hormones.

Acute hypoxia causes increased sodium and water excretion. Animal studies suggest that this renal response is largely driven by direct peripheral arterial chemoreceptor stimulation, independent of accompanying changes in ventilation and acid-base status. Whether the diuresis and natriuresis observed in humans made acutely hypoxic are caused by peripheral chemoreceptor stimulation is not known, but, if so, we hypothesized that people with a high ventilatory response to hypoxia (high peripheral chemosensitivity) should have greater diuresis and natriuresis than those with a low ventilatory response to hypoxia. The isocapnic hypoxic ventilatory response (HVR) of 16 subjects on a fixed sodium intake was measured, as were their urinary volume and sodium and bicarbonate losses during 6 h of breathing air (in a normobaric environmental chamber) and, on the subsequent day, 12% O2. The isocapnic HVR correlated positively with hypoxic diuresis (r = 0.87) and natriuresis (r = 0.76). In contrast, the isocapnic HVR did not correlate with bicarbonate excretion, despite the expected respiratory alkalosis of acute hypoxia. The magnitude of diuresis and natriuresis with hypoxia did not correlate with changes in circulating aldosterone, renin, atrial natriuretic peptide, vasopressin, or a digoxin-like immunoreactive substance. These findings are compatible with a role of the peripheral arterial chemoreceptors in mediating the renal response to hypoxia in humans. The efferent pathway remains unknown.

Acute Disease↗

PubMed2002

Chromosome 1 blood pressure QTL region influences renal function curve and salt sensitivity in SHR.

One or more quantitative trait locus (QTL) for blood pressure (BP) exists on rat chromosome 1, in the vicinity of the Sa gene. The present work examined whether this QTL region: 1) alters pressure-natriuresis relationship and 2) affects the BP response to salt load. Male spontaneously hypertensive rats (SHR), Wistar-Kyoto (WKY) rats, and rats from an SHR congenic strain that contains a WKY chromosome 1 segment spanning the BP QTL region (SHR. WKY-Sa) were used. In an acute study in anesthetized animals, renal function was measured at several levels of renal perfusion pressure. In a chronic study, BP was measured in freely moving rats using telemetry during normal and high sodium intake (2% NaCl as drinking water for 2 wk). WKY rats showed a significantly higher glomerular filtration rate and increased pressure-natriuresis compared with SHR. SHR.WKY-Sa also demonstrated an increased glomerular filtration rate and enhanced pressure-natriuresis, associated with a lower tubular sodium reabsorption, compared with SHR. These modifications were accompanied by a lower basal BP in SHR.WKY-Sa compared with SHR and a markedly reduced BP response to salt load. These findings suggest that the BP QTL(s) present in this region of chromosome 1 influences BP and salt sensitivity, at least partly, by modulating pressure-natriuresis.

Animals↗

PubMed1967

The Effects of Angiotensin II on Renal Water and Electrolyte Excretion in Normal and Caval Dogs.

The effects of intravenous administration of angiotensin II on renal water and electrolyte excretion were examined during hydropenia, water diuresis, and hypotonic saline diuresis in anesthetized normal dogs and dogs with thoracic inferior vena cava constriction and ascites (caval dogs). The effects of unilateral renal artery infusion of a subpressor dose were also examined.During hydropenia angiotensin produced a decrease in tubular sodium reabsorption, with a considerably greater natriuresis in caval dogs, and associated with a decrease in free water reabsorption (T(c) (H(2)O)). Water and hypotonic saline diuresis resulted in an augmented angiotensin natriuresis, with a greater effect still observed in caval dogs. In these experiments free water excretion (C(H(2)O)) was limited to 8-10% of the glomerular filtration rate (GFR), although distal sodium load increased in every instance. In the renal artery infusion experiments a significant ipsilateral decrease in tubular sodium reabsorption was induced, particularly in caval dogs.These findings indicate that angiotensin has a direct effect on renal sodium reabsorption unrelated to a systemic circulatory alteration. The attenuation or prevention of the falls in GFR and effective renal plasma flow (ERPF) usually induced by angiotensin may partially account for the greater natriuretic response in caval dogs and the augmentation during water or hypotonic saline diuresis. However, a correlation between renal hemodynamics and the degree of natriuresis induced was not always present and, furthermore, GFR and ERPF decreased significantly during the intrarenal artery infusion experiments. Therefore, the present experiments indicate that another mechanism is operative in the control of the angiotensin natriuresis and suggest that alterations in intrarenal hemodynamics may play a role.The decrease in T(c) (H(2)O) and the apparent limitation of C(H(2)O) associated with an increase in distal sodium load localize the site of action of angiotensin to the ascending limb of Henle's loop and the proximal tubule.

