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PubMed1988

Additive and synergistic interaction of atrial natriuretic peptide and volume expansion.

To investigate whether atrial natriuretic peptides (ANP) are entirely responsible for the natriuresis of volume expansion (VE), we studied the natriuresis from acutely snared and nonsnared kidneys of rats undergoing sustained saline VE and subsequent infusion of maximal doses of ANP (atriopeptin II), or vice versa. Fractional excretion of Na (FENa) was increased from control (0.15 +/- 0.03%) to 4.6 +/- 0.6% by VE and to 10.9 +/- 1.5% by subsequent ANP infusion. With ANP alone FENa increased from control (0.24 +/- 0.04%) to 2.6 +/- 0.3%, and to 10.8 +/- 0.9% with VE, showing additive effects by both. Natriuresis with VE was significantly greater than with ANP alone (P less than 0.01) and both exhibited synergism, producing significantly greater natriuresis in the presence of the other than alone (P less than 0.05 for both). A reduction in perfusion pressure inhibited the effects of ANP and reduced that of VE. Natriuresis was produced by ANP independently of changes in glomerular filtration rate. It is concluded that 1) VE and ANP produce natriuresis by different renal mechanisms and that therefore, ANP can only account for part of the natriuresis of sustained VE; 2) the two have a synergistic interaction on natriuresis, probably through an intrarenal mechanism.

Animals↗

PubMed1998

Acute volume expansion and salt-loading studies in rats. The role of atrial natriuretic peptide and catecholamines.

Differences have been postulated for the mechanism of natriuresis due to atrial natriuretic peptide (ANP), salt loading with high salt diet (HS) and acute volume expansion (AcVE), in particular between AcVE and ANP based on the observed synergism between the two. Therefore the effects of and the interaction between the three were investigated in rats. ANP and AcVE produced the same natriuresis in HS as in normal salt (NS) rats and, in both, the actions of ANP and AcVe were significantly additive showing similarity in mechanisms. Synergism [(AcVE + ANP) - AcVE] was, however, present only in the NS rats. Proximal tubular sodium transport was the same with AcVE and ANP+AcVE suggesting that synergism is a property of more distal nephron segments. In conscious HS rats, plasma ANP was significantly less but natriuresis was higher than in NS rats. ANP therefore probably has some causative role in the natriuresis of AcVE but none in that of HS loading. Urinary dopamine was significantly increased by HS and further increased by AcVE in both NS and HS rats, the relationship between dopamine and natriuresis being significantly positive (r2 = 0.328) reaching equivalent levels in both NS and HS rats. Systemic benserazide prevented the increase in urinary dopamine but only attenuated the natriuresis of AcVE. We conclude that HS does not potentiate the natriuresis of AcVE or ANP, synergism between AcVE and ANP is not a proximal tubule event and dopamine accounts for significant natriuresis of VE in addition to other natriuretic factors.

Animals↗

PubMed2000

Neuropeptide Y enhances potassium excretion by mechanisms distinct from those controlling sodium excretion.

Neuropeptide Y (NPY) is an established modulator of renal function. Although NPY reduces renal blood flow and does not alter glomerular filtration rate, it enhances diuresis and natriuresis. Although initial studies on natriuresis did not detect kaliuresis, we now report that a retrospective analysis of previous studies regarding natriuresis demonstrates NPY-induced kaliuresis under several experimental conditions. Kaliuresis was observed despite a marked reduction in urinary potassium concentrations, which may explain why it has not been noted in some initial studies. In a direct comparison of NPY-induced kaliuresis and natriuresis, both effects were slow in onset (requiring >45 min to develop fully) and blocked by the cyclooxygenase inhibitor indomethacin. While natriuresis occurred solely via a Y5 receptor, kaliuresis involved a Y1 receptor and an additional receptor subtype, possibly Y2. The L-type Ca2+ entry blocker nifedipine abolished natriuresis but did not inhibit kaliuresis. A combination of experiments with the bradykinin B2 receptor antagonist icatibant, the angiotensin II receptor antagonist losartan, and the converting enzyme inhibitor ramiprilat revealed that NPY-induced natriuresis involves bradykinin while kaliuresis involves angiotensin II. We conclude that NPY-induced kaliuresis is much less pronounced than natriuresis and is mediated by distinct mechanisms.

