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PubMed1991

Endogenous atrial natriuretic factor is involved in the natriuresis following sodium loading in rats with chronic heart failure.

STUDY OBJECTIVE: Plasma levels of atrial natriuretic factor are increased in chronic heart failure; however, it is still controversial whether these raised levels contribute to the diuresis and natriuresis in this setting. To address this issue the potential contribution of endogenous atrial natriuretic factor in the renal excretion of a moderate oral sodium load in a rat model of chronic heart failure was studied. DESIGN: A monoclonal antibody against atrial natriuretic factor was used for specific antagonisation of its in vivo effects. Animals were subjected to oral sodium loading (30 ml.kg-1 0.9% NaCl, 2.5% dextrose) at baseline, immediately after, and 5 d after injection of monoclonal antibody or control solvent. EXPERIMENTAL MATERIAL: Sham operated rats and rats with chronic heart failure due to myocardial infarction (infarct size 35(SEM 4)% of left ventricle) were studied 4-5 weeks after surgery. MEASUREMENTS AND MAIN RESULTS: The renal excretion of cyclic guanosine monophosphate (cGMP), which represents a specific marker for the activation of the atrial natriuretic factor system, was markedly increased in infarcted rats, at 17.9(SEM 3.4) vs 5.8(1.2) nmol.kg-1, p less than 0.01. Atrial natriuretic factor antibody given immediately before sodium loading reduced the natriuretic response (0-4 h period) in infarcted rats from 1270(171) to 805(76) mumol.kg-1 (p less than 0.01) but not in sham operated animals. Similarly, the excretion of cGMP was only decreased by atrial natriuretic factor antibody in infarcted rats, from 29.8(6.3) to 20.7(3.7) nmol.kg-1. The reduction in sodium and cGMP excretion in infarcted rats was confirmed with a purified antibody preparation. CONCLUSIONS: Endogenous atrial natriuretic factor appears to be involved in the natriuresis following a moderate oral volume load in chronic heart failure. Thus the raised concentrations found in chronic heart failure may contribute to the regulation of urinary sodium excretion under these conditions despite the fact that the diuretic effects of exogenous atrial natriuretic factor are attenuated in chronic heart failure.

Animals↗
PubMed1994

Diuresis and natriuresis in non-seizing and in kindled rats from a genetically audiogenic susceptible strain.

Audiogenic seizures are evoked by acoustic stimulation in susceptible (S) but not in resistant (R) rats. Repeated audiogenic seizures recruit limbic areas, a model called audiogenic kindling. In order to evaluate excretory patterns (urinary volume, Na+ and K+ excretion), S and R animals were non-stimulated, submitted to one (acute) or 10 (kindled) stimulations or to two aqueous overloads (5% b.w.). Non-stimulated S animals displayed a significant increase (p < 0.05) in Na+ excretion at 60, 80, 100 and 120 min. Acutely stimulated S animals showed greater natriuresis than non-stimulated animals at 40, 60, 80 and 100 min. Kindled S animals displayed the greatest natriuresis (p < 0.005) at 40, 60, 80, 100 and 120 min and the highest diuretic response (p < 0.05) at 40, 60 and 80 min. Abnormalities of the endogenous hydroelectrolytic profile of non-stimulated S animals and their overt expression in kindled rats may be related to alterations in neuroendocrine systems regulating hydroelectrolytic balance, in addition to the long-lasting effects of kindled seizures.

Acoustic Stimulation↗
PubMed1988

Pressure natriuresis and control of arterial pressure during chronic norepinephrine infusion.

