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PubMed1969

Some determinants of the effects of VAL-5-angiotensin II amide on glomerular filtration rate and sodium excretion in dogs.

In 12 dogs anesthetized with chloralose, angiotensin (angiotensin II amide) given intravenously increased the glomerular filtration rate (GFR) of an ischemic kidney while simultaneously having little effect on the GFR of the contralateral kidney. In the ischemic kidney, in 14 of 30 observations, increments of GFR greater than 100% of mean control GFR (9 ml/min) occurred in response to angiotensin. The magnitude of the increase in GFR produced by angiotensin was independent of dose (range 0.005-0.050 mug/kg per min), the degree of accompanying pressor response, and alterations in renal blood flow (RBF) (electromagnetic flow-meter). In the ischemic kidney, increments of GFR could be produced by sub-pressor doses of angiotensin. Dissociations between increments of GFR and sodium excretion occurred. Equivalent increments of GFR in the ischemic kidney in dogs receiving either 5% glucose in water or 10% mannitol in 0.3% saline were associated with natriuresis only in the latter group: a) as an initial response of the contralateral kidney to renal arterial constriction (RAC) in spite of a concomitant reduction in RBF and an unchanged GFR; b) in the ischemic kidney on giving angiotensin. The natriuresis produced by angiotensin was independent of the magnitude of elevations in blood pressure, altered filtration fraction, and was associated with a further reduction in RBF. After release of RAC in the dogs receiving mannitol, an antinatriuresis was again observed in response to angiotensin. The presence of unilateral renal ischemia allowed the demonstration of a differential action of angiotensin on the GFR of an ischemic and nonischemic kidney. The natriuresis in response to angiotensin requires, in addition to mannitol, the participation of undefined factors invoked by unilateral renal ischemia.

Angiotensin II↗

PubMed1972

A micropuncture study of postobstructive diuresis in the rat.

In order to investigate the syndrome of postobstructive diuresis, clearance and micropuncture studies were carried out in rats after relief of 24 hr of bilateral (BUL) or unilateral (UUL) ureteral ligation. In rats with BUL, a striking diuresis and natriuresis occurred when the obstruction to one kidney (the experimental kidney) was relieved. The results were not influenced by administration of vasopressin or d-aldosterone. Whole kidney clearances of inulin and p-aminohippuric acid (PAH) in the experimental kidney were reduced to 10% and 20% of normal, respectively. Superficial nephron inulin and PAH clearances were also reduced, but only to 40% and 45%, respectively. These findings suggest a heterogeneity of nephron function in which deep nephrons were functioning poorly or not at all. To investigate the site of impaired tubular reabsorption in the surface nephrons, absolute and fractional water reabsorption was measured. Absolute reabsorption was found to be decreased all along the nephron. Fractional reabsorption in proximal tubules was normal, as indicated by an average endproximal tubular fluid per plasma inulin (TF/P(In)) of 2.16 vs. 2.30 in controls. TF/P(In) was markedly decreased in distal tubules (2.91 vs. 8.02) and final urine (5.56 vs. 263). These observations indicate that the major sites of impaired sodium reabsorption leading to the diuresis were beyond the proximal tubule.Rats with 24 hr of UUL did not demonstrate a comparable natriuresis or diuresis either spontaneously when the obstruction was relieved or after i.v. infusion of urea. A major difference between the BUL and UUL rats was that prerelease intrarenal hydrostatic pressure was markedly elevated (30.1 mm Hg) in the former but was below normal free-flow values (9.2 mm Hg) in the latter. Thus, elevation of intrarenal pressure during the period of obstruction may be causally related to the natriuresis and diuresis which occurs after the obstruction is relieved.

Aminohippuric Acids↗

PubMed1975

An inhibitor of sodium transport in the urine of dogs with normal renal function.

The urine and serum of chronically uremic patients and dogs contain an inhibitor of sodium transport that reduces short-circuit current (SCC) in the toad bladder and produces natriuresis in the rat. The present studies represent an effort to determine whether the same inhibitor is detectable in urine of normal dogs maintained on a dosium intake varying from 3 to 258 meq/day. Observations were made with and without fludrocortisone. The same Sephadex G-25 gel filtration fraction previously shown to contain the "uremic" inhibitor was tested in both the isolated toad bladder and rat bioassay systems. The fraction from dogs maintained on 258 meq qodium plus 0.2 mg fludrocortisone/day consistently inhibited SCC in the toad bladder and induced a natriuresis in the rat (P less than 0.001). The fraction from dogs on the same sodium intake without fludrocortisone was also natriuretic (P less than 0.01) but did not inhibit SCC significantly. In contrast, the fraction from dogs fed 3 meq sodium with fludrocortisone or 91 meq sodium without fludrocortisone had no significant effect in either assay system. Thus, an inhibitor of sodium transport has been found in the urine of nonuremic dogs. Both the degree of natriuresis in the rat and the degree of inhibition of SCC in the toad bladder correlated with the state of sodium balance which ensued in the dog.

Animals↗

PubMed1988

Effect of human atrial natriuretic peptide on 1-deamino-D-Arg8-vasopressin-induced antidiuresis in man.