Aldosterone↗

PubMed1992

Stress-induced changes in the rate of sodium excretion in healthy black and white men.

The effects of exposure to competitive mental stressors on rates of excretion of sodium (Na), potassium (K) and fluid, together with cardiovascular responses, were evaluated in 14 black and 14 white normotensive men after 3 days of controlled diet (200 mEq Na, 100 mEq K daily). In the first hour of a 5-hr protocol, subjects ingested a standard dinner and drank 1 liter of water. In hours 2-5, they voided to provide urine collections every 30 min, and drank 200 ml additional water after each collection. Hours 1-2 were for stabilization of excretion, hour 3 was baseline, hour 4 was stress and hour 5 was post-stress rest. During stress, 20 men showed faster natriuresis and 8 showed slower natriuresis than at baseline. These subgroups did not differ in any excretion measure at baseline. During stress, the slow stress natriuresis group showed slower excretion of potassium and fluid as well as sodium; slow natriuresis and kaliuresis persisted 30 min after stress. Creatinine clearance rate was also decreased, but only during the first 30 min of stress. Slow stress natriuresis subjects were found to have higher blood pressures during baseline and stress, greater heart rate and cardiac output increases during stress, and a larger percentage had hypertensive parents (63 vs 37%) compared to fast stress natriuresis subjects. Slow stress natriuresis was observed in 50 vs 17% of men with resting diastolic levels above vs below 80 mmHg, and in 43% of blacks vs 18% of whites tested. Overall, black subjects tended to excrete sodium more slowly than whites at baseline, and showed significantly lesser increases in sodium excretion rate when pressures rose during stress.

Adult↗

PubMed1999

Diuretics in cardiovascular therapy: the new clinicopharmacological bases that matter.

Diuretics in current use include early distal tubular (i.e., thiazide-type), loop (i.e., furosemide-type), and potassium-and-hydrogen-retaining substances. Available oral formulations of diuretics differ in terms of their renal excretory potency in man, as formally assessed through the effect of a single dose on 24-hour natriuresis in healthy subjects. The 2.5 mg formulation of the loop diuretic torasemide does not increase mean 24-hour natriuresis, and it is therefore considered a very-low-dose formulation. Amiloride 5 mg and torasemide 5 mg and 10 mg, which increase mean 24-hour natriuresis by less than 40%, are considered low-dose or low-potency diuretic formulations of diuretic substances. Hydrochlorothiazide 25 and 50 mg, furosemide 40 and 80 mg, and torasemide 20 mg, which increase mean 24-hour natriuresis by more than 40%, are considered high-dose or high-potency formulations. A rebound in natriuresis follows the early-after-dosing increase in this variables caused by loop diuretics; hence many oral formulations of loop substances are less potent natriuretics than most oral formulations of thiazide-type diuretics. Hydrochlorothiazide 25 mg and furosemide 80 mg have similar natriuretic potencies. During once-daily administration of diuretic formulations of diuretics to subjects without edema and normal renal function, the increases in 24-hour natriuresis and diuresis that follow the first dose disappear or attenuate markedly. This is due to neuroendocrine reactions to diuretic-induced sodium loss and its attendant hemodynamic shifts. Some of these reactions, e.g. the increase in plasma aldosterone that takes place, account for an elevation in kaliuresis that occurs during once-daily treatment with a high-dose formulation of a thiazide-type diuretic. Common fixed-dose combinations of a thiazide-type or a loop diuretic and a potassium-and-hydrogen-retaining substance generally do not change kaliuresis, but they increase natriuresis strikingly. Thiazide-type and loop diuretics decrease and increase calciuresis respectively; none of these actions wanes during prolonged administration. Plasma renin activity and aldosterone do not rise in response to very-low-dose formulations of loop diuretics taken once daily. Glomerular filtration rate tends to fall in the course of once-daily administration of high-dose formulations of diuretics, but not during prolonged once-daily treatment with very-low-dose formulations of loop diuretics.

Aldosterone↗

PubMed1986

Humoral control of water and electrolyte excretion during water restriction.

