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PubMed1997

Pressure natriuresis after adrenomedullin in anesthetized spontaneously hypertensive rats.

Adrenomedullin (ADM), a peptide with potent vasodilatory and natriuretic actions, is elevated in patients with essential hypertension. Because pharmacological doses of ADM result in renal vasodilation and natriuresis, it has been suggested that ADM may play a modulatory role in hypertension through potential actions on renal pressure natriuresis. However, it is unclear whether elevation of plasma ADM within the pathophysiological range has similar actions. To determine the effects of pathophysiological doses of ADM on blood pressure and on the relationship between renal perfusion pressure (RPP) and renal hemodynamics and sodium excretion, renal function was determined at RPPs of 80, 105, 130, and 155 mm Hg in spontaneously hypertensive rats (SHR) infused with ADM at 50 ng x kg(-1) x min(-1) (ADM-50, n=5) and at 100 ng x kg(-1) x min(-1) (ADM-100, n=5) and in control SHR (n=5). Decreasing RPP from 155 to 80 mm Hg in control SHR decreased (P<.05) absolute sodium excretion from 0.81+/-0.25 to 0.04+/-0.02 microEq/min, fractional sodium excretion from 0.32+/-0.11% to 0.06+/-0.04%, and urine flow rate from 11.5+/-2.8 to 1.03+/-0.31 microL/min. ADM infusion elevated (P<.05) plasma ADM levels in ADM-infused SHR (679+/-47 pg/mL in ADM-50, 858+/-79 in ADM-100) compared with control (79.5+/-27.8). However, although reduction of RPP from 155 to 80 mm Hg in ADM rats decreased absolute sodium excretion (ADM-50, 0.98+/-0.10 to 0.09+/-0.04 microEq/min; ADM-100, 0.95+/-0.09 to 0.07+/-0.02 microEq/min), fractional sodium excretion (ADM-50, 0.31+/-0.03% to 0.17+/-0.04%; ADM-100, 0.33+/-0.02% to 0.09+/-0.01%), and urine flow (ADM-50, 13.6+/-1.4 to 1.73+/-0.75 microL/min; ADM-100, 13.5+/-1.5 to 1.07+/-0.16 microL/min), these decreases were not different from values found in controls. Renal plasma flow and glomerular filtration rate were also similar in control and ADM-treated SHR at each level of RPP. Thus, acute increases in ADM to levels found in pathophysiological conditions have no effect on blood pressure, pressure natriuresis, or renal autoregulation in the SHR. These findings do not support the hypothesis that ADM serves as a modulating factor in hypertension, at least in the SHR.

Adrenomedullin↗

PubMed1997

A peptide released by pepsin from kininogen domain 1 is a potent blocker of ANP-mediated diuresis-natriuresis in the rat.

A 20-amino acid peptide, KYEIKEGDCPVQSGKTWQDC (PU-D1), released by pepsin hydrolysis of LMW kininogen domain 1 was tested for its ability to antagonize the diuretic and natriuretic effect of ANP(103-125) in anesthetized rats. A single dose of 10.8 or 21.6 pmol (25 or 50 ng) PU-D1 given intravenously or into the duodenal lumen suppressed the diuresis-natriuresis induced by 209 pmol (500 ng) ANP by 43% to 59% and 69% to 96%, respectively. None of the doses tested (2.16 to 432 pmol, 5 ng to 1 microg) modified systemic blood pressure. Strikingly, a single IV dose of 10.8 pmol PU-D1 blocked the action of ANP for more than 3 hours. ANP blockade by PU-D1 was annulled completely by the bradykinin (BK) B2 receptor inhibitor Hoe 140. On a molar basis, PU-D1 is more effective than BK and kinins of 15, 16, and 18 amino acids for blocking the ANP-mediated diuresis-natriuresis. As with BK and other kinins, the inhibitory effect of Pu-D1 on ANP is obtained only within a small range of picomol doses. A single dose of 2.16 or 4.32 pmol PU-D1 or 47 pmol (50 ng) BK is ineffective against ANP if injected alone. However, when both substances are administered concomitantly at these subthreshold doses, they totally suppress ANP-induced diuresis-natriuresis. These results raise the question of whether PU-D1, released from kininogen domain 1, either alone or associated with BK, may interact with ANP in the regulation of urinary water and electrolyte excretion in physiological and pathological conditions.