Journal Article↗

PubMed1993

Concurrent neutral endopeptidase and ACE inhibition in experimental heart failure: renal and hormonal effects.

Neutral endopeptidase (NEP) inhibitors have been shown to strengthen the effects of endogenous atrial natriuretic peptide (ANP). It has been well documented that angiotensin I-converting enzyme (ACE) inhibitors act beneficially in chronic congestive heart failure (CHF). In the present study, renal and hormonal effects of SCH 34826, an orally active NEP inhibitor, were studied in a coronary-ligation model of experimental CHF in the rat. The effects were compared to those of captopril. The drugs were also administered in combination. In anaesthetized rats with CHF, SCH 34826 (90 mg kg-1 sc) elevated plasma ANP from 382 +/- 85 to 658 +/- 120 ng l-1 compared with vehicle (p = 0.002). In sham-operated control rats, plasma ANP also increased slightly from 52 +/- 6 to 70 +/- 9 ng l-1 (p = 0.05). Plasma renin activity did not change in either group. When given orally for 36 h (90 mg kg-1 b.i.d.), SCH 34826 enhanced natriuresis in controls but not in rats with CHF. Captopril (0.2 mg ml-1 in drinking water) enhanced natriuresis in CHF rats and both natriuresis and kaliuresis in controls. When SCH 34826 and captopril were combined, natriuresis was potentiated in control rats as compared with captopril alone; in rats with CHF, however, a brisk kaliuresis was seen. The excretion of cyclic guanosine monophosphate was enhanced in CHF rats by 52% during treatment with SCH 34826 but not with captopril or combination of the two drugs. Moreover, captopril suppressed aldosterone excretion both in CHF rats and controls when administered alone but not when combined with SCH 34826.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1981

Influence of insulin and glucagon on sodium balance in obese subjects during fasting and refeeding.

To delineate the hormonal mechanism of dietary-induced changes in sodium balance, the role of insulin and glucagon in natriuresis of fast was evaluated in obese subjects submitted to a total starvation and given either glucagon or somatostatin infusion on day 4 of fast. While large amounts of glucagon (1 mg over 6 h) stimulated concomitantly ketonaemia, ketonuria and renal sodium losses, the ten-times lower amounts of glucagon induced an increase in renal ketone body and sodium excretion without any significant change in ketonaemia. It was concluded, therefore, that elevated plasma glucagon level may enhance renal sodium loss in ketotic states, through a direct renal effect reducing tubular ketone body reabsorption, hence increased ketonuria and natriuresis. It appears nevertheless that decreased insulin secretion, rather than an increase in plasma glucagon level must be considered as a key hormonal factor responsible for natriuresis attending starvation. Indeed, the concomitant reduction in plasma glucagon and insulin levels, resulting from somatostatin infusion on day 4 of fast, was followed by significant increase in natriuresis. The latter observation supports several previous studies indicating that insulin stimulates sodium reabsorption by the kidney and that the reduction in insulin secretion may induce an increase in renal sodium excretion. It was concluded, therefore, that not only sodium intake but also the carbohydrate content of the diet should be reduced in an attempt to induce a negative sodium balance and to correct hypertension in obese subjects.

3-Hydroxybutyric Acid↗

PubMedDate not supplied

In vivo evidence for a defect in the dopamine DA1 receptor in the prehypertensive Dahl salt-sensitive rat.

