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PubMed1982

Nocturnal natriuresis in hyperthyroidism.

We measured urine flow and the renal excretion of total solute, sodium, potassium and calcium in eleven patients with hyperthyroidism before and after treatment. Mean nocturnal sodium excretion was significantly greater (P less than 0.05) during hyperthyroidism and was unaccompanied by any significant alterations in day time or 24-h values. As a result of this nocturnal natriuresis in hyperthyroidism significant changes were noted in the ratios of day/night sodium excretion (P less than 0.005) and urinary flow (P less than 0.05). The change in ratio of day/night sodium excretion resulting from treatment of hyperthyroidism was shown to correlate significantly with the change in plasma total triiodothyronine (r=0.73, P less than 0.01). Twenty-four hour urinary calcium output was significantly greater (P less than 0.02) in hyperthyroidism but there was no significant alteration in the day/night pattern of excretion.

Adult↗
PubMed1985

Renal water and sodium handling in compensated liver cirrhosis: mechanism of the impaired natriuresis after saline loading.

The present study was attempted to evaluate sodium and water balance in compensated liver cirrhosis. Renal sodium and water handling was studied in six cirrhotic patients without ascites and/or oedema and in six controls before and after saline loading. Fractional sodium reabsorption at the various nephron sites (proximal, diluting and distal) was evaluated by means of clearance techniques during maximal water diuresis and hypotonic saline infusion. Compensated cirrhotic patients showed a normal baseline sodium and water balance but a blunted natriuretic response when saline loaded (urinary sodium excretion after saline load = 338 +/- 290 compared to 933 +/- 504 mumol min-1 of controls; P less than 0.05). The impaired natriuresis was found to be related to an increased reabsorption of sodium in the proximal tubule (proximal fractional sodium reabsorption = 88.4 +/- 3.8 compared to 81.7 +/- 4.3% of controls; P less than 0.05). These findings confirm the hypothesis that renal sodium handling abnormalities might precede ascites formation. Additional studies, however, are necessary to further define renal factors mediating the increased reabsorption of sodium in compensated liver cirrhosis.

Adult↗
PubMed1995

Effects of NG-nitro-L-arginine on pressure natriuresis in anaesthetized rabbits.

1. We tested the effects of blockade of nitric oxide synthesis on renal function under conditions of controlled renal artery pressure. Our hypothesis was that endogenous nitric oxides plays a role in the natriuresis that accompanies increased renal perfusion pressure. We used a novel technique which employed an extracorporeal circuit to produce step changes over a wide range of renal artery pressures in pentobarbitone-anaesthetized rabbits. 2. Rabbits were treated with either NG-nitro-L-arginine (NOLA, 20 mg/kg, i.v.; n = 8) or its vehicle (n = 8). Renal artery pressure was set (by adjusting the extracorporeal circuit) at 65, 80, 95, 110 and then 130 mmHg respectively, at the beginning of each of five 30 min experimental periods. 3. NOLA treatment caused profound renal vasoconstriction that was largely independent of the level of renal artery pressure, renal blood flow being 35-43% lower in NOLA-treated than in vehicle-treated rabbits across the range of renal artery pressures tested (P = 0.002). NOLA treatment increased filtration fraction (P = 0.02), and tended to reduce glomerular filtration rate (P = 0.09). 4. NOLA-treatment affected sodium excretion in a manner dependent on the legel of renal artery pressure, with the slope of the relationship between sodium excretion and renal artery pressure being lower in NOLA-treated than in vehicle-treated rabbits (P = 0.006). 5. These data provide direct evidence that in anaesthetized rabbits endogenous nitric oxide (i) tonically dilates the renal vasculature across a wide range of renal perfusion pressures, and (ii) enhances sodium excretion to a progressively greater degree as renal artery pressure is increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Effects of zaprinast on renal nerve stimulation-induced anti-natriuresis in anaesthetized dogs.

