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PubMed2001

Furosemide-induced natriuresis as a test to identify cirrhotic patients with refractory ascites.

The diagnosis of refractory ascites in cirrhotic patients carries a poor prognosis and liver transplantation should always be considered in this situation. Identification of patients who will not respond to diuretic therapy usually requires several weeks of observation during which a trial of diuretics is instituted using stepwise increases in dosage in order to classify ascites as refractory. In the present study we evaluated the effect of a single dose of 80 mg intravenous furosemide on urinary sodium excretion over 8 hours in cirrhotic patients with ascites responsive to diuretic treatment (group 1; n = 14) and patients with refractory ascites (group 2; n = 15). The test was performed after 3 days without diuretics and patients were on a 80 mEq sodium/day diet. Refractory ascites was defined by the absence of response after 3 months of high doses of diuretics (spironolactone 200 mg/d + furosemide 80 mg/d + metolazone 2.5 mg/d) and the need for repeated paracentesis. The two groups had similar degrees of liver and renal dysfunction as assessed by the Pugh score and creatinine clearance. The effects of furosemide on 8-hour natriuresis was much higher in patients with responsive ascites as compared with patients with refractory ascites (125 +/- 46 vs. 30 +/- 16 mEq; mean +/- SD; P <.0001). A natriuresis lower than 50 mEq/8 hours was observed in all group-2 patients as compared with none from group 1. The present study shows that patients with refractory ascites can be identified quickly and accurately by using this simple furosemide-induced natriuresis test, which could be very useful to select patients for liver transplantation.

Ascites↗
PubMed1988

Antihypertensive drugs and sodium restriction. Analysis of their interaction based on pressure-natriuresis relationship.

The hypotensive effects of some antihypertensive drugs are augmented under sodium restriction, while those of others are not. The mechanisms of these interactions were theoretically analyzed based on the arterial pressure-natriuresis relationship. Four-week studies were performed in 24 patients with essential hypertension who were given a regular sodium diet (12-15 g of NaCl/d) in the first and third weeks and a sodium-restricted diet (1-3 g/d) in the second and fourth weeks. One of three antihypertensive drugs, 60 mg/d of nicardipine (Ca-antagonist), 120 mg/d of propranolol (beta-blocker) or 150 mg/d of captopril (converting-enzyme inhibitor) was administered in the third and fourth weeks. The mean arterial pressure and urinary sodium excretion were measured on the last three days of each week. The degree of interaction between the antihypertensive drugs and sodium restriction was statistically compared. The hypotensive effect of nicardipine and propranolol did not differ with the change in sodium intake, whereas that of captopril was greater under sodium restriction than under the regular sodium diet. Urinary sodium excretion was plotted on the ordinate as a function of arterial pressure before and after administration of the antihypertensive drugs. The pressure-natriuresis curve was shifted left, without a change in the slope, by nicardipine and propranolol and also left, but with a decrease in the slope, by captopril. The hypotensive effect of nicardipine and propranolol, being independent of the amount of sodium intake, was based on the leftward shift of the pressure-natriuresis curve that was probably due to the decrease in renal vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗
PubMed1989

Effects of oral calcium, potassium, digoxin, and nifedipine on natriuresis in normal humans.

Many factors influence renal sodium excretion and blood pressure. We tested the independent effects of dietary calcium (Ca; 500 mg twice daily), potassium (KCl; 20 mEq three times daily), sodium-potassium dependent ATPase inhibition (digoxin), calcium channel blockade (nifedipine), and placebo, on acute natriuresis in 14 normal subjects while receiving 150 mEq/d sodium diets and 2 L normal saline intravenously over four hours. Each subject received each regimen in random sequence. Sodium balance before infusion was not different among the regimens. Plasma renin activity (PRA) was increased in subjects receiving nifedipine, while the plasma aldosterone concentration (PA) was not different among the regimens. None of the regimens influenced the clearance of inulin or paraaminohippurate (PAH) either before or after saline infusion. 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-hour sodium excretion on that day to above that of the other regimens. The data support the notion that potassium and nifedipine may decrease blood pressure by facilitating sodium excretion. Nifedipine may also uncouple renin from aldosterone. Oral calcium supplementation and sodium-potassium dependent ATPase inhibition did not facilitate natriuresis.