A defective dopamine DA1 receptor has been suggested to be involved in the salt-sensitive hypertension in Dahl-S rats (DS). To investigate the consequences of this defect, the influence of DA1 receptor blockade (SCH23390) and of dopamine-synthesis inhibition (benserazide) on volume expansion (VE)-induced sodium and dopamine excretion was studied in anesthetized prehypertensive DS and salt-resistant Dahl rats (DR). Under control conditions all measured variables were equal in DR and DS. During VE (5% of BW), sodium and dopamine excretion increased similarly in the two strains. During peak natriuresis mean arterial blood pressure was 119 +/- 3 and 122 +/- 3 mm Hg, respectively. In DR treated with SCH23390, sodium excretion was only 72% of that in vehicle-treated DR. Dopamine excretion increased, however, as in vehicle-treated DR. In DS, treatment with SCH23390 did not attenuate natriuresis and dopamine excretion also increased as in vehicle-treated DS. In benserazide-pretreated DR and DS, sodium excretion during VE was similar, but only 50-51% of that in the respective vehicle-treated group. Dopamine excretion decreased by about 80% in both strains. In conclusion, prehypertensive DR and DS have a similar capacity to acutely excrete an intravenous saline load and to generate dopamine. The total dopamine involvement in VE-induced natriuresis is also comparable in the two strains, but the natriuresis mediated by DA1 receptors is pronounced in DR and non-existent in DS.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

PubMed1998

Factors determining cardiac hypertrophy in hypertensive patients with or without peripheral vascular disease.

1. Coronary ischaemic disease and congestive heart failure are the principal causes of mortality in patients with peripheral vascular disease. Whether cardiac hypertrophy is present and even more pronounced in peripheral vascular disease than in other populations has never been explored.2.Twenty-five hypertensive patients were investigated, 11 without and 14 with peripheral vascular disease, matched for age, sex, mean arterial pressure and antihypertensive drug treatment. Cardiac mass was determined using echocardiography together with measurement of systemic blood pressure, ratio between ankle systolic pressure (ASP) and brachial systolic pressure (BSP), and standard biochemical parameters including natriuresis per 24 h.3. At the same mean arterial pressure, patients with peripheral vascular disease had a significantly higher cardiac mass (157+/-12 versus 116+/-6 g/m2; P<0.01), pulse pressure (81+/-5 versus 55+/-4 mmHg; P<0.01) and natriuresis (180+/-17 versus 144+/-6 mmol/24h; P<0. 01) than controls. Using univariate correlations, cardiac mass was positively associated with pulse pressure, mean arterial pressure and natriuresis, and negatively with the ASP/BSP ratio. On the basis of multivariate regression analysis, only natriuresis was positively correlated to cardiac mass.4. Patients with peripheral vascular disease develop a higher degree of cardiac hypertrophy in comparison with hypertensive subjects with the same level of mean arterial pressure. Sodium intake rather than mechanical factors seems to be the major modulating factor which influences the degree of cardiac hypertrophy.

Aged↗

PubMed1990

Saluretic effect of the loop diuretic torasemide in chronic renal failure. Interdependence of electrolyte excretion.

The effects of torasemide have been studied in 7 healthy controls and 9 patients with stable chronic renal failure of various degrees. After a control period of 3 days torasemide 20 mg i.v. caused a dramatic increase in diuresis and electrolyte excretion without affecting the glomerular filtration rate. The duration of action of torasemide, tau, averaged 6 h and was independent of the creatinine clearance, CLCR. When related to tau the drug-induced excretion of Cl-, Na+, K+, Ca2+ and Mg2+ showed strong linear dependence on CLCR. Both the kaliuresis and the calciuresis during tau were tightly correlated with the natriuresis over the broad range of CLCR. Similarly, the excretion of Mg2+ was dependent on the kaliuresis. The torasemide-induced kaliuresis amounted to 12% of natriuresis, as after furosemide. The kaliuretic effect of loop diuretics is smaller than that of the thiazides. After tau, e.g. over a 24 h period, kaliuresis was not correlated with natriuresis. The magnitude of the rebound effect was diminished with increasing renal impairment.

Adult↗

PubMed1990

The role of posture on the changes in plasma atrial natriuretic factor and arginine vasopressin levels during immersion.

In seven healthy male volunteers we investigated changes in plasma atrial natriuretic factor [( ANF]), arginine vasopressin [( AVP]) and plasma volume (PV) during supine immersion. Twenty minutes head-out water immersion in a supine position in a thermo-neutral water bath attenuated the increase in PV induced by 20 min in a supine position in air, but increased the mean plasma [ANF] from 32.0 pg.ml-1, SEM 5.1 to 53.3 pg.ml-1, SEM 3.6 and decreased the mean plasma [AVP] from 1.4 pg.ml-1, SEM 0.1 to 0.9 pg.ml-1, SEM 0.04. Simultaneously, diuresis and natriuresis increased markedly. During a 20-min control period in the supine posture without immersion, PV, plasma [ANF] and [AVP] remained unaffected while diuresis and natriuresis did not increase to the same extent. These data suggest that an increase in the central blood volume induced by a weak external hydrostatic pressure during supine immersion triggered the changes in plasma [ANF] and [AVP] and that the increase was probably due to a shift of blood volume from peripheral to central vessels. The changes in plasma [ANF] contributed to the changes in natriuresis.