Amino Acid Sequence↗

PubMed2000

Role of kinins in the control of renal papillary blood flow, pressure natriuresis, and arterial pressure.

The present study evaluated the effects of blocking kinins with the bradykinin B(2) receptor antagonist Hoe140 on the relationship between renal perfusion pressure, papillary blood flow (PBF), and sodium excretion. To determine the relevance of renal kinins in the long-term control of arterial pressure, the effect of a chronic intrarenal infusion of Hoe140 on arterial pressure and sodium balance was also studied. PBF was not autoregulated in volume-expanded rats, and the administration of Hoe140 reduced PBF (-30%) and improved PBF autoregulation. The kinin antagonist also decreased sodium excretion (-35%) and blunted pressure natriuresis with no whole-kidney renal hemodynamic changes. These effects may be mediated through nitric oxide (NO), because in rats pretreated with N(G)-nitro-L-arginine methyl ester, Hoe140 had no additional effects on PBF or pressure natriuresis. A role for NO in mediating the renal response to Hoe140 is also supported by the finding that Hoe140 reduced basal urinary NO(3)(-)/NO(2)(-) excretion (-33%), and it blunted the arterial pressure-induced increase in NO(3)(-)/NO(2)(-) excretion, which is compatible with the idea that the pressure-natriuresis response may be mediated through kinins and NO. The importance of kinins in long-term regulation of arterial pressure is demonstrated by the severe arterial hypertension (172+/-6 mm Hg) induced during the chronic intrarenal infusion of Hoe140 associated with sodium and volume retention. These data suggest that renal kinins and NO may be a part of the renal mechanism coupling changes in arterial pressure with modifications in PBF and sodium excretion, therefore contributing to the long-term control of arterial pressure.

Adrenergic beta-Antagonists↗

PubMed1992

Diurnal and nocturnal diuresis and natriuresis in obstructive sleep apnea. Effects of nasal continuous positive airway pressure therapy.

Excessive nocturnal diuresis and natriuresis have been reported in patients with sleep apnea. The mechanisms responsible for these alternations in nocturnal renal function have not been clearly identified. To gain further insight into this matter, we studied 12 patients (one woman) with a mean +/- SD age of 50 +/- 9 yr and body mass index of 36.9 +/- 8.6 kg/m2. Polysomnography showed in all a sleep apnea syndrome with an apnea-hyponea index (AHI) of 81.3 +/- 41.7. Treatment with nasal continuous positive airway pressure (nCPAP) resulted in an AHI of 19.4 +/- 13.7 and in normalization of sleep characteristics. Diurnal renal function was normal in all subjects. Although untreated, patients showed an abolition of the well-known decrease in diuresis and natriuresis during the night (diurnal and nocturnal diuresis 56.3 +/- 26.8 and 77.2 +/- 33.4 ml/h, respectively, p = NS; diurnal and nocturnal fractional urinary Na+ excretion 0.42 +/- 0.09 and 0.70 +/- 0.55 ml/100 ml glomerular filtration [GF], respectively, p = NS). Results of nocturnal studies under nCPAP therapy showed a significant decrease in diuresis and natriuresis (nocturnal diuresis before and under nCPAP, respectively: 90.4 +/- 27.3 and 70.6 +/- 25.1 ml/h, p less than 0.02; nocturnal fractional urinary sodium excretion before and under nCPAP, respectively: 0.76 +/- 0.53 and 0.44 +/- 0.37 ml/100 ml GF, p less than 0.03). Morning blood levels of renin, aldosterone, antidiuretic hormone, epinephrine, and atrial natriuretic factor showed no significant difference before and under nCPAP, whereas norepinephrine significantly decreased from 309.5 +/- 104.2 before to 230.4 +/- 88.4 pg/ml under nCPAP (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Circadian Rhythm↗

PubMed1991

Oxytocin produces natriuresis in rats at physiological plasma concentrations.