1. We examined whether zaprinast, a putative cGMP-specific phosphodiesterase inhibitor, affects neural control of renal function in pentobarbital-anaesthetized dogs. 2. Renal nerve stimulation (1 Hz, 1 ms duration) reduced urine flow rate, urinary Na+ excretion (UNaV) and fractional excretion of Na+ (FENa) with little change in either renal blood flow (RBF) or glomerular filtration rate (GFR). 3. Intrarenal arterial infusion of zaprinast (10 and 100 micrograms/kg per min) increased basal urine flow rate, UNaV and FENa but not RBF or GFR. Zaprinast infusion (100 micrograms/kg per min) also increased renal venous plasma cGMP concentration and urinary cGMP excretion. 4. Renal nerve stimulation-induced reductions in UNaV and FENa were attenuated during zaprinast infusion, whereas the reduction in urine flow rate was resistant to zaprinast. 5. Renal nerve stimulation increased the renal venous plasma noradrenaline concentration and renal noradrenaline efflux, which remained unaffected during infusion of zaprinast (100 micrograms/kg per min). 6. The results of the present study suggest that zaprinast induces natriuresis and counteracts adrenergically induced antinatriuresis by acting on renal tubular sites in the dog kidney in vivo.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1998

Natriuresis and inhibition of Na+/K(+)-ATPase: modulation of response by physiological manipulation.

1. There is considerable evidence for the existence of an endogenous inhibitor of Na+/K(+)-ATPase. The exact physiological nature and role of this postulated agent remains unclear, although it would be predicted that one of its actions would be stimulation of renal sodium excretion. 2. The natriuretic effect of renal arterial infusion of ouabain is relatively slow in onset and is sustained. 3. The natriuresis is not modified by changes in sodium status, unlike the natriuretic effect of atrial natriuretic peptide. 4. The natriuretic action of ouabain is enhanced dramatically by acute volume expansion or chronic mineralocorticoid treatment, which both result in hypokalaemia, hypertension and hypervolaemia. 5. The natriuretic response to small increments in blood pressure is markedly enhanced by treatment with ouabain. 6. We hypothesize that the interaction between the inhibition of Na+/K(+)-ATPase and elevated blood pressure could result in the shedding of sodium in conditions where there are increased levels of circulating endogenous digitalis-like factors.

Animals↗
PubMed2001

Early effects of renal denervation in the anaesthetised rat: natriuresis and increased cortical blood flow.

A novel method of renal denervation was developed based on electro-coagulation of tissue containing most of the sympathetic fibres travelling towards the kidney. Kidney tissue noradrenaline was decreased to 4.7 % of the content measured in the contralateral innervated kidney when studied 3 days postdenervation. The method was utilised in anaesthetised rats to examine the effects of denervation within the heretofore unexplored first 75 min period postdenervation. Sodium excretion (UNaV) increased significantly (+82 %, P < 0.03) over the 25-50 min after denervation. In a parallel group, with a lower baseline UNaV, there was also a significant increase in UNaV (+54 %, P < 0.03) within the first 25 min. The renal perfusion pressure was maintained at a constant value and the glomerular filtration rate did not change after denervation. Renal cortical and medullary blood flows (CBF, MBF) were estimated as laser Doppler flux and medullary tissue ion concentration was estimated as electrical admittance (Y). Following denervation, in both groups CBF increased significantly within the first 25 min (+12 %, P < 0.01 and +8 %, P < 0.05, respectively) while MBF did not change or decreased slightly; Y did not change. The data document the development of natriuresis within the first 25-50 min after denervation. The increase in CBF indicated that, prior to denervation, the cortical, but not medullary, circulation was under a tonic vasoconstrictor influence of the renal nerves. Such a dissociation of neural effects on the renal cortical vs. medullary vasculature has not been previously described.

Animals↗
PubMed1995

Natriuresis obtained by intracerebroventricular infusion of hypertonic NaCl in rats with papillary necrosis.

Raising the sodium concentration in the third cerebral ventricle increases renal sodium, potassium and water excretion. The identification and characterization of the factor(s) mediating the centrally evoked natriuresis would be greatly facilitated if the exact intrarenal effector site were known. We have assessed the importance of inner medullary structures for the effects of CNS stimulation by examining its ability to alter renal excretion in rats with papillary necrosis, induced 2 d earlier with 2-bromoethylamine hydrobromide (BEA), 250 mg kg-1 body wt i.v. Male Lewis x DA rats were divided into a BEA-treated group (n = 6) and a control group receiving vehicle alone (n = 6). In contrast to the white papillae normally seen, the papillae of BEA-treated animals were bright red and showed a clear line of demarcation at their base. The rats were anaesthetized i.p. with Inactin (120 mg kg-1 body wt). Artificial cerebrospinal fluid (CSF) was infused (520 nL min-1) via a cannula into the left lateral ventricle. After 45 min CSF containing 1 M NaCl was used. Stimulation of the control rats with hypertonic CSF increased urine flow rate five-fold (5.4 +/- 0.8 to 27.1 +/- 6.1 microL min-1), Na excretion 23-fold (0.4 +/- 0.1 to 7.6 +/- 1.8 mumol min-1) and K excretion fourfold (0.6 +/- 0.18 to 3.8 +/- 0.5 mumol min-1). When the concentration mechanisms were damaged with BEA, the basal excretion rates of water and Na increased. The natriuretic response to ICV stimulation was severely impaired in these rats, but the kaliuretic effect was sustained.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Mechanisms of pressure natriuresis: how blood pressure regulates renal sodium transport.