Adult↗

PubMed1995

Furosemide dynamics in conscious rabbits: modulation by arginine vasopressin.

The aims of this study were to assess the influence of arginine-vasopressin (AVP) on the pharmacodynamics and kinetics of furosemide. To this purpose, the response and the kinetics of furosemide (5 mg/kg i.v.) were studied in two groups of rabbits, one control and one receiving an infusion of AVP (2.5 ng/kg/min). The infusion of AVP generated mean plasma levels of 35 pg/ml, and in these rabbits osmolal clearance was increased, free water clearance was reduced, and renal plasma flow was reduced by 25% (p < 0.05). High AVP plasma levels increased the natriuresis (p < 0.01) and the urinary excretion of prostaglandin E2 (UPgE2V; p < 0.01). The increase in UPgE2V was associated with AVP plasma concentrations (r = 0.8248; p < 0.001). AVP reduced the increment in natriuresis and diuresis elicited by furosemide from 163 +/- 20 to 87 +/- 20 mumol/min (p < 0.05) and from 1.22 +/- 0.11 to 0.83 +/- 0.13 ml/min (p < 0.05). The infusion of AVP enhanced furosemide metabolic clearance but diminished its renal clearance, resulting in a decrease in the rate of furosemide urinary secretion. It was concluded that high plasma levels of AVP reduce furosemide natriuresis, presumably because of a decrease in furosemide urinary secretion.

Analysis of Variance↗

PubMed1990

Drag-reducing polymers: a novel class of diuretic and natriuretic compounds.

Previous studies have demonstrated that Separan AP-30, a drag-reducing polymer, significantly decreased the formation of atherosclerotic plaques in rabbits fed a high-cholesterol diet. Furthermore, Separan AP-273, a polymer similar to but longer than Separan AP-30, markedly increased cardiac output in open-chest rats. Preliminary studies in our laboratory have described diuresis and natriuresis following the intravenous infusion of Separan AP-273. These studies did not determine whether this natriuresis was common to drag-reducing polymers or unique to Separan. In the present study the renal effects of two chemically dissimilar drag-reducing polymers of molecular lengths approaching approximately 100 microns were compared. Sprague-Dawley rats (250-300 g) were anesthetized (Nembutal) and a tracheostomy was performed. A baseline level of sodium and water excretion was established by the infusion of saline (0.097 ml/min, IV). Separan (0.004%), an anionic polyacrylamide; Polyox (0.4%), a poly(ethylene oxide); or mannitol (20%), an osmotic diuretic, was infused into the jugular vein at 0.0034 ml/min. Separan and Polyox both increased the excretion of sodium and water (p less than 0.05). At the doses tested, potassium excretion was unaltered in both groups. Separan, but not Polyox, produced a modest increase in blood pressure. Creatinine clearance was unaltered. At this infusion rate, only hypertonic concentrations of mannitol (20%) induced a similar effect. These results indicate that drag-reducing polymers may represent a novel class of potassium-sparing diuretic and natriuretic compounds. The ability of this class of polymers to decrease the formation of atherosclerotic plaques, increase blood flow, and produce a potassium-sparing natriuresis may be of practical clinical significance.

Acrylic Resins↗

PubMed1992

Dehydration increases the renal response to atrial natriuretic peptide in fetal sheep.