Administration, Oral↗
PubMed1990

Role of endogenous dopamine in the natriuresis accompanying various sodium challenges.

The contribution of endogenous dopamine (DA) to the natriuresis accompanying various sodium challenges is reviewed. Data are presented suggesting that DA participates in the control of sodium excretion produced by a normal sodium diet, increments in sodium consumption, and an acute infusion of isoosmotic saline. In contrast, the natriuresis accompanying a high sodium diet in the dog and extracellular fluid volume expansion with hypoosmotic saline or a very large volume of isoosmotic saline is independent of DA activity. Thus, the evidence suggests that DA contributes to the natriuresis produced by some, but not all, forms of sodium loading.

Animals↗
PubMed1993

Tubular site of the natriuresis after unilateral nephrectomy in the rat.

Unilateral nephrectomy (UNX) is followed by a prompt increase in sodium excretion from the remaining kidney. Recently, an important role for atrial natriuretic peptide (ANP) in mediating the UNX-associated natriuresis has been suggested. The present studies were undertaken to gain insight into the intrarenal mechanisms participating in the post-UNX natriuresis in circumstances in which the release or the action of endogenous ANP were suppressed by prior removal of the right atrial appendage and by administration of monoclonal anti-ANP antibodies, respectively. In anesthetized euvolemic untreated rats, UNX resulted in a twofold increase in urinary excretion of sodium (from 0.93 +/- 0.23 to 2.14 +/- 0.34 microE/min; p < 0.03), whereas glomerular filtration rate did not change significantly. Fractional excretion of lithium, an index of proximal tubular handling of sodium, increased from 30.7 +/- 3.4% to 39.4 +/- 4.0%, and fractional distal reabsorption of sodium decreased from 98.6 +/- 0.2% to 96.5% +/- 0.4% (both p < 0.006). Neither sham atrial appendectomy nor the administration of nonspecific antibodies affect the natriuretic response of the remaining kidney. The natriuretic response to UNX was abolished in right atrial appendectomized rats, as well as in rats receiving anti-ANP antibodies. Post-UNX changes in both proximal and distal tubular reabsorption of sodium were also suppressed in these animals. These observations indicate that ANP may be an important mediator of the natriuretic response to UNX and that the proximal and the distal part of the nephron contribute to the postnephrectomy natriuresis.

Animals↗
PubMedDate not supplied

Mechanisms mediating pressure natriuresis: what we know and what we need to find out.

1. It is well established that pressure natriuresis plays a key role in long-term blood pressure regulation, but our understanding of the mechanisms underlying this process is incomplete. 2. Pressure natriuresis is chiefly mediated by inhibition of tubular sodium reabsorption, because both total renal blood flow and glomerular filtration rate are efficiently autoregulated. Inhibition of active sodium transport within both the proximal and distal tubules likely makes a contribution. Increased renal interstitial hydrostatic pressure (RIHP) likely inhibits sodium reabsorption by altering passive diffusion through paracellular pathways in 'leaky' tubular elements. 3. Nitric oxide and products of cytochrome P450-dependent arachidonic acid metabolism are key signalling mechanisms in pressure natriuresis, although their precise roles remain to be determined. 4. The key unresolved question is, how is increased renal artery pressure 'sensed' by the kidney? One proposal rests on the notion that blood flow in the renal medulla is poorly autoregulated, so that increased renal artery pressure leads to increased renal medullary blood flow (MBF), which, in turn, leads to increased RIHP. An alternative proposal is that the process of autoregulation of renal blood flow leads to increased shear stress in the preglomerular vasculature and, so, release of nitric oxide and perhaps products of cytochrome P450-dependent arachidonic acid metabolism, which, in turn, drive the cascade of events that inhibit sodium reabsorption. 5. Central to the arguments underlying these opposing hypotheses is the extent to which MBF is autoregulated. This remains highly controversial, largely because of the limitations of presently available methods for measurement of MBF.

Animals↗
PubMed1981

Renal nerve activity and exaggerated natriuresis in conscious spontaneously hypertensive rats.