The goal of this study was to quantitate changes in mean arterial pressure (MAP) and renal function during chronic increases in plasma levels of norepinephrine, and to determine the role of the renal pressure natriuresis mechanism in controlling sodium balance in norepinephrine hypertension. In six conscious dogs in which renal artery pressure (RAP) was allowed to increase during 7 days of norepinephrine infusion (0.2 micrograms/kg per min), sodium excretion (UNaV) rose from 66 +/- 3 to 112 +/- 15 mmol/day and MAP increased from 100 +/- 3 to 109 +/- 3 mmHg on the first day. On days 2-7, UNaV returned toward the control level while MAP averaged 108 +/- 2 mmHg. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) did not change significantly, averaging 85.9 +/- 4.0 and 235 +/- 17 ml/min, respectively, during 7 days of norepinephrine, compared to controls of 84.1 +/- 3.9 and 252 +/- 20 ml/min. When RAP was servo-controlled for 7 days during norepinephrine infusion, the natriuresis was abolished; UNaV averaged 76 +/- 8 during control, 77 +/- 13 during the first day of norepinephrine and 65 +/- 4 mmol/day during 7 days of norepinephrine. GFR and ERPF did not change significantly during norepinephrine infusion with RAP held constant. MAP did not reach a plateau but continued to rise from 102 +/- 3 to 137 +/- 3 mmHg after 7 days of norepinephrine and servo-control of RAP.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1988

Exaggerated natriuresis and lithium clearance in spontaneously hypertensive rats.

Since hypertension is associated with changes in the handling of various cations (including sodium and lithium) across the cell membrane, the present study investigated the validity of the lithium clearance method in hypertension by comparing two measures of proximal reabsorption. Thus, fractional lithium excretion and transit time (TT)-occlusion time (OT; e-TT/T) were determined successively in the same spontaneously hypertensive rat (SHR, Okamoto strain). The rats were examined both before and after an acute saline load. The results show that the lithium clearance method can be used for the determination of proximal reabsorption in SHR. Utilizing the lithium clearance method, the changes in renal sodium handling underlying the exaggerated natriuresis were investigated in unanaesthetized catheterized rats. It was found that the exaggerated natriuresis was associated with an increased output from the proximal tubule, whereas no difference in distal sodium handling could be detected between SHR and normotensive Wistar-Kyoto rats (WKY).

Animals↗
PubMed1989

Atrial natriuretic peptide and exaggerated natriuresis during acute hypertonic volume expansion in essential hypertension.

In patients with essential hypertension and healthy controls, plasma levels of atrial natriuretic peptide (ANP), angiotensin II (Ang II), aldosterone (Aldo), arginine vasopressin (AVP) and urinary excretion of prostaglandin E2 (PGE2) were measured under basal conditions, and before and after acute volume expansion with a 2.5% hypertonic sodium chloride solution. Tubular sodium handling was assessed by the lithium clearance technique. Under basal conditions ANP was increased in patients compared with controls (9.0 pmol/l versus 7.5 pmol/l, P less than 0.01). In response to acute volume expansion patients exhibited exaggerated increases in ANP (5.3 pmol/l versus 3.0 pmol/l, P less than 0.05), exaggerated natriuresis, and an abnormal decrease in fractional proximal and distal tubular sodium reabsorption (PFRNa and DFRNa, respectively). Furthermore, during comparable urinary flow rates, urinary PGE2 excretion was decreased in patients compared with controls (266 pg/min versus 705 pg/min, P less than 0.05). No differences were found between patients and controls in Ang II, Aldo or AVP under basal conditions. Both groups responded to hypertonic acute volume expansion with comparable decreases in Ang II and Aldo, and an increase in AVP. It is concluded that in essential hypertension ANP is increased under basal conditions and the increase in natriuresis and ANP is exaggerated during acute volume expansion. The exaggerated natriuretic response to acute volume expansion resulted from an altered handling of sodium in both proximal and distal tubules.

Adult↗
PubMed1998

Exaggerated natriuresis as a candidate intermediate phenotype in spontaneously hypertensive rats.