An acute increase in blood pressure provokes a rapid decrease in proximal tubule salt and water reabsorption that is central to tubuloglomerular feedback regulation of renal blood flow and glomerular filtration rate and contributes to pressure natriuresis. The molecular mechanisms responsible for this critical homeostatic adjustment were studied. When blood pressure is acutely elevated, apical proximal tubule NHE3 are rapidly redistributed out of the microvilli to intermicrovillar clefts and then endosomal pools, and Na,K-ATPase activity is suppressed. Depressing apical Na(+) entry without hypertension is not sufficient to decrease Na,K-ATPase activity, and depressing Na,K-ATPase activity alone is not sufficient to decrease proximal tubule Na(+) and water reabsorption; thus, it appears that coordinated decreases in both NHE3 surface distribution and Na,K-ATPase activity may be important for the response to acute hypertension. Clamping plasma angiotensin II levels blunts the retraction of NHE3 from the cell surface to endosomal pools. The increased volume flow of salt and water to the loop of Henle stimulates Na,K-ATPase activity in this region and provides evidence for a downstream shift in sodium transport during acute hypertension. These same responses in the proximal tubule and loop develop and persist in the spontaneously hypertensive rat. These studies demonstrate that sodium transporters along the nephron are very dynamic, responding quickly to normal fluctuations of blood pressure, and are key to generating the macula densa tubuloglomerular feedback signal and for accommodating increased volume flow through the loop of Henle.

Animals↗
PubMed1981

The role of renal nerves in the diuresis and natriuresis caused by stimulation of atrial receptors.

The diuretic response to stimulation of left atrial receptors by distending balloons located either at the pulmonary vein-left atrial junctions or in the body of the left atrium, was studied in anaesthetized dogs in which on kidney had been surgically denervated. In these dogs diuretic and natriuretic responses to stimulation of atrial receptors were obtained in the denervated and the intact kidney; both responses were significantly greater in the intact kidney than in the denervated kidney. In the denervated kidney the natriuretic response showed a significant correlation to increases in heart rate resulting from stimulating of atrial receptors. It is concluded that the renal nerves contribute significantly to the increases in urine flow and sodium excretion in response to stimulation of atrial receptors. In the denervated kidney, the diuresis appeared to be mediated by a humoral mechanism and the natriuresis was associated with concomitant increases in heart rate.

Animals↗
PubMed1986

Retrograde infusion of blood into a pulmonary vein promotes natriuresis in anaesthetized dogs.

Retrograde infusion of blood into a pulmonary vein raised the pressure by 0.5-1 kPa in the cannulated vein. There were no changes in heart rate, arterial blood pressure, left atrial pressure, right atrial pressure or the pressure in the other pulmonary veins. The rise in pulmonary venous pressure was associated with an increase in urinary sodium concentration and excretion. However, there was no change in urine volume. The natriuresis was abolished by cooling the vagi to 9 degrees C. It is argued that receptors up-stream in the pulmonary veins themselves may be involved in the increase in sodium excretion that follows a rise in left atrial pressure.

Anesthesia↗
PubMed1996

Natriuresis caused by blood volume expansion in dogs is not mediated by the renal nerves.

The influence of renal denervation on the renal response to rapid blood volume expansion was investigated by measurement of urine volume, sodium and osmolar excretion rates, sodium p-aminohippurate and free water clearances, and systemic haemodynamic and plasma hormone (atrial natriuretic peptide, arginine vasopressin and plasma renin activity (PRA)) changes in ten control and ten renal-denervated chloralose-anaesthetized mongrel dogs. Following renal denervation, blood volume expansion caused a similar increase in sodium excretion to that in the control group. Renal denervation resulted in systemic vasodilatation and decreased PRA. During fluid loading the right atrial pressure and pulmonary capillary wedge pressure were significantly higher in the control group. In the control group, volume expansion caused a large fall in PRA, whereas in the renal-denervated dogs, PRA remained suppressed. We conclude, from the fact that natriuresis is preserved after renal denervation, that this response is not mediated by a reflex with efferent limb in the renal nerves.