Exaggerated natriuresis upon volume loading occurs in both human and animal hypertension and is mainly due to suppressed tubular reabsorption. To explore whether altered renal sympathetic activity contributes to this response, conscious male spontaneously hypertensive rats (SHR) were exposed to isotonic saline loading in comparison with normotensive male Wistar Kyoto rats (WKR). After a 60 min control hydropenic period, during which mean arterial pressure, heart rate, renal sympathetic nerve activity and urinary sodium excretion were followed, a 60 min period of intravenous volume expansion with isotonic saline (0.2 ml/min X 100 g b.w.) was started followed by a 60 min hydropenic recovery period. Already during the control period sodium excretion was significantly higher in SHR. During the volume load and subsequent recovery period a clearly exaggerated natriuresis occurred in SHR compared with WKR. Further, volume loading reduced renal sympathetic nerve activity in all animals, but significantly more in SHR. Moreover, volume loading reduced mean arterial pressure and heart rate in both groups. It is suggested that the accentuated reflex inhibition of renal sympathetic activity in SHR upon volume loading emanates from cardiac mechanoreceptors and partly explains the exaggerated natriuresis in SHR. This augmented "volume' reflex response is probably due to reduced systemic venous compliance in SHR with a consequently increased central filling and cardiac receptor activation.

Animals↗
PubMed1989

Renal denervation does not prevent dehydration-induced natriuresis in sheep.

Normal sheep or sheep in which the renal nerves had been extirpated were deprived of water for 2 days in order to determine whether changes in renal nerve activity contribute to natriuresis during water deprivation. Both groups of sheep showed a considerable natriuresis throughout the period of water deprivation and increases in plasma osmolality and plasma Na concentration. Renal denervation, as indicated by the absence of catecholamine fluorescence in kidney sections, was extensive. Previous experiments have suggested cerebral involvement in the induction of dehydration-induced natriuresis. The present results indicate that the efferent pathway mediating this cerebral influence on renal sodium excretion does not involve the renal nerves, suggesting a hormonal mechanism as the likely pathway.

Animals↗
PubMed1994

Reducing brain sodium concentration prevents post-prandial and dehydration-induced natriuresis in sheep.

Renal Na excretion during the 24 h following feeding was studied in sheep. A pronounced natriuresis occurred 3.5-5.5 h after feeding. Na excretion then fell to low levels in animals allowed to drink water, but was significantly elevated above this level in water-deprived sheep for most of the remaining period. Both the post-prandial and dehydration-induced natriuresis were prevented by intracerebroventricular (icv) infusions of low Na concentration 0.3 mol l-1 mannitol at 1 ml h-1, and a water diuresis also occurred. These effects were not caused by icv infusion of artificial cerebrospinal fluid (Na concentration = 150 mmol l-1). As a result, there was a much greater increase in plasma Na concentration and osmolality in the sheep given icv mannitol. Intravenous infusion of vasopressin prevented the water diuresis induced by icv mannitol, but the inhibition of natriuresis was still observed and plasma Na concentration increased by 8 mmol l-1 over 24 h compared with an increase of 3 mmol l-1 in dehydrated sheep infused icv with artificial cerebrospinal fluid. The results show that the ambient Na concentration in the brain plays an important role in the normal homeostatic regulation of Na balance by the kidney in sheep.

Animals↗
PubMed1990

Normalization of arterial pressure after barodenervation: role of pressure natriuresis.

Studies in several species have demonstrated that mean arterial pressure (MAP) is normal or only slightly elevated after chronic arterial baroreceptor denervation. We hypothesized that the absence of sustained hypertension after barodenervation was the result of a pressure natriuresis response, secondary to sympathetic vasoconstriction of nonrenal vasculature. To test this hypothesis, MAP, sodium balance (NaBal), and water balance were measured before and after aortic baroreceptor denervation (ABD), sinoaortic denervation (SAD), or sham surgery in conscious rats. MAP was increased 20.0 +/- 3.7 mmHg 1 day after ABD but returned to control by day 3. ABD had no significant effect on daily NaBal or water balance. The responses to SAD were similar to those after ABD, with the exception that a significant natriuresis was observed the first day after SAD. However, this was followed by a significant antinatriuresis on day 2, when MAP was still elevated. By day 3 after SAD, MAP, NaBal, and water balance were not significantly different from control. These results suggest that the normalization of MAP after ABD or SAD is not the result of pressure natriuresis but rather failure to maintain a chronic elevation of sympathetic activity after barodenervation.