OBJECTIVE: In sheep, maternal water deprivation results in urinary natriuresis in spite of suppression of plasma atrial natriuretic factor levels. Near-term fetal sheep also have a urinary natriuresis without change in plasma atrial natriuretic factor during maternal dehydration. This study was designed to explore the role of plasma atrial natriuretic factor levels in fetal dehydration-natriuresis. STUDY DESIGN: Eight chronically instrumented preterm (113 +/- 1 days) ovine fetuses received two atrial natriuretic factor infusions (3 and 15 ng/kg/min) in a euhydrated state and after 48 +/- 1 hours of maternal water deprivation. RESULTS: Dehydration significantly increased maternal plasma osmolality (302 +/- 2 to 313 +/- 2 mOsm/kg water), sodium (148.1 +/- 0.8 to 154.3 +/- 0.4 mEq/L), chloride (112.4 +/- 0.6 to 116.8 +/- 0.9 mEq/L), and arginine vasopressin (4.2 +/- 1.2 to 23.0 +/- 4.0 pg/ml) and significantly decreased plasma atrial natriuretic factor (36 +/- 6 to 19 +/- 4 pg/ml) concentrations. Fetal plasma osmolality (296 +/- 1 to 308 +/- 2 mOsm/kg), atrial natriuretic factor (128 +/- 16 to 241 +/- 36 pg/ml), and arginine vasopressin (3.5 +/- 0.8 to 12.3 +/- 4.8 pg/ml) concentrations and urine osmolality (170 +/- 10 to 253 +/- 10 mOsm/kg), osmolar clearance (0.80 +/- 0.02 to 0.14 +/- 0.02 ml/kg/min), and fractional sodium excretion (3.3% +/- 1.7% to 8.5% +/- 2.1%) increased significantly with dehydration, whereas the plasma atrial natriuretic factor clearance decreased from 127 +/- 27 to 63 +/- 10 ml/kg/min. Dehydration had no effect on fetal hematocrit, vascular pressures, glomerular filtration rate, urine flow, or free water clearance. In euhydrated fetuses plasma atrial natriuretic factor increased from 128 +/- 16 to 287 +/- 46 pg/ml with sequential atrial natriuretic factor infusion, and no significant increases were observed in urine flow, fractional sodium excretion, and glomerular filtration rate. In contrast, atrial natriuretic factor infusion to dehydrated fetuses significantly increased urine flow (0.17 +/- 0.03 to 0.32 +/- 0.07 ml/kg/min), osmolar clearance (0.14 +/- 0.02 to 0.28 +/- 0.06 ml/kg/min), and fractional sodium excretion (8.5% +/- 2.1% to 14.8% +/- 4.0%). CONCLUSION: These results demonstrate that in the fetus at 113 days' gestation plasma atrial natriuretic factor levels increase with dehydration, probably a result of decreased plasma atrial natriuretic factor clearance, and the fetal renal responsiveness to atrial natriuretic factor infusion increases during maternal dehydration.

Animals↗

PubMed1986

The rapid adjustment of renal sodium excretion to changes in dietary sodium intake in sheep.

The rapidity with which the kidney alters sodium excretion (ENa) in response to changes in dietary Na was studied in Merino sheep by analyzing hourly ENa for three control days, and then for three days after a change in Na intake. On a control diet of 117 mmol Na, sheep had a pre-feeding ENa of 3.5 mmol/hr., a striking post-feeding natriuresis that began 2 hours after feeding (less than 0.01), peaked at 4 hrs. and then declined to pre-feeding levels 7 hrs. after feeding. When in balance on a high Na diet the feeding of a low Na meal resulted in marked depression of ENa within 4 hours after feeding. On a low Na diet, a 100 mmol Na meal resulted in an increase in ENa within 4 hours but a 50 mmol Na meal did not. Thus, the sensitivity of post-feeding natriuresis is between 50 and 100 mmols Na. As post feeding natriuresis is a naturally occurring physiological event it should provide a useful paradigm for the investigation of mechanisms controlling Na balance.

Animals↗

PubMed1993

Endogenous natriuretic factors 1: sodium pump inhibition does not correlate with natriuretic or pressor activities from uremic urine.

It is our purpose to isolate and characterize the putative "Natriuretic Hormone", ostensibly responsible for ECF homeostasis, as well as identify endogenous pressors and compounds that induce prolonged natriuresis; we report here our initial progress in this area. Large volumes of pooled urine collected from uremic patients were fractionated, and the resulting isolates were evaluated for in vivo natriuretic and pressor effects and Na+/K(+)-ATPase inhibitory activity in renal cells. The purification steps involved ultrafiltration to obtain materials of less than 3000 da, gel filtration, and sequential reversed-phase high performance liquid chromatography (HPLC). After each HPLC step, the fractions were evaluated for their ability to elicit significant natriuresis and/or influence mean arterial pressure in the normal conscious female rat. Each fraction was also assayed for its ability to inhibit Na+/K(+)-ATPase as determined by the inhibition of 86Rb+ uptake into MDBK renal cells. While several of the fractions elicited profound natriuresis and/or pressor activity and other fractions inhibited Na+/K(+)-ATPase, there was no correlation among the activities in individual fractions. We have concluded that this plethora of bioactivities is responsible for much of the confusion and multiplicity of crude isolates claimed to be the putative hormone. Presently we are attempting to purify each of these activities to chemical homogeneity for structure determination.