Animals↗
PubMed1977

Increased urinary kallikrein excretion during prostaglandin E1 infusion in anaesthetized dogs and its relation to natriuresis and diuresis.

. The effect of intra-arterial prostaglandin E1 (PGE1) infusion on urinary kallikrein, sodium, potassium and water excretion was studied in normal anaesthetized dogs. 2. Infusion of PGE1 caused a dose-related increase in urinary excretion of kallikrein, sodium, potassium and water as well as an increase in renal blood flow (R.B.F.) and a fall in urinary osmolality and renal vascular resistance. 3. The changes occurred in the absence of appreciable changes in inulin clearance (Cin), arterial blood pressure, haematocrit, and plasma sodium and potassium concentrations. 4. The increased urinary kallikrein excretion correlated positively with the natriuresis, diuresis and kaliuresis and the increase in renal blood flow, but negatively with the urinary osmolality and renal vascular resistance. 5. It is concluded that renal kallikrein is involved in the renal response to arterial infusion of PGE1.

Animals↗
PubMed2003

Inhibition of Rho-kinase reduces renal Na-H exchanger activity and causes natriuresis in rat.

Rho-kinase regulates the actin cytoskeleton and therefore modulates transport. The role of Rho-kinase in Na-H exchanger (NHE) activity of rat proximal convoluted tubules (PCTs) was investigated using (R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide (Y-27632), a specific inhibitor of Rho-kinase. In spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats, apical and basolateral NHE activities were determined by measuring cell pH recovery following luminal NH4+ prepulse and basolateral sodium removal, respectively. Apical NHE activity was greater in 8 to 9 week old hypertensive SHR compared with WKY. Although Y-27632 suppressed pH(i) recovery in both strains, sensitivity was 50-fold higher in adult SHR. Y-27632 suppressed basolateral NHE in both strains with similar sensitivity. Apical NHE activity was not greater in 5-week-old, not yet hypertensive, SHR rats compared with WKY. In clearance studies, Na excretion was less in SHR than in WKY rats. Y-27632 increased Na excretion and fractional excretion Na in both strains but more so in SHR. (22)Na uptake of the brush border membrane vesicle taken from Y-27632-treated rats decreased more than that from vehicle-treated animals in both adult SHR and WKY. We conclude that apical NHE activity is increased in SHR PCT compared with controls and that inhibition of Rho-kinase reduces PCT NHE activities and causes natriuresis.

Amides↗
PubMed1975

Natriuresis following fourth ventricle perfusion with high-sodium artificial CSF.

Perfusion of the fourth cerebral ventricle with high-sodium artificial cerebrospinal fluid was found to result in an increase in urinary sodium excretion in anesthetized cats. The natriuresis was accompanied by an increase in blood pressure and glomerular filtration rate. However, in animals with the changes in blood pressure and glomerular filtration rate prevented by alpha adrenergic blockade (phenoxybenzamine), the increase in urinary sodium excretion persisted. the data suggest the presence of a neural mechanism in the vicinity of the fourth ventricle sensitive to cerebrospinal fluid sodium levels and capable of affecting urinary sodium excretion independent of changes in blood pressure or glomerular filtration rate. The possible role of the area postrema and adjacent medulla is considered.

Adrenergic alpha-Antagonists↗
PubMed1984

Renal venous pressure and volume natriuresis in the rat.

Anesthetized rats were surgically prepared so that left renal venous pressure could be maintained at its normal level (near 1 mmHg) (1 mmHg = 133.322 Pa) while right renal venous pressure was free to change in response to acute isoncotic blood volume expansion (n = 10). The purpose of the study was to test whether the renal venous pressure changes normally accompanying a 33% blood volume expansion have an effect on inulin clearance (CIn) and on the rates of excretion of water (V) or sodium (UNaV) by the kidneys. In 10 control rats blood volume was not expanded. The results showed that the volume expansion used resulted in a peak pressure of 5.3 +/- 0.5 (SEM) mmHg in the right renal vein. Both kidneys showed significant increases in CIn, V, and UNaV over their respective preexpansion values. However, there were no significant differences between these parameters measured in the right or in the left kidney even though the differences between the two renal venous pressures were highly significant during the infusion and for the next 20 min. In a further six rats, a caval snare was placed superior to the right renal vein so that both renal venous pressures could be held at normal during blood volume expansion. The ensuing diuresis and natriuresis were not different from those observed in the preceding group. It is concluded that changes in renal venous pressure, of the magnitude associated with volume expansion, have no significant effect on renal excretion rates.