The goals of the present study were twofold: first, to assess the renal excretory and hormonal responses to chronic water restriction in dogs whose sodium retaining mechanisms had been stimulated through dietary sodium (Na+) deprivation; second, to determine the mediator(s) of the natriuresis which was observed with water restriction in these sodium deprived dogs. Three groups of dogs maintained on a low Na+ diet (5 mEq/day) for two weeks underwent a three day period of water restriction. In normal, intact dogs Group 1 (N = 5), water restriction resulted in a significant increase in Na+ excretion with a net cumulative loss of 26.3 +/- 2.6 mEq over three days. The natriuresis was associated with a significant increase in plasma vasopressin (PAVP) (1.7 to 10.2 pg/mliter) and a significant fall in plasma aldosterone (PALDO) from the levels observed with Na+ restriction alone (24.9 to 12.4 ng/dliter). The natriuresis could not be explained by decreases in food intake as determined by control studies in four dogs. Group 2 (N = 6) dogs had a decrease in PALDO with water restriction that was prevented by means of continuous i.v. aldosterone infusion (6.0 micrograms/kg/day). Dogs in this group failed to demonstrate a natriuresis during three days of water restriction, despite the fact that PAVP rose from 3.3 +/- 0.8 to a peak level of 14.95 +/- 1.9 pg/mliter. Group 3 (N = 6) dogs underwent selective neurohypophysectomy, thus preventing the rise in PAVP during three days of water restriction. In this group, PALDO also remained unchanged from the Na+ deprived level during water restriction, and no natriuresis was observed. We conclude: 1) that the natriuresis which occurs with water restriction is a potent physiological response that occurs even in the Na+ restricted state; and 2) this natriuresis can be explained by a fall in PALDO and not the rise in PAVP.

Aldosterone↗

PubMed1989

Arginine vasopressin potentiates natriuretic effect of atrial peptide.

We investigated potentiation of atrial peptide (AP)-induced natriuresis by vasopressin in anesthetized rats. Increasing doses of vasopressin potentiated AP-induced natriuresis in a dose-dependent manner, e.g., sodium excretion during AP administration (290 ng/min) was 0.66 +/- 0.16, 2.02 +/- 0.68, 5.21 +/- 1.38 and 7.08 +/- 1.96 mu eq/min during infusion of 0.00, 0.78, 1.56, and 3.12 ng.kg-1.min-1 of vasopressin, respectively. Vasopressin alone had no effect on sodium excretion. In a second experiment, vasopressin (1.56 ng.kg-1.min-1) potentiated AP (128 ng/min)-induced natriuresis similar to that seen in the first experiment. In this experiment, glomerular filtration rate (GFR) and mean arterial pressure were monitored. Mean arterial pressure was no different between the groups treated with AP plus vasopressin and AP alone. Glomerular filtration was actually reduced in the group treated with vasopressin plus AP, suggesting that neither changes in GFR nor blood pressure were responsible for potentiation of the natriuresis. A third experiment compared the ability of 1-desamino-8-D-arginine vasopressin (dDAVP), a nonpressor analogue of vasopressin, to vasopressin in enhancing AP (145 ng/min)-induced natriuresis. The nonpressor analogue did not potentiate AP-induced natriuresis, whereas vasopressin had the same effect as in the first two experiments. These are the first studies to report a functional interaction between AP and vasopressin. They show that vasopressin potentiates AP-induced natriuresis without altering mean arterial pressure or GFR.

Animals↗

PubMed1996

Pressure-volume regulation in hypertension.

In all forms of hypertension, including human essential hypertension, pressure natriuresis is abnormal because sodium excretion is the same as in normotension despite increased arterial pressure. Considerable evidence indicates that this resetting of pressure natriuresis plays a key role in causing hypertension, rather than merely occurring as an adaptation to increased blood pressure. Because human essential hypertension is a heterogeneous disease, it is likely that multiple neurohumoral and intrarenal defects contribute to abnormal pressure natriuresis and increased blood pressure. Physiological studies have shown that renal abnormalities that cause increased distal and collecting tubule reabsorption, decreased glomerular filtration coefficient or loss of nephrons also cause decreased slope of pressure natriuresis (salt-sensitive hypertension), whereas increased preglomerular resistance causes a parallel shift of pressure natriuresis (salt-insensitive hypertension). Comparison of the characteristics of pressure natriuresis (such as salt-sensitivity of blood pressure) in hypertensive subjects with those forms of experimental hypertension of known origin can provide insight into the etiology of human hypertension. With long-standing hypertension, pathological changes in the glomeruli and renal arterioles may further shift pressure natriuresis and exacerbate hypertension.