Animals↗

PubMed1988

Effect of protein intake and urea on sodium excretion during inappropriate antidiuresis in rats.

Administration of urea to patients with the syndrome of inappropriate antidiuresis (SIAD) is thought to ameliorate hyponatremia by both producing an osmotic diuresis and diminishing ongoing natriuresis. The present study evaluated these effects in a rat model of SIAD utilizing dilutional hyponatremia induced by continuous infusion of 1-deamino-[8-D-arginine] vasopressin. Following 48 hours of sustained hyponatremia, separate groups of rats were then refed with either: (1) 5% dextrose alone, (2) a 20% protein chow, (3) an isocaloric protein deficient (0%) chow, or (4) the isocaloric protein-deficient chow supplemented with oral urea. Our results demonstrate that rats refed a 20% protein diet significantly improved their plasma [Na+] as compared to rats refed protein deficient diets, and this improvement was accompanied by decreases in natriuresis despite an increased glomerular filtration rate and an unchanged negative free water clearance. Identical effects were observed in rats refed a protein deficient diet but supplemented with oral urea, suggesting that urea generation from catabolism of dietary protein is responsible for the effect of protein refeeding to decrease urinary sodium excretion. Both the protein and urea refed rats had significantly higher inner medullary urea contents and concentrations compared to rats refed protein-deficient diets and also to rats studied immediately before protein refeeding, supporting the hypothesis that urea and dietary protein decrease natriuresis in patients with SIAD in association with increased inner medullary urea concentrations.

Animals↗

PubMed1996

Antihypertensive effect of thymectomy in Lyon hypertensive rats. Vascular reactivity, renal histology, and sodium excretion.

The aim of this study was to search for the possible mechanisms involved in the antihypertensive effect of neonatal thymectomy that we previously observed in Lyon hypertensive (LH) rats. To that end, we studied in LH and normotensive control (LN) rats the consequences of neonatal thymectomy on vascular reactivity, renal structure, and pressure-natriuresis. The increase in pressor responses to angiotensin I and phenylephrine noted in LH rats as compared to LN animals was abolished by neonatal thymectomy. Histological study showed that kidneys from LH rats exhibited arterial wall hypertrophy, segmental hyalinization of the glomeruli, and were infiltrated by mononuclear cells. All these features of kidney injury were reduced in neonatally thymectomized LH rats. Lastly, the responses of isolated perfused kidneys from LH rats to stepwise reductions in renal perfusion pressure differed from those of LN rats by decreased renal perfusion flow and natriuresis. Neonatal thymectomy tended to improve sodium excretion in parallel with a slight decrease in renal vascular resistances. It is concluded that the normalization of vascular responsiveness to vasoconstrictor factors, the alleviation of renal lesions and, to a lesser extent, the moderate improvement of pressure natriuresis may account, at least in part, for the antihypertensive effect of neonatal thymectomy in LH rats.

Animals↗

PubMed1988

Strategies for the in vivo inhibition of endogenous atriopeptin.

Pharmacological strategies have been employed to manipulate the response to atriopeptin (AP-28; ANF 99-126) in rats. These approaches include: heparin infusion which blocks the natriuresis-diuresis produced by exogenous AP infusion or by acute volume expansion; and autoimmune rats with endogenous antibody that blocks the natriuresis-diuresis produced by administration of exogenous AP or by acute volume expansion in anesthetized rats. Administration of the pressor analog 1-deamino-arg8-vasopressin (dAVP) to rats produces an elevation in systemic and right atrial blood pressure and markedly increases atriopeptin blood levels. The dAVP also produces a delayed natriuresis-diuresis which is effectively blunted in the autoimmune or heparin treated rats. The above approaches provide tools, in the absence of a specific receptor antagonist, with which to validate the intrinsic involvement of AP in physiological, pharmacological, or pathophysiological events.

Animals↗