Oxytocin (OT) is known to stimulate natriuresis in rats when administered in large doses that produce high plasma levels. We examined the effects of physiological plasma OT levels on renal sodium excretion by infusing graded doses of OT sc in conscious adult male rats maintained on a sodium-deficient diet. Our results demonstrate that OT causes a dose-related increase in urinary sodium excretion during the initial day of infusion. The lowest plasma OT levels associated with increases in urinary sodium excretion (5-6 pmol/liter) were well within the range of physiological OT secretion in rats. However, this natriuretic effect was not sustained during subsequent days of maintenance on a sodium-deficient diet, suggesting that the OT-induced natriuresis was limited in part by receptor desensitization and/or a decreased exchangeable sodium pool in combination with secretion of opposing antinatriuretic factors such as aldosterone. Pretreatment with an OT receptor antagonist completely blocked the natriuresis produced by a 20 pmol/h infusion of OT, but urinary sodium excretion was not affected by a vasopressin V1 antagonist and was blocked only partially by a combined vasopressin V1 and V2 antagonist. Together with previous studies in rats demonstrating an inverse relation between pituitary OT secretion and sodium appetite, these results support the hypothesis that peripherally and centrally secreted OT act in concert in rats to produce a negative sodium balance by stimulating sodium excretion while inhibiting sodium ingestion.

Angiotensin Receptor Antagonists↗

PubMed1994

Management of neurosurgical patients with hyponatremia and natriuresis.

The main objective of our study was to evolve a practical management protocol for neurosurgical patients with hyponatremia and natriuresis, based on their blood volume status and hematocrit. Twenty-one patients with hyponatremia and natriuresis and 3 control patients were studied. Patients with hyponatremia were categorized on the basis of their hematocrit, central venous pressure, and total blood volume. Group A consisted of patients with hypovolemia and anemia (16 patients); Group B patients had hypovolemia but no anemia (5 patients); Group C included those with hypervolemia (0 patients). Patients in Groups A and B received isotonic saline (> 50 ml/kg/d) and oral salt (12 g/d). Additionally, those in Group A were transfused with 500 ml of whole blood. The end points in the study were 72 hours after entry or two consecutive serum sodium values of > 130 mEq/L, whichever was earlier. Hyponatremia was corrected in all the patients within 72 hours (1 patient, < 24 h; 13 patients, < 48 h; and 7 patients, < 72 h). We conclude that most neurosurgical patients with hyponatremia and natriuresis have hypovolemia, with or without anemia. Fluid and salt replacement and a blood transfusion rather than fluid restriction often results in the correction of the hyponatremia. Our findings offer indirect evidence to support the hypothesis that in most of these patients, hyponatremia is caused by cerebral salt wasting syndrome, rather than the syndrome of inappropriate secretion of antidiuretic hormone.

Adolescent↗

PubMed1981

Studies on the mechanism of "exaggerated natriuresis" in essential hypertension.

Prompt and exaggerated natriuresis and diuresis were seen one to two hours after the starting of an infusion of 300 ml of 3% saline for one hour in patients with essential hypertension on a high sodium chloride intake. There were no significant differences in urinary volume and sodium excretion after the saline load in patients with normal and low plasma renin activity. The inhibition of angiotensin converting enzyme with SQ 14225 in patients with normal plasma renin activity did not produce additional natriuresis and diuresis after the saline load. Mean arterial blood pressure and/or changes in mean arterial blood pressure after the saline load showed a positive correlation with urinary volume and sodium excretion in each collection period in hypertensive subjects. Free water reabsorption in hypertensives was lower at high levels of osmolar clearance than that in control subjects. These results suggest that "exaggerated natriuresis" in essential hypertension is due to a decrease in tubular sodium reabsorption, which may be the result of intrarenal hemodynamic changes related to high blood pressure per se. The decreased medullary osmolar gradient is a possible contributing factor in the enhanced sodium and water excretion, while the renin-angiotensin-aldosterone system does not seem to play an important role.

Aldosterone↗

PubMed1990

[A study on the relationship between natriuresis and renally formed dopamine in the rat].

This study was undertaken to elucidate the relationship between natriuresis and renally formed dopamine in pentobarbital-anesthetized rats that were loaded with 0.9% NaCl. Infusion of dopamine resulted in marked increases in urinary free dopamine excretion, plasma free dopamine concentration, urine volume and urinary sodium excretion. Infusion of carbidopa markedly decreased urinary free dopamine excretion, but did not affect urine volume and urinary sodium excretion. Infusion of L-dopa markedly increased urinary free dopamine excretion and plasma free dopamine concentration, but did not affect urine volume and urinary sodium excretion. When carbidopa was infused with L-dopa or dopamine, carbidopa significantly inhibited the increase in urinary and plasma free dopamine induced by L-dopa, but did not inhibit the increases in urinary and plasma free dopamine, urinary sodium excretion and urine volume induced by dopamine. These data indicated that there is no correlation between renally formed dopamine and natriuresis, and furthermore suggested that renally formed dopamine is not essential for natriuresis.