Animals↗

PubMed1993

Renal excretory responses to single and repeated administration of diuretics in healthy subjects: clinical connotations.

Administration of an initial oral dose of hydrochlorothiazide 25 mg to healthy subjects is followed by increased 24-hour urinary outputs of sodium, chloride, and potassium. On the fourth day of once-daily dosing with hydrochlorothiazide 25 mg, 24-hour natriuresis and chloriuresis are no longer augmented, but the elevation in 24-hour kaliuresis that follows the first dose remains unchanged. Twenty-four-hour urinary calcium output is consistently reduced during repeated once-daily administration of hydrochlorothiazide 25 mg. The first oral dose of the loop diuretic torasemide augments the average natriuresis and kaliuresis in the 6 hours immediately after dosing in healthy subjects, in a dose-dependent fashion, within the 2.5 to 10-mg range. These increased urinary outputs are followed by rebounds below postplacebo values between 6 and 24 hours after dosing. As a result of this biphasic response, torasemide 2.5 mg qualifies as a nondiuretic formulation (it does not elevate 24-hour natriuresis), whereas torasemide 5 and 10 mg qualify as diuretic formulations. After the seventh dose of torasemide 5 or 10 mg during a regimen of once-daily therapy, 24-hour urinary sodium and chloride outputs no longer differ from their postplacebo counterparts. Twenty-four-hour kaliuresis tends to increase in a dose-dependent fashion after the first dose of torasemide (torasemide 2.5 and 5 mg do not augment it significantly), but this tendency is no longer present after the seventh once-daily dose, when torasemide (2.5, 5, or 10 mg) does not elevate the mean 24-hour kaliuresis. Twenty-four-hour calciuresis tends to increase in a dose-dependent manner (torasemide 2.5 mg does not elevate it significantly) after the first dose of torasemide; this calciuretic effect does not change in intensity after 7 days of once-daily treatment. The time course of natriuresis over the 24 hours following the administration of any given formulation of a loop or of an early distal tubular diuretic to healthy subjects is alike after the first and after the nth once-daily dose; therefore, it constitutes a definite characteristic of any given oral formulation. In the case of torasemide, lower doses have more protracted effects on natriuresis, to the extent that the time course of natriuresis over the 24 hours after administration of torasemide 2.5 mg to healthy subjects resembles the time course after administration of hydrochlorothiazide 25 mg, rather than the time course after administration of the overtly diuretic formulation torasemide 10 mg.

Calcium↗

PubMed1997

Mechanism of the natriuretic action of gamma-melanocyte-stimulating hormone.

To explore the mechanism underlying the natriuretic effect of gamma-melanocyte-stimulating hormone (gamma-MSH), we infused the peptide intravenously at 200 pmol/min into anesthetized rats. gamma-MSH led to a progressive increase in urinary sodium excretion (UNaV), whereas continuous infusion of the vehicle did not affect UNaV. Plasma immunoreactive gamma-MSH was nine times greater at 120 min after the start of the infusion than in vehicle-infused rats. Plasma atrial natriuretic peptide (ANP) concentration also increased as a consequence of the gamma-MSH infusion, and a strong correlation existed between the concentrations of the two peptides (n = 17, r = 0.81, P < 0.001). Urinary excretion of guanosine 3',5'-cyclic monophosphate and adenosine 3',5'-cyclic monophosphate increased as a result of the infusion. Antiserum to rat ANP blunted the natriuresis only slightly, suggesting that the increase in plasma ANP concentration was not a critical element in gamma-MSH natriuresis. gamma-MSH had no effect on ANP release from isolated rat right atrial strips superfused in vitro. Infusion of gamma-MSH (500 fmol/min) directly into one renal artery led to an ipsilateral natriuresis without change in UNaV from the contralateral kidney. Prior denervation of the infused kidney prevented the natriuresis resulting from intrarenal infusion. Intrarenal infusion of ANP (800 fmol/min) also produced ipsilateral natriuresis, which, however, was not affected by renal denervation. These studies confirm that the natriuretic action of gamma-MSH occurs primarily by an interaction with the renal nerves. Intravenous infusion of the peptide sufficient to produce a supraphysiological plasma gamma-MSH concentration also results in an increase in plasma ANP concentration; however, this increase at best plays only a minor role in the natriuresis following intravenous gamma-MSH infusion.