Animals↗
PubMed1995

Involvement of renin-angiotensin system in the reduced pressure natriuresis response of hyperthyroid rats.

Previous studies have indicated that the pressure diuresis and natriuresis (PDN) response is greatly impaired in thyroxine-treated hypertensive rats. In the present study, we have examined the role of the renin angiotensin system (RAS) as a mediator of these alterations by characterizing the relationships between renal perfusion pressure and urine flow and sodium excretion in hyperthyroid rats acutely treated with a converting-enzyme inhibitor (captopril, 2 mg/kg) or an AT1 angiotensin II receptor blocker (losartan, 10 mg/kg). In the control animals, captopril did not change mean arterial pressure (MAP) or renal blood flow (RBF) but significantly decreased MAP and increased RBF and glomerular filtration rate in the hyperthyroid rats. Captopril did not change the PDN response of the control animals but improved significantly that of the hyperthyroid rats, although it was not completely normalized. Losartan also significantly improved renal hemodynamics and excretion in hyperthyroid rats. These results indicate that an increased intrarenal activity of the RAS is partly responsible for the blunted renal PDN mechanism of the hyperthyroid rats.

Animals↗
PubMed1993

Pressure diuresis and natriuresis in cirrhotic rats.

Arterial hypotension in liver cirrhosis has been proposed as a major mechanism contributing to renal sodium and water retention. To evaluate kidney excretory responses at different levels of arterial pressure (AP), we have characterized the relationships between renal perfusion pressure (RPP) and sodium and water excretion in carbon tetrachloride cirrhotic rats. Experiments were performed in anesthetized control (n = 9) and cirrhotic rats with (Asc, n = 6) and without ascites (Cir, n = 6) by mechanically adjusting vascular resistance in animals with renal denervation and infused with main systemic hormones. Control and Cir animals showed similar glomerular filtration rates (GFR), renal blood flows, hematocrits (Hct), and plasma proteins (PP). However, Hct, PP, and GFR were significantly lower in the Asc rats. For the same level of RPP, both cirrhotic groups excreted significantly less water and sodium than controls. Then, the pressure diuresis and natriuresis relationships of the Cir animals were significantly depressed, but those of the Asc animals were more reduced than those of the Cir rats. These results indicate that the cirrhotic kidney is not able to normally increase the sodium and water excretion in response to changes in AP. Intrarenal mechanisms, and not mainly RPP, are likely mediators of the renal alterations of liver cirrhosis.

Animals↗
PubMed1990

Atrial natriuretic factor release and natriuresis in rats with high-output heart failure.

We investigated whether rats with high-output heart failure [aortocaval (AC) shunts] release atrial natriuretic factor (ANF) and excrete sodium after moderate volume expansion (VE) as do sham-operated controls. Mean arterial blood pressure was lower (92.5 +/- 4.4 vs. 114.0 +/- 1.3 mmHg) and relative heart weight was higher (545.6 +/- 35.1 vs. 253.8 +/- 9.8 mg/100 g body wt) in animals with AC shunts than in their controls. Central venous pressure (CVP) was elevated (3.61 +/- 0.36 vs. 0.37 +/- 0.94 mmHg) and heart rate decreased (332.5 +/- 8 vs. 370.0 +/- 9.9 beats/min) in AC rats. This group also presented lower basal urinary sodium excretion (UNaV), urinary volume, and hematocrit than their sham-operated controls. Basal plasma COOH- and NH2-terminal ANF levels were greatly elevated in AC shunt animals (165.43 +/- 55.73 and 1,692.98 +/- 305.63 fmol/ml, respectively) when compared with the controls (14.27 +/- 1.49 and 331.67 +/- 29.84 fmol/ml, respectively). VE was performed in conscious rats 3 times at 15-min intervals with human plasma protein fraction. The effect of VE on CVP, left-ventricular end-diastolic pressure, the increases in plasma COOH- and NH2-terminal ANF, and the diuretic and natriuretic responses were similar in both experimental groups. U(NA)V was positively correlated with plasma COOH- (r = 0.50, P less than 0.01) and NH2- (r = 0.60, P less than 0.001) terminal ANF only in the controls. One main peak of immunoreactive ANF corresponding to the elution time of a small peptide such as ANF-(99-126) was detected in the plasma of AC animals after VE. We conclude that ANF release and natriuresis are conserved after moderate VE in a rat model of moderate high-output experimental heart failure.

Animals↗