Animals↗

PubMed1977

Natriuresis of fasting in intact and adrenalectomized rats.

Experiments were carried out in an attempt to elucidate the mechanism of fasting-induced natriuresis in conscious rats. Female animals were given low sodium diet and saline in a fixed concentration for at least three days, and deprived of food thereafter. The sodium balance significantly shifted to negative independently of potassium supply in intact rats. Such was also observed in the dexamethasone-replaced, adrenalectomized rats and was not affected by further administration of aldosterone. In addition, the diuretic effect of insulin in fasted intact rats was not evident in the fed diabetic rats in which diabetes had been induced by streptozotocin. Such findings suggested participation of factors other than insulin. The natriuresis of fasting in intact rats appears to involve two factors, one of which is independent of the sodium intake level. Dependence on the sodium intake level may be derived from alteration of the solute diuresis-like effect of drinking saline w hen animals are fasted. These results suggest that neither aldosterone nor insulin is a major causal factor involved in fasting-induced natriuresis.

Adrenalectomy↗

PubMed1995

Oxytocin-induced natriuresis mediated by the renal kallikrein-kinin system in anesthetized male rats.

Intravenous infusion of oxytocin (OT) (10-100 nmol/kg/30 min) to 8-week-old anesthetized male rats resulted in a dose-dependent increase in urine volume, which showed a peak value 30-45 min after the start of OT-infusion. Urinary excretions of sodium, chloride and potassium were also increased by OT, showing peak values at 30-45 min, without any increase in the creatinine level. The natriuresis by OT was accompanied by increased excretion of urinary active kallikrein, which showed a peak value 15 min after the start of OT-infusion. The urinary kinin level was also increased. Intravenous infusion of a kallikrein inhibitor, aprotinin (15 mg/kg/90 min), when started 30 min before the OT-infusion, significantly inhibited the OT-induced increase in urine volume and urinary excretion of sodium, chloride and potassium. Intravenous infusion of a bradykinin B2 antagonist, Hoe 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]BK, 4.5 mg/kg/90 min), when started 30 min before the OT-infusion, significantly inhibited the OT-induced increases in urine volume and urinary excretion of sodium and chloride, but not that of potassium. These results indicate that the OT-infusion induces natriuresis in male rats, and more than half of the natriuresis is mediated by a concomitant increase in excretion of urinary active kallikrein and the kinin generated.

Anesthesia↗

PubMed1995

Role of atrial natriuretic peptide in interleukin 1 beta-induced natriuresis in conscious rats.

To assess whether atrial natriuretic peptide (ANP) plays a role in the natriuresis induced by interleukin 1 beta (IL-1 beta), the following experiments were carried out. Experiment (Ex) I: IL-1 beta (7.5 micrograms/kg BW) was given intravenously (i.v.) in conscious hydrated rats (n = 6). Plasma ANP, vasopressin (AVP) osmolality (Posm), Na and K, urine Na (UNa V) and K excretion (UK V), osmolality and flow (UF), and mean arterial blood pressure (MABP) and heart rate were simultaneously determined. In the control group (n = 6), the drug was omitted, and the same protocols were carried out. Ex II: Three mg/kg BW of the specific ANP antagonist, HS-142-1 (HS), was administered i.v. and then, IL-1 beta (7.5 micrograms/kg BW) was given i.v. (n = 6). In the HS alone group (n = 6), IL-1 beta was omitted. The experimental protocols were the same as those in Ex I. IL-1 beta increased significantly plasma ANP and AVP and UNa V, but not UF, accompanied by decreases in Posm and UKV and increases in MABP (ExI). HS inhibited the natriuresis mediated by IL-1 beta, despite increases in plasma ANP and had no influence on plasma AVP and MABP. In the control (ExI) and HS alone (ExII) groups, these parameters did not change, except for decreases in Posm in both groups and increased plasma ANP in the latter. These results suggest that plasma ANP may play an essential role in the IL-1 beta-mediated natriuresis.

Animals↗

PubMed1991

A role for atrial natriuretic peptide in endothelin-induced natriuresis.