Animals↗

PubMed2003

The kidney, hypertension, and obesity.

This paper provides a personal perspective of the role of abnormal renal-pressure natriuresis in the pathogenesis of hypertension. Direct support for a major role of renal-pressure natriuresis in long-term control of arterial pressure and sodium balance comes from studies demonstrating that (1) pressure natriuresis is impaired in all forms of chronic hypertension and (2) prevention of pressure natriuresis from operating, by servo-control of renal perfusion pressure, also prevents the maintenance of sodium balance hypertension. Although the precise mechanisms of impaired pressure natriuresis in essential hypertension have remained elusive, recent evidence suggests that obesity and overweight may play a major role. Obesity increases renal sodium reabsorption and impairs pressure natriuresis by activation of the renin-angiotensin and sympathetic nervous systems and by altered intrarenal physical forces. Chronic obesity also causes marked structural changes in the kidneys that eventually lead to a loss of nephron function, further increases in arterial pressure, and severe renal injury in some cases. Although there are many unanswered questions about the mechanisms of obesity hypertension and renal disease, this is one of the most promising areas for future research, especially in view of the growing, worldwide "epidemic" of obesity.

Blood Pressure↗

PubMed1987

Effects of atrial natriuretic peptides and furosemide in conscious dogs.

Effects of ANF(8-33) and Auriculin A on renal variables were investigated in conscious water-diuretic dogs. The two substances were injected intravenously (1.08 micrograms/kg in 3 min) or ANF(8-33) was infused (0.2 microgram/kg X min in 20 min). The effects were compared to those of an equinatriuretic dose of furosemide (1.0 microgram/kg X min). Injections caused increases in sodium excretion, diuresis, and osmolar clearance. No significant change in exogenous creatine clearance (CCREA) occurred. Infusion of ANF(8-33) decreased blood pressure by 14% (P less than 0.01) and increased sodium excretion by a factor of 10 (P less than 0.01). The natriuresis was a function of increases in diuresis and urinary sodium concentration, the latter by a factor of 6 (P less than 0.01). Diuresis and free-water clearance (CH2O) increased by 60% (P less than 0.01), but urine osmolality did not change significantly. After the infusion a significant decrease in PAH clearance (CPAH) (P less than 0.01) was observed. Filtration fraction (FF) did not change. The furosemide natriuresis appeared later than that of ANF without significant deviations in diuresis, CH2O, CCREA, CPAH, and FF; urine osmolality increased by 35% (P less than 0.01). The effects of ANF(8-33) differ from those of furosemide in several ways. First, the onset of natriuresis is faster, second, the natriuresis is associated by marked increases in diuresis and free-water clearance but not in urine osmolality; and third, natriuresis is followed by a reduction in renal blood flow. The rapid natriuresis of ANF can occur without changes in glomerular filtration rate.

Animals↗

PubMed1997

Receptor subtypes Y1 and Y5 are involved in the renal effects of neuropeptide Y.

1. Systemic infusion of neuropeptide Y (NPY) reduces renal blood flow and can concomitantly increase diuresis, natriuresis and calciuresis in anaesthetized rats. The present study was designed to investigate whether the apparently contradictory NPY effects on renal blood flow and urine formation and composition are mediated by distinct NPY receptor subtypes. 2. NPY and its analogues, peptide YY (PYY), [Leu31, Pro34]NPY and NPY13-36, were infused in incremental doses of 0.3, 1 and 3 micrograms kg-1 min-1 for 45 min each and the results compared to those obtained in vehicle-infused rats. Renal blood flow was monitored in 1-5 min intervals, while urine excretion and composition were determined in 15 min collection periods. Plasma renin activity and aldosterone concentrations were measured at the end of the final infusion period. 3. Relative to vehicle NPY, PYY and [Leu31, Pro34]NPY dose-dependently reduced renal blood flow and increased diuresis, natriuresis and calciuresis with roughly similar potency; NPY13-36 slightly but significantly increased renal blood flow but had no effect on diuresis, natriuresis and calciuresis. None of the peptides significantly affected endogenous creatinine clearance or kaliuresis. 4. Plasma renin activity was significantly reduced by PYY. Quantitatively similar reductions were observed with NPY and [Leu31, Pro34]NPY but failed to reach statistical significance with the given number of experiments. NPY13-36 did not reduce plasma renin activity. None of the peptides significantly affected plasma aldosterone concentrations. 5. In another series of experiments infusion of PYY3-36 (2 micrograms kg-1 min-1 for 120 min) did not reduce renal blood flow but significantly enhanced diuresis and natriuresis to a similar extent as the NPY 2 micrograms kg-1 min-1. 6. In a final series of experiments the Y1-selective antagonist, BIBP 3226 (1 or 10 micrograms kg-1 min-1) dose-dependently antagonized reductions of renal blood flow elicited by bolus injections of NPY (0.1-30 micrograms kg-1). BIBP 3226 (10 micrograms kg-1 min-1) also inhibited the effects of a 120 min infusion of NPY (2 micrograms kg-1 min-1) on renal blood flow but had only minor inhibitory effects on enhancements of diuresis and did not significantly affect enhancements of natriuresis. 7. We conclude that NPY reduces renal blood via a classical Y1 subtype of NPY receptor. In contrast enhancements of diuresis, natriuresis and calciuresis occur via a distinct subtype which resembles the receptor that mediates NPY-induced enhancement of food intake.