Animals↗
PubMed1993

Evaluation of renal hormones in natriuresis induced by renal arterial saline infusion.

Low rates of unilateral renal arterial infusion with isotonic saline (154 mM NaCl) produce a natriuresis in both kidneys in anesthetized rats, with the involvement of a blood-borne factor. We investigated whether this response was modulated by known renal or adrenal hormones. The response to saline infusion at 0.05 ml/min was tested after acute adrenalectomy (n = 7), in the presence of various blocking agents [captopril (3 mg.kg-1.h-1, n = 7), indomethacin (5 mg/kg, n = 8), aprotinin (25 KIU/min, n = 8), propranolol (1 micrograms/min, n = 6), or benserazide (15 micrograms/min, n = 6)], and after lignocaine infusion around the renal artery (12.5 micrograms/min, n = 5). In all cases, the overall increase in sodium excretion by both kidneys was not significantly less (alpha < or = 0.01) than that in untreated rats; it was increased by aprotinin, renal nerve blockade, and propranolol. Plasma levels of angiotensin II, aldosterone, and atrial natriuretic peptide were unchanged by renal arterial saline infusion. We conclude that the saline-induced natriuresis is not reduced by inhibition of the production of angiotensin II, prostaglandins, kinins, dopamine, or adrenal hormones, or by factors released by the renal nerves, indicating that none of these is directly responsible for the saline-induced natriuresis.

Adrenalectomy↗
PubMed1997

Dopamine and diltiazem-induced natriuresis in the spontaneously hypertensive rat.

An attenuated natriuretic response to dopamine and D1 agonists in genetic hypertension has been attributed to an uncoupling of the renal D1 dopamine receptor from its G protein-effector protein complex. We have reported that in normotensive Wistar-Kyoto (WKY) rats the natriuresis induced by calcium channel blockers is caused in part by activation of renal D1 dopamine receptors. We tested the interaction between the renal D1 receptor and a calcium channel blocker, diltiazem, infused into a renal artery of anesthetized spontaneously hypertensive rats (SHR) acutely loaded with 5% saline. Diltiazem produced a 50% increase in renal blood flow and nearly tripled absolute and fractional sodium excretion; urine flow rate more than doubled, but glomerular filtration rate did not change. However, the D1 receptor antagonist SKF-83742, which had no effect by itself, did not diminish the response to diltiazem. In a separate group of concurrent experiments, we found that the diltiazem-induced natriuresis was associated with a decrease in Na(+)-K(+)-adenosinetriphosphatase activity in the renal medulla of SHR. In contrast, in WKY rats, no changes were noted in the renal medulla but a decrease in Na(+)-K(+)-adenosinetriphosphatase activity was noted in the renal cortex. Diltiazem had no effect on urinary dopamine excretion in either rat strain. We conclude that diltiazem induces natriuresis differently in SHR and WKY rats; it is independent of D1 receptors in SHR and is in great part mediated by renal hemodynamic, rather than by cortical tubular, effects. These studies support previous findings of a defective renal cortical tubular D1 mechanism in SHR.

Animals↗
PubMed1997

Long-term captopril treatment restores natriuresis after carotid baroreceptor activation in the SHR.