OBJECTIVE: To determine whether exaggerated natriuresis and exaggerated renal sympathoinhibition during volume loading constitute an intermediate phenotype in spontaneously hypertensive rats. DESIGN: The borderline hypertensive rat, the F1 of a cross between a spontaneously hypertensive rat and a normotensive Wistar-Kyoto rat, is a NaCl-sensitive model of genetic hypertension. In addition to hypertension, borderline hypertensive rats fed 8% NaCl food develop characteristic alterations in regulation of renal sympathetic nerve activity and neural regulation of renal function similar to those in the spontaneously hypertensive rat parent. Like the Wistar-Kyoto rat parent, borderline hypertensive rats fed 1% NaCl food remain normotensive and do not exhibit these alterations in renal sympathetic neural mechanisms. These renal sympathetic neural mechanisms constitute a complex quantitative trait that could represent an intermediate phenotype. METHODS: A backcross population, developed by mating borderline hypertensive rats with Wistar-Kyoto rats, was fed 8% NaCl food for 12 weeks from age 4 to 16 weeks. Responses to intravenous isotonic saline volume loading (10% body weight/30 min) in 81 backcross rats chronically instrumented for measurement of mean arterial pressure, renal sympathetic nerve activity, and urinary sodium excretion were determined. RESULTS: Mean arterial pressure was 105-180 mmHg and was not correlated to the magnitude either of the decrease in renal sympathetic nerve activity or of the increase in urinary sodium excretion during volume loading. CONCLUSIONS: These two aspects of the complex quantitative trait, exaggerated natriuresis and exaggerated renal sympathoinhibition during volume loading, are not part of an intermediate phenotype in spontaneously hypertensive rats.

Animals↗
PubMed1988

Facilitation of natriuresis with nifedipine in normal humans.

We tested the effect of dietary potassium (KCl, 20 mEq three times daily), calcium (Ca, 500 mg twice daily), sodium-potassium-dependent ATPase inhibition (digoxin), calcium channel blockade (nifedipine), and placebo on acute natriuresis in 14 normal subjects who received 2 L normal saline intravenously over 4 h. Plasma renin activity (PRA) was increased in subjects receiving nifedipine, while plasma aldosterone (PA) concentrations were not different among the regimens. Only KCl and nifedipine affected sodium excretion compared to controls. KCl and nifedipine increased the amount of sodium excreted after the infusion was terminated. In the case of nifedipine, this natriuresis was sufficient to increase the 24 h sodium excretion on that day to above that of the other regimens.

Adolescent↗
PubMed1993

Is the renal natriuretic peptide urodilatin involved in the regulation of natriuresis?

Recent evidence has shown that the kidneys produce and secrete a member of the atrial natriuretic peptide family, named urodilatin. This 32-amino acid peptide does not circulate in blood, but is secreted into urine. Urodilatin excretion closely parallels renal sodium excretion under various conditions that influence body fluid regulation, such as circadian rhythm, salt ingestion, acute intravenous sodium loading, water immersion, atrial distension, and cerebral hypernatremia. In contrast, the plasma concentration of the atrial member of the natriuretic peptide family often is only weakly and occasionally even negatively associated with natriuresis under these conditions. We conclude from these observations that urodilatin rather than atrial natriuretic peptide might be the member of the natriuretic peptide family that is involved in the regulation of natriuresis in normal physiology.

Animals↗
PubMed2000

Unmasking of endothelin-1-induced natriuresis and renal vasodilation in the dog by enrasentan (SB 217242).

Infusion of endothelin-1 (ET-1) into conscious, chronically instrumented dogs (1, 3 and 10 ng/kg/min i.v.) resulted in decreases in renal plasma flow, urine flow and sodium excretion. Intravenous ET-1 infusion in the presence of enrasentan at 30 microg/kg/min, resulted in an increase in renal plasma flow and sodium excretion; however, at a higher infusion rate (100 microg/kg/min) no renal vasodilation or natriuresis was observed. These data indicate that enrasentan can unmask ET(B)-receptor-induced renal vasodilation and natriuresis.

Animals↗
PubMed2003

Pressure natriuresis in AT(2) receptor-deficient mice with L-NAME hypertension.