Animals↗

PubMed2006

Indomethacin differentiates the renal effects of sphingosine-1-phosphate and sphingosylphosphorylcholine.

The sphingomyelin breakdown products sphingosine-1-phosphate (S1P) and sphingosylphosphorylcholine (SPC) constrict intrarenal microvessels in vitro in a pertussis toxin (PTX) sensitive manner, and S1P also reduces renal blood flow in vivo. Nevertheless, both S1P and SPC have been reported to enhance diuresis and natriuresis. This pattern is similar to that of neuropeptide Y, which also reduces renal blood flow and enhances diuresis and natriuresis. The latter effects are inhibited by the cyclooxygenase inhibitor indomethacin, and various S1P and SPC responses have also been linked to the cyclooxygenase pathway. Therefore, we have investigated whether indomethacin can alter the renal effects of S1P and SPC in anaesthetised rats in vivo. In line with earlier experiments S1P bolus injections dose-dependently reduced renal blood flow (by up to 4.8 +/- 0.5 ml min(-1)), and this was not significantly affected by indomethacin treatment (5 mg kg(-1) i.p.). Infusion of S1P but not of SPC (30 microg kg(-1) min(-1) each) for 60 min reduced renal blood flow by up to 0.8 +/- 0.2 ml min(-1), and this was not markedly altered by indomethacin. Despite the differential renovascular effect, both S1P and SPC enhanced diuresis by up to 215 +/- 65 and 201 +/- 58 microl 15 min(-1) respectively, and natriuresis by up to 25 +/- 9 and 29 +/- 11 micromol 15 min(-1) respectively. While indomethacin abolished the SPC-induced diuresis and natriuresis, it, if anything, slightly enhanced the diuretic and natriuretic effect of S1P. To determine whether tubular SPC effects are receptor-mediated, PTX experiments were performed. SPC-induced enhancements of diuresis and natriuresis were abolished by PTX. We conclude that S1P, SPC and neuropeptide Y exhibit distinct patterns of modulation of renal function and that indomethacin allows such effects to be differentiated.

Animals↗

PubMed1983

Identification of pathways involved in the natriuretic, kaliuretic and diuretic responses induced by cholinergic stimulation of the medial septal area (MSA).

Natriuresis, kaliuresis and diuresis have been studied in rats following water loading and cholinergic stimulation in the MSA before and after bilateral electrolitic lesion of the habenula, or medullary stria, or supraoptic nucleus or paraventricular nucleus, or fornix. Carbachol injection in MSA elicited an increase of natriuresis and kaliuresis. These responses were blocked by bilateral electrolytic lesion of the habenula, medullary stria, or supraoptic nucleus but not of the paraventricular nucleus or the fornix. Urinary output plotted as a function of time showed antidiuresis in periods of 20 and 40 minutes after carbachol injection into the MSA. The lesion of the supraoptic nucleus inhibited this antidiuresis and natriuresis. The lesion of the habenula or medullary stria blocked natriuresis but not antidiuresis suggesting an independence between the mechanisms of antidiuretic hormone release and natriuresis regulation. The integrity of the habenula, medullary stria and supraoptic nucleus seems to be important in the mediation of the natriuretic response induced by carbachol injection into the MSA.