In anesthetized Sprague-Dawley rats, intermittent bilateral carotid artery traction (BilCAT) caused a transient decrease in mean arterial pressure (MAP) of 28 +/- 3 mmHg and led to a progressive increase in sodium excretion (UNaV) that nearly doubled 45-90 min after initiation of the repetitive application of BilCAT (P < 0.001). This natriuresis was accompanied by an increase in glomerular filtration rate (GFR) from 2.70 +/- 0.3 to 3.2 +/- 0.3 ml/min (P < 0.001), no change in renal plasma flow [clearance of p-aminohippurate (PAH)], and an increase in the fractional excretion of lithium. Rats with bilateral renal denervation exhibited neither natriuresis nor an increase in GFR in response to BilCAT despite similar vasodepression caused by the maneuver. Normotensive Wistar-Kyoto (WKY) rats responded to BilCAT like Sprague-Dawley rats, whereas spontaneously hypertensive rats (SHR) exhibited an exaggerated vasodepressor response to BilCAT (-51 +/- 3 mmHg) without increasing either UNaV or GFR. Separate groups of WKY and SHR were treated from 4 wk of age with captopril added to the drinking water at a concentration of 1 g/l. At 12-14 wk, both groups had lower MAP compared with untreated animals. Captopril treatment did not alter either the natriuretic response or the increase in GFR seen in untreated WKY after BilCAT, and the maneuver produced equivalent degrees of vasodepression as in controls. However, treated SHR now responded to BilCAT with increases in both UNaV and GFR that closely resembled the responses seen in Sprague-Dawley and WKY rats. These results suggest that BilCAT produces natriuresis through a pathway dependent on the renal nerves. This pathway does not function in untreated SHR despite similar vasodepression. Long-term treatment with captopril restores this reflex pathway in SHR, lending support to the concept that angiotensin II is critically linked to heightened sympathetic nerve activity and abnormal sodium metabolism in this strain.

Analysis of Variance↗
PubMed2000

Determinants of the natriuresis after acute, slow sodium loading in conscious dogs.

The relative importance of systemic volume, concentration, and pressure signals in sodium homeostasis was investigated by intravenous infusion of isotonic (IsoLoad) or hypertonic (HyperLoad) saline at a rate (1 micromol Na(+) x kg(-1) x s(-1)), similar to the rate of postprandial sodium absorption. IsoLoad decreased plasma vasopressin (-35%) and plasma ANG II (-77%) and increased renal sodium excretion (95-fold), arterial blood pressure (DeltaBP; +6 mmHg), and heart rate (HR; +36%). HyperLoad caused similar changes in plasma ANG II and sodium excretion, but augmented vasopressin (12-fold) and doubled DeltaBP (+12 mm Hg) without changing HR. IsoLoad during vasopressin clamping (constant vasopressin infusion) caused comparable natriuresis at augmented DeltaBP (+14 mm Hg), but constant HR. Thus vasopressin abolished the Bainbridge reflex. IsoLoad during normotensive angiotensin clamping (enalaprilate plus constant angiotensin infusion) caused marginal natriuresis (9% of unclamped response) despite augmented DeltaBP (+14 mm Hg). Cessation of angiotensin infusion during IsoLoad immediately decreased BP (-13 mm Hg) and increased glomerular filtration rate by 20% and sodium excretion by 45-fold. The results suggest that fading of ANG II is the cause of acute "volume-expansion" natriuresis, that physiological ANG II deviations override the effects of modest systemic blood pressure changes, and that endocrine rather than hemodynamic mechanisms are the pivot of normal sodium homeostasis.

Angiotensin II↗
PubMed2000

Volume expansion natriuresis during servo control of systemic blood pressure in conscious dogs.

The importance of arterial blood pressure (BP) and ANG II for the renal natriuretic response (NaEx) to volume expansion (3.5% body wt) was investigated during converting enzyme blockade (enalaprilate, 2 mg/kg). In separate experiments, BP was clamped either 30 mm Hg above or a few millimeters mercury below baseline by servo-controlled infusion of ANG II or sodium nitroprusside, respectively, so that volume expansion did not change BP. Enalapril decreased BP by 8 mm Hg. Without clamping, volume expansion returned BP to that of preenalapril control and increased NaEx 10-fold (40+/-10 to 377+/-69 micromol/min). During high pressure clamping (133+/-2 mm Hg), peak NaEx after volume expansion was 6% of control experiments. During low pressure clamping, NaEx was 68% of control experiments (45+/-15 to 256+/-64 micromol/min). The results show that 1) in absence of ANG II, volume expansion elicited pronounced natriuresis without increases in BP beyond baseline, 2) in the presence of hypertensive amounts of ANG II, the volume expansion-induced natriuresis was almost eliminated, and 3) nitroprusside prevented the increase in BP but not sodium excretion during volume expansion. ANG II appears to dominate the control of NaEx; however, when absent, volume expansion may still induce marked natriuresis even at constant BP, possibly via nitric oxide-mediated mechanisms.

Angiotensin II↗
PubMed1985

Fasting induces denervation natriuresis in the conscious rat.