AT(2) receptor-disrupted (AT(2) -/-) mice provide a unique opportunity to investigate the cardiovascular and BP-related effects of NO depletion. This study compared the pressure-diuresis-natriuresis relationship in (AT(2) -/-) and wild-type (AT(2) +/+) mice after treating the animals with L-NAME (130 mg/kg body wt per day) for 1 wk. L-NAME increased mean arterial pressure (MAP) more in AT(2) -/- than in AT(2) +/+ mice (118 +/- 2 versus 108 +/- 4 mmHg). This difference occurred even though L-NAME-treated AT(2) +/+ mice had a greater sodium excretion than AT(2) -/- mice (10.9 +/- 0.5 versus 8.0 +/- 1.0 micro mol/h). The pressure-natriuresis relationship in conscious AT(2) -/- mice was shifted rightward compared with controls. RBF was decreased in AT(2) -/- compared with AT(2) +/+ mice. L-NAME decreased RBF in these mice further from 4.08 +/- 0.43 to 2.79 +/- 0.15 ml/min per g of kidney wt. GFR was not significantly different between AT(2) +/+ and AT(2) -/- mice (1.09 +/- 0.08 versus 1.21 +/- 0.09 ml/min per g of kidney wt). L-NAME reduced GFR in AT(2) -/- to 0.87 +/- 0.07 ml/min per g of kidney wt. Fractional sodium (FE(Na)) and water (FE(H2O)) curves were shifted more strongly to the right by L-NAME in AT(2) -/- mice than in AT(2) +/+ mice. AT(1) receptor blocker treatment lowered BP in both L-NAME-treated strains to basal values. It is concluded that the AT(1) receptor plays a key role in the impaired renal sodium and water excretion induced by NO synthesis blockade. Changes in RBF, GFR, and tubular sodium and water reabsorption are involved and may be also responsible for the greater BP increase in L-NAME-treated AT(2) -/- mice.

Animals↗
PubMed2004

Increased activity of cGMP-specific phosphodiesterase (PDE5) contributes to resistance to atrial natriuretic peptide natriuresis in the pregnant rat.

Increased cGMP-specific phosphodiesterase (PDE5) activity in renal inner medullary collecting duct (IMCD) cells contributes to resistance to atrial natriuretic peptide (ANP) and the excessive sodium retention seen in experimental nephrotic syndrome and liver cirrhosis. Normal pregnancy is also accompanied by sodium retention and plasma volume expansion, and pregnant rats are resistant to the natriuretic action of ANP. The authors investigated a possible role of increased renal PDE5 activity in the physiologic sodium retention of normal rat pregnancy. The natriuresis and increased urinary cGMP excretion (U(cGMP)V) evoked by acute volume expansion (a measure of renal responsiveness to endogeneous ANP) was blunted in 16-d pregnant versus virgin rats, despite equivalent increases in circulating ANP in pregnants and virgins. The ANP-dependent cGMP accumulation in isolated IMCD cells from pregnants was blunted versus virgins and restored by the PDE5-selective antagonist DMPPO (10(-7) mol/L). PDE5 activity in vitro and PDE5 protein abundance in IMCD were greater in pregnants. Four days postpartum, volume expansion natriuresis, U(cGMP)V, and PDE5 protein levels in IMCD cell homogenates had returned to virgin values. These results demonstrate that normal rat pregnancy leads to in vivo and in vitro renal resistance to ANP, in association with heightened activity of the cGMP-specific PDE5 in IMCD. This may contribute to the physiologic sodium retention of normal pregnancy.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1976

Natriuresis and renin release by the denervated dog kidney during furosemide administration.

Renal excretion of sodium and water, renal venous plasma renin activity and renin secretion rate were measured during the administration of furosemide (5 mg/kg) to 10 anesthetized dogs, previously subjected to unilateral splanchnicotomy ("renal denervation"). Denervation diuresis and natriuresis, observed during control periods, did not occur when the diuretic was given and there were no significant changes in glomerular filtration rate or renal plasma flow in either the intact or denervated kidneys. Despite the abolition of denervation natriuresis with furosemide, plasma renin activity and renin secretion rate were depressed by splanchnicotomy. Thus, changes in the sodium load to the macula densa do not seem to play a decisive role in decreasing renin release following renal denervation.

Animals↗
PubMed1997

Nitric oxide in the mediation of pressure natriuresis.