Animals↗

PubMed1994

Renal sodium handling in cirrhosis with ascites: mechanisms of impaired natriuretic response to reclining.

We recently showed that patients with compensated cirrhosis can dispose of their fluid overload while reclining. In contrast, patients with ascites fail to develop supine-induced natriuresis. To assess the effect of reclining on renal sodium handling in patients with advanced cirrhosis and the mechanisms blunting natriuresis in this situation, renal function and plasma concentrations of atrial natriuretic factor, aldosterone and norepinephrine were evaluated in 10 nonazotemic patients with cirrhosis and ascites and 10 healthy controls standing for 2 h and reclining for 2 h. While standing, all patients showed marked sodium retention and significantly elevated plasma atrial natriuretic factor levels, aldosterone and norepinephrine. Glomerular filtration rate did not differ from healthy controls. The reclining increased renal sodium excretion in both groups, but this change was far less marked in patients; natriuresis only rose to the control range in two of them. An increase in atrial natriuretic factor and a depression of plasma aldosterone and norepinephrine was seen in both controls and patients. In the latter, despite the greater change in atrial natriuretic factor and aldosterone, the aldosterone to atrial natriuretic factor ratio, which was inversely correlated with natriuresis during both standing and reclining remained significantly elevated. In the two patients who achieved normal natriuresis during reclining, reclining was associated with both the normalization of the aldosterone/atrial natriuretic factor ratio, and with an increase in glomerular filtration rate. The supine-induced increase in atrial natriuretic factor was not only preserved but was even enhanced in cirrhosis with ascites.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Renal effects of nifedipine in healthy normotensive volunteers. Effects of dose, formulation, duration of treatment, and chlorothiazide coadministration.

Renal effects of nifedipine were assessed in 3 groups of healthy normotensive volunteers. In the first group (N = 10), a single 20-mg dose of the slow-release formulation caused an increase in 8-h sodium excretion (P less than 0.025) and urine volume (P less than 0.005). Natriuresis (P less than 0.05) and diuresis (P less than 0.05) were still evident after 1 wk of pretreatment, but were significantly attenuated (P less than 0.05), in each case, compared to levels after a single dose. Natriuresis and diuresis after 2 wk of intake were indistinguishable from control levels. In another group of 8, a single 10 mg dose of the conventional formulation (capsule) effected natriuresis (P less than 0.01) and diuresis (P less than 0.001) similar to those associated with intake of a single 20-mg dose of the slow-release formulation. Natriuresis and diuresis associated with a 20-mg single dose of the conventional formulation were not different from control but were less than those following intake of the 10-mg dose (P less than 0.025 in each case). In the third group of 6, nifedipine, though weaker than chlorothiazide, promoted natriuresis (P less than 0.025) and diuresis (P less than 0.025) of the thiazide without augmenting its kaliuresis. In all the groups, there were no changes in creatinine clearance, and nifedipine did not alter kaliuresis. It is suggested that natriuretic and diuretic effects of nifedipine in healthy normotensive individuals are dependent on the dose employed, the formulation used, and the duration of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1975

Time course of onset and decay of humoral natriuretic activity in the rat.

The natriuretic mechanism.tic activity shown in earlier cross-circulation experiments to develop in the blood of rats undergoing sustained vascular expansion has been further characterized. Following whole blood infusion and urine reinfusion of the donor rat, a cross-circulated isovolaemic partner exhibits a natriuresis of gradual onset, requiring 60-80 min to reach a peak (0.04-3.24 muequiv./min per gram kidney weight). The gradual feature of recipient natriuresis was unchanged by infusing the donor rat 1 h prior to cross-circulation. Once developed, the recipient natriuresis was sustained when fluid depletion by the renal response was prevented, but was reversible with a half-life of about 30 min on interruption of the cross-circulation; reconnection of cross-circulation promptly restored recipient natriuresis. No significant natriuresis (0.04-0.16 muequiv/min per gram kidney weight) occurred in the recipients if the donors in comparable cross-circulations were not infused. These findings confirm that a natriuretic activity develops in the blood as a consequence of vascular expansion, and reveal that the activity has a slowly developing and reversible action on the renal natriure

Animals↗