The participation of renal nerves in the regulation of sodium excretion was studied in fed and overnight-fasted rats subjected to acute or chronic left kidney denervation or sham operation. Clearance experiments were performed on conscious restrained animals. Urine flow, glomerular filtration rate (GFR), and urinary sodium excretion were not different in left and right kidneys of sham-operated rats. In fed conscious rats, urine flow, GFR, and urinary sodium excretion of innervated (I) and denervated (D) kidneys were similar. In fasted conscious rats, significant denervation natriuresis was observed after both acute (I, 1.06 +/- 0.27; D, 1.56 +/- 0.40 mumol . min-1 . g-1, P less than 0.05) and chronic (I, 1.55 +/- 0.19; D, 2.20 +/- 0.18 mumol . min-1 . g-1, P less than 0.01) renal sympathectomy, whereas urine flow and GFR in I and D kidneys were not different. Additional experiments revealed that extracellular fluid and plasma volumes of fasted rats were decreased by approximately 10% compared with those of fed animals due to a significant overnight natriuresis and negative water balance. In fed conscious rats, the renal nerves do not seem to participate in the regulation of sodium excretion. The presence of denervation natriuresis in conscious fasted rats suggests that renal nerves are involved in sodium conservation during fasting to maintain extracellular fluid and plasma volume.

Animals↗
PubMed1985

Natriuresis induced by arginine vasopressin infusion in sheep.

The aim of this study was to investigate whether arginine vasopressin (AVP) is natriuretic in sheep at plasma concentrations comparable to those induced by water deprivation. AVP was infused intravenously at 0.1, 0.2, and 0.5 microgram/h for 24-48 h in sheep allowed free access to water. Infusion of AVP at 0.1 microgram/h did not alter renal Na output, whereas infusion of AVP at both 0.2 and 0.5 microgram/h significantly increased daily output of Na in urine. Significant natriuresis did not occur until 3.5 h after the start of AVP infusion at 0.2 microgram/h. Plasma AVP levels induced by these infusions were 9.8 +/- 1.6 (0.1 microgram/h AVP), 21.9 +/- 7.7 (0.2 microgram/h AVP), and 32.5 +/- 9.0 pg/ml (0.5 microgram/h AVP) after 24 h. These concentrations are within the range found in sheep deprived of water for 3 days. Hypophysectomy abolished increases in plasma AVP concentration but not natriuresis in response to water deprivation. This suggests that increased plasma AVP concentration does not play an essential role in the mechanisms subserving dehydration-induced natriuresis.

Animals↗
PubMed1986

Cholinergic stimulation of the hypothalamus and natriuresis in rats: role of the renal nerves.

The role of the renal nerves in the natriuresis seen after cholinergic stimulation of the hypothalamus was studied in anesthetized rats treated with injection into the lateral hypothalamus (LH) of 1 microgram of carbamylcholine chloride (carbachol) in 1 microliter of 0.15 M NaCl or NaCl alone. Injection of carbachol exhibited diuresis and natriuresis both in acutely denervated kidneys (P less than 0.01) and in contralateral innervated kidneys (P less than 0.01) without changes in glomerular filtration rate (GFR) or renal plasma flow (RPF) (n = 10). Salt and water excretion was unchanged in 10 rats after injection of NaCl. Micropuncture studies in denervated kidneys showed that, after carbachol injection, tubular fluid-to-plasma inulin concentration ratio [(F/P)In] in the late proximal tubule fell from 1.86 +/- 0.08 to 1.64 +/- 0.07 (P less than 0.01) without changes in single-nephron GFR. In nine other carbachol-treated rats in which renal perfusion pressure was maintained low and constant, diuresis and natriuresis, although attenuated, were again observed both in denervated (P less than 0.01) and in contralateral innervated kidneys (P less than 0.05). In another group of 11 animals, efferent renal nerve activity (ERNA) was recorded before and after LH injection of carbachol and isotonic saline. ERNA was significantly depressed for 30 min, only after carbachol injection. Our results suggest that the renal nerves, although involved, are not essential for the natriuretic response after cholinergic stimulation of LH. By exclusion, other factors, presumably hormones, must contribute to the response.

Animals↗