Systemic administration of low-dose endothelin increases urinary sodium excretion rate despite mild to moderate reductions in renal plasma flow and glomerular filtration rates. The role of atrial natriuretic peptide in endothelin-induced natriuresis was investigated. Administration of 2.50 pmol/min of endothelin to euvolemic rats resulted in increases in plasma atrial natriuretic peptide levels from 127 +/- 18 to 169 +/- 23 pg/mL. However, a lower dose of endothelin (0.63 pmol/min) or saline did not increase plasma levels of atrial natriuretic peptide. Mean arterial pressure was unchanged at the lower dose of endothelin and increased only slightly in rats receiving 2.5 pmol/min. To assess functional significance, renal responses to endothelin (2.5 pmol/min) in the absence and presence of a specific anti-rat atrial natriuretic peptide antibody were compared. Equivalent reductions in renal blood flow were observed. Urinary sodium excretion rates increased significantly in non-ANP-antibody-treated rats by 33 +/- 7 and 82 +/- 20% at 10 and 30 min, respectively. Atrial natriuretic peptide antibody blunted markedly endothelin-induced natriuresis: urinary sodium excretion rates changed insignificantly by 18 +/- 10 and 30 +/- 14%, respectively. Thus, endothelin infusion results in increases in plasma atrial natriuretic peptide levels, which may contribute to endothelin-induced natriuresis, providing evidence for potentially significant interactions between these peptide hormones in the regulation of sodium balance and renal vascular tone.

Animals↗

PubMed1996

Dopamine does not enhance furosemide-induced natriuresis in patients with congestive heart failure.

The objective of this study was to determine whether the addition of low-dose (renal-dose) dopamine to furosemide therapy enhances natriuresis in patients with compensated congestive heart failure, New York Heart Association Class II or III. We performed a randomized, controlled, open-label, crossover study wherein urinary sodium, creatinine, and furosemide excretion rates and GFR determined by inulin clearance rates were measured during each of three treatment interventions: furosemide infusion alone, dopamine infusion alone, and furosemide and dopamine infusions administered concurrently. Six of eight recruited subjects (4 male, 2 female) were able to complete the study. The baseline sodium excretion rate after equilibration on a metabolic diet was 6.7 +/- 0.7 mEq (mean +/- SE) over 3 h. Infusion of dopamine alone caused a slight nonsignificant increase in natriuresis to 36.7 +/- 8.5 mEq/3 h. Furosemide alone markedly increased sodium excretion to 276.6 +/- 47.2 mEq/3 h. No significant additional increment in natriuresis occurred when dopamine and furosemide were administered concurrently (253.8 +/- 73.6 mEq/3 h). Neither dopamine, furosemide, or their coadministration affected GFR. In conclusion, infusion of low-dose dopamine does not enhance furosemide-induced urinary sodium excretion rates in patients with compensated congestive heart failure, New York Heart Association Class II or III.

Aged↗

PubMed1990

Role of intrarenal renin-angiotensin system on pressure-natriuresis in spontaneously hypertensive rats.

The pressure-natriuresis relationships in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were characterized with or without intrarenal renin-angiotensin system (RAS) blockade. The pressure-natriuresis relationship in SHR was shifted toward higher pressure in comparison to WKY. The inhibition of intrarenal RAS by MK-422 (0.3 ug/kg/min) in SHR enabled to excrete more sodium at the same pressure (P less than 0.05), whereas no significant changes were observed in WKY. In SHR, during administration of Thi5,8, D-Phe7-bradykinin (50 micrograms/kg/min), the natriuretic responses to MK-422 were maintained. Intrarenal infusion of Sar1, Ile8-angiotensin (70 ng/kg/min) into SHR increased sodium excretion accompanied by an increase in renal plasma flow. Intrarenally administered angiotensin I (10 ng/kg/min) into WKY showed antinatriuretic effects with minimal changes in renal hemodynamics. These results indicate that alteration of intrarenal RAS in SHR might contribute to reset the pressure-natriuresis relationship.

Angiotensins↗

PubMed1990

Exaggerated natriuresis in salt-sensitive essential hypertension.