1. Recent studies have indicated that nitric oxide (NO) production in the kidney contributes to the regulation of renal haemodynamics and excretory function. Inhibition of nitric oxide synthase (NOS) reduces renal blood flow by approximately 25% and markedly reduces sodium excretion without reductions in filtered load. In particular, inhibition of NO synthesis markedly suppresses the slope of the arterial pressure-mediated response in sodium excretion. 2. Further studies have shown that constant intrarenal infusion of a NO donor in dogs treated with a NOS inhibitor produced diuretic and natriuretic responses but failed to restore the slope of the pressure-induced natriuretic response. These data indicate that an alteration in intrarenal NO activity, rather than the simple presence of NO during changes in arterial pressure is required for full expression of pressure natriuretic responses. 3. In support of the hypothesis that NO is involved in the mediation of pressure natriuresis, we also recently demonstrated a direct relationship between changes in arterial pressure and urinary excretion rate of sodium as well as nitrate and nitrite (a marker for endogenous NO activity) in the presence of efficient autoregulation of cortical and medullary blood flow. 4. The direct inhibitory actions of NO on tubular sodium reabsorption have also been observed in cultured tubular cells as well as isolated, perfused cortical collecting duct segments. 5. Thus, the collective data suggest that acute changes in arterial pressure induce changes in intrarenal NO production, which may directly alter tubular reabsorptive function to manifest the phenomenon of pressure natriuresis.

Animals↗
PubMed2005

CNS-induced natriuresis, neurohypophyseal peptides and renal dopamine and noradrenaline excretion in prehypertensive salt-sensitive Dahl rats.

To identify defects in the salt-sensitive Dahl rat (Dahl-S), the natriuretic, catecholaminergic and pressor responses to 60-min elevation of the cerebroventricular sodium concentration (CNS-induced natriuresis) were compared between prehypertensive salt-sensitive Dahl-S and salt-resistant Dahl rats (Dahl-R). The plasma concentrations of the rat natriuretic hormone oxytocin, which has implications for the development of hypertension, and vasopressin (AVP) were also measured. Basal sodium and catecholamine excretion and mean arterial blood pressure (MAP) were similar in both strains. Sodium excretion during CNS stimulation increased more than 15-fold in Dahl-R but only 10-fold in Dahl-S. Dopamine excretion increased only transiently and similarly in both strains. Noradrenaline excretion and response to CNS stimulation were similar, suggesting a comparable sympathetic nervous activity between the strains. MAP increased comparably in Dahl-R and Dahl-S. Plasma AVP concentration was similar in both strains while plasma oxytocin concentration after CNS stimulation was more than 2-fold higher in Dahl-S than in Dahl-R. In conclusion, the prehypertensive Dahl-S has an attenuated natriuretic response to elevations of the cerebroventricular fluid sodium concentration and a higher plasma level of the natriuretic hormone oxytocin. Dopamine is not a mediator of CNS-induced natriuresis in neither strain. The attenuated natriuretic response may partly explain the salt-sensitivity in Dahl-S, and the higher plasma oxytocin value may either represent an effort to compensate for the deficient natriuretic response or reflect a primary defect in this system. Due to the known involvement of oxytocin in central MAP regulation in some hypertensive animal models, the findings warrant further investigation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Vasopressin-induced natriuresis in the conscious rat: role of blood pressure, renal prostaglandin synthesis and the peptide ANF.

1. The response to arginine vasopressin (AVP) at doses of 5 and 10 pmol (100 g body weight)-1 h-1 was studied in conscious rats during the infusion of 1% (w/v) dextrose at 11.6 ml h-1 with and without pre-treatment with indomethacin. 2. In the absence of indomethacin AVP infusion induced dose-related increases in sodium output that were positively correlated with increases in mean arterial blood pressure (MAP) and plasma atrial natriuretic factor (ANF) immunoreactivity. Increases in renal prostaglandin E2 (PGE2) synthesis were also associated with AVP infusion. 3. Indomethacin pre-treatment abolished the AVP-induced increases in renal PGE2 synthesis and also the dose-related differences in ANF immunoreactivity. Increases in MAP and sodium output were unaffected at the 10 pmol (100 g body weight)-1 h-1 dose of AVP and only slightly attenuated for the 5 pmol (100 g body weight)-1 h-1 dose. 4. For both series AVP induced marked falls in glomerular filtration rate (GFR) but only small transient falls in effective renal plasma flow. The observed falls in GFR support the view that the natriuresis is due to changes in tubular handling and not in the filtered load of sodium. 5. It is concluded that the natriuresis elicited by AVP is closely related to the pressor action of the hormone but renal PGE2 synthesis and plasma ANF are not responsible for mediating this response.

Animals↗
PubMed1990

Atrial peptide natriuresis in the rat without genuine rise in filtration rate or wash-out of medullary electrolytes.

1. Effects of synthetic atrial natriuretic peptide (ANP) on renal excretion, total renal blood flow (RBF), glomerular filtration rate (GFR) and tissue electrical admittance (reciprocal impedance, an estimate of tissue electrolytes) were determined in pentobarbitone-anaesthetized rats. GFR was measured both as inulin clearance (Cin) and as a product of renal plasma flow (RPF) and inulin extraction ratio (Ein). 2. With the lowest dose of ANP (0.35 micrograms/(kg min) I.V.) a 5-fold increase in sodium excretion occurred without measurable change in Cin, RPF x Ein nor medullary electrolyte concentration estimated from tissue electrical admittance. 3. With medium and high dosage (2 and 6 micrograms/(kg min), respectively), major and rapid increases in sodium excretion and urine flow were associated with an acute increase in Cin but not RPF x Ein. 4. The RBF increase observed in all groups of rats was not dose-related and did not parallel the natriuresis. Electrolyte concentration in the medullary tissue showed a modest transient decrease in rats given medium and high ANP doses. 5. We conclude that pronounced ANP natriuresis can develop in the absence of a measurable increase of GFR, estimated by a method not subject to urinary dead space error (RPF x Ein). The small transient decrease in medullary tissue electrolytes observed with higher peptide doses does not support solute wash-out as an important mechanism of increased sodium excretion.

Animals↗
PubMed2003

Mechanisms of acute natriuresis in normal humans on low sodium diet.

This study evaluates the relative importance of several mechanisms possibly involved in the natriuresis elicited by slow sodium loading, i.e. the renin-angiotensin-aldosterone system (RAAS), mean arterial blood pressure (MAP), glomerular filtration rate (GFR), atrial natriuretic peptide (ANP), oxytocin and nitric oxide (NO). Eight seated subjects on standardised sodium intake (30 mmol NaCl day(-1)) received isotonic saline intravenously (NaLoading: 20 micromol Na(+) kg(-1) min(-1) or approximately 11 ml min(-1) for 240 min). NaLoading did not change MAP or GFR (by clearance of (51)Cr-EDTA). Significant natriuresis occurred within 1 h (from 9 +/- 3 to 13 +/- 2 micromol min(-1)). A 6-fold increase was found during the last hour of infusion as plasma renin activity, angiotensin II (ANGII) and aldosterone decreased markedly. Sodium excretion continued to increase after NaLoading. During NaLoading, plasma renin activity and ANGII were linearly related (R = 0.997) as were ANGII and aldosterone (R = 0.999). The slopes were 0.40 pM ANGII (mi.u. renin activity)(-1) and 22 pM aldosterone (pM ANGII)(-1). Plasma ANP and oxytocin remained unchanged, as did the urinary excretion rates of cGMP and NO metabolites (NO(x)). In conclusion, sodium excretion may increase 7-fold without changes in MAP, GFR, plasma ANP, plasma oxytocin, and cGMP- and NO(x) excretion, but concomitant with marked decreases in circulating RAAS components. The immediate renal response to sodium excess appears to be fading of ANGII-mediated tubular sodium reabsorption. Subsequently the decrease in aldosterone may become important.

Adult↗
PubMed1984

Mechanism of polyuria and natriuresis in atrioventricular nodal tachycardia.

A woman with tachycardia associated with polyuria was investigated. Electrophysiological analysis showed that the tachycardia was an atrioventricular nodal re-entrant tachycardia. Programmed stimulation was then used to provoke and sustain the tachycardia for 40 minutes. Polyuria, with an appreciable increase in free water clearance, was observed. This was associated with reduction in plasma and urinary arginine vasopressin concentrations. Appreciable natriuresis also developed. These results support the hypothesis that the polyuria with increased free water clearance and the natriuresis occurring during sustained tachycardia in man are due to inhibition of secretion of vasopressin and the release of natriuretic factor.

Arginine Vasopressin↗