Acute responses of blood pressure and natriuresis to intravenous injection of furosemide and saline infusion were evaluated in 38 patients with essential hypertension. Twelve patients whose mean arterial blood pressure decreased by more than 5% at two hours after intravenous administration of 20 mg furosemide were classified as salt-sensitive (SS); the remainders as salt-resistant (SR). The extent of natriuresis induced by furosemide was not different between the two subgroups. During 2-liter isotonic saline infusion the SS subjects excreted more sodium than the SR subjects did (108.7 +/- 11.9 vs 55.9 +/- 6.6 mmole, p less than 0.001). There was a significant correlation (r = 0.57, p less than 0.001) between the hypotensive effect of furosemide and the 4-hour sodium excretion during saline infusion. A reverse correlation between the sodium excretion during saline infusion and the increase in mean blood pressure at the end of infusion was shown in the SS subgroup (r = -0.72, p less than 0.01), but not in the SR subgroup (r = 0.045). The results suggest that prompt natriuresis on saline infusion in the SS hypertensives may function as a protective mechanism to prevent abrupt increase in blood volume and blood pressure during acute sodium loading.

Adult↗

PubMed1994

Effects of a calcium channel blocker, nicardipine, on pressure-natriuresis in Dahl salt-sensitive rats.

The effects of a calcium channel blocker, nicardipine, on pressure-natriuresis responses were studied in Dahl salt sensitive (DS) and resistant (DR) rats. Differences in the neural and endocrine background were minimized by renal denervation and by holding plasma vasopressin, aldosterone, corticosterone, and norepinephrine levels constant by intravenous infusion. The renal plasma flow (RPF) and glomerular filtration rate (GFR) of DS rats were disautoregulated in the low renal perfusion pressure range, while those of DR rats were autoregulated. Administration of nicardipine (0.3 microgram/kg/min) into the renal artery significantly increased RPF and GFR and abolished the autoregulation in both strains of rats. Nicardipine also sharpened the pressure-natriuresis responses in both strains without changes in fractional excretion of sodium. These findings suggest that nicardipine increased GFR and thereby improved the pressure-natriuresis responses of DS rats.

Animals↗

PubMed1984

Hyponatremia and natriuresis following subarachnoid hemorrhage in a monkey model.

A monkey model of subarachnoid hemorrhage (SAH) was used to study both the incidence of hyponatremia and natriuresis and the associated changes in antidiuretic hormone (ADH) secretion and salt and water balance. Following SAH, seven of nine monkeys became natriuretic and hyponatremic. The natriuretic period lasted an average of 4.4 +/- 0.4 days. The mean nadir of serum sodium content was 125.7 +/- 1.6 mEq/liter, and occurred on the average on the 5th day following SAH. The sodium balance after SAH was negative as compared to the preoperative positive sodium balance (p less than 0.001). The plasma vasopressin level was usually elevated for a day following surgery, but there was no significant difference in the levels during the preoperative period and during the period of natriuresis following SAH. The daily urine output and aldosterone levels were not significantly different, and the plasma volume was slightly, but not significantly, decreased after SAH. Four of the animals that had a hyponatremic and natriuretic response following SAH showed a normal regulation of vasopressin in response to both a water challenge and hypertonic saline challenge. The three monkeys that underwent sham procedures did not become hyponatremic and natriuretic postoperatively. The sham-operated monkeys did not show significant differences in their plasma vasopressin levels, urine volume, plasma volume, and aldosterone levels following surgery. These observations are more consistent with primary natriuresis as the cause of hyponatremia rather than the syndrome of inappropriate secretion of ADH. The cause of the renal loss of sodium is not known, but the possibility of a brain natriuretic factor or an alteration in the neural control of the kidney should be considered.

Animals↗

PubMed1984

Renal response to captopril in severe heart failure: role of furosemide in natriuresis and reversal of hyponatremia.

To assess the effect of furosemide and captopril on renal function and hyponatremia in patients with severe heart failure, we studied two groups of patients with hyponatremia who were receiving digoxin therapy and whose sodium intake was 40 meq/d. One group received captopril and furosemide, the second received captopril. The first group responded to combination therapy with a brisk natriuresis and diuresis, weight reduction, and an increase in serum sodium concentration. Patients who received captopril alone did not respond, despite a similar increase in renal plasma flow and glomerular filtration rate. When furosemide was then administered to patients who had received captopril alone, a brisk natriuresis, weight loss, and correction of hyponatremia followed. Treatment with furosemide is necessary to promote natriuresis and correction of hyponatremia in patients with severe heart failure treated with captopril; the renal vascular action of captopril enhances the effectiveness of furosemide.

Adult↗