The interaction of exogenous synthetic human atrial natriuretic peptide (hANP), given in iv bolus doses of 100, 200, and 400 micrograms, and of various bolus-primed infusion of 1-deamino-D-Arg8-vasopressin (dDAVP), a nonpressor analog of antidiuretic hormone, were investigated in six normal men. A marked dose-dependent rise in plasma hANP concentrations occurred after the administration of hANP. The antidiuretic effect of dDAVP (P less than 0.01) was partially but not completely reversed by the concomitant administration of hANP (P less than 0.01). hANP-induced natriuresis was similar in the presence and absence of dDAVP-induced antidiuresis. While these results do not prove that hANP-dependent natriuresis and diuresis are independent phenomena, it is of clinical interest that natriuresis without diuresis can be induced by the simultaneous administration of hANP and dDAVP.

Adult↗

PubMed2002

Effects of benidipine on glomerular hemodynamics and proteinuria in patients with nondiabetic nephropathy.

Experimental studies suggest that some long-acting calcium antagonists decrease glomerular hypertension and suppress the progression of nephropathy, but clinical evidence is lacking. To investigate clinically whether a long-acting calcium antagonist, benidipine, lowers glomerular capillary hydraulic pressure via a decrease in efferent arteriolar resistance and decreases proteinuria, we examined hypertensive patients with nondiabetic nephropathy. The subjects were 7 patients with chronic glomerulonephritis or glomerulosclerosis. Before and during the administration of benidipine (4 mg/day), systemic pressure, glomerular hemodynamics, the sodium sensitivity index (reciprocal of the pressure-natriuresis curve), and urinary excretion of proteins (total protein, albumin, and immunoglobulin G) were investigated. The glomerular hemodynamics in terms of glomerular capillary hydraulic pressure and resistance of afferent and efferent arterioles were calculated from the renal clearance, plasma total protein concentration, and pressure-natriuresis relationship. Benidipine lowered the mean arterial pressure from 105 +/-5 to 99 +/- 4 mm Hg (p = 0.002; mean +/- SD) and glomerular pressure from 48 +/- 8 to 39 +/- 5 mmHg (p = 0.006) by decreasing the resistance of efferent arterioles. Benidipine made the pressure-natriuresis curve steeper and decreased the median sodium sensitivity index from 0.099 (0.084 and 0.117; 25th and 75th percentiles) to 0.048 (0.017 and 0.058; p = 0.018). Urinary excretion of proteins did not change. Our clinical study showed that benidipine lowered the glomerular pressure by decreasing the resistance of efferent arterioles and decreased the sodium sensitivity of blood pressure, but did not affect proteinuria in patients with nondiabetic nephropathy.

Aged↗

PubMedDate not supplied

K+ channel blockers: natriuretic potency correlates to vascular ATP-sensitive K+ channel blockade.

Using analogs of known vascular ATP-sensitive K+ channel (KATP) blockers, we identified compounds with a wide range of potencies (over 500-fold) in their capacity to block the hypotensive response of 0.2 mg/kg pinacidil in rats. The most potent of these, U-97025E, belongs to a newly disclosed class of compounds, the cyanoguanidines. U-97025E at 0.04 mg/kg blocked 50% of the depressor response induced by 0.2 mg/kg pinacidil. The maximal natriuresis induced by U-97025E (0.4 mg/kg i.v.) increased Na+ excretion by approximately 60%. This natriuresis is of the same magnitude as that induced by thiazide without any effect on K+ excretion. We found a high degree of correlation between natriuretic potency and the capacity to block the blood pressure lowering effects of pinacidil, both among closely related analogs and dissimilar compounds. These findings imply an obligatory rather than incidental relationship between vascular KATP blockade and natriuresis. The exact molecular link of the vascular and renal effects remains to be determined.

ATP-Binding Cassette Transporters↗

PubMed1978

Sodium metabolism in essential hypertension. Natriuretic response to acute hypertonic saline load.

In order to investigate the mechanism of the "exaggerated natriuresis" in hypertension, 300 ml of 3% saline was infused for 1 hour during hydropenia in 13 patients with normal renin essential hypertension and 5 normotensive subjects on a daily ingestion of 4 Gm and 16 Gm of NaCl. At the end of the infusion, the circulating blood volume indicated by the change in serum total protein concentration and the glomerular filtered load were increased in a similar manner in both groups. Prompt the enhanced natriuresis and diuresis were seen within 1--2 hours after starting the infusion in the hypertensives on a daily ingestion of 16 Gm of NaCl. Significant positive correlations were found between the change in mean arterial blood pressure (deltaMAP) and UV, and between deltaMAP and UNa V in the hypertensives either on a daily 4 Gm or 16 Gm ingestion of NaCl. Free water reabsorption (Tc H2O) was lower in the hypertensives than that in the controls at high levels of osmolar clearance (Cosm). Plasma renin activity (PRA) did not differ in either group on either NaCl ingestion and was equally suppressed on a daily ingestion of 4 Gm of NaCl, while little changed on a high salt intake. Plasma aldosterone levels changed in parallel with PRA. It is suggested that the "exaggerated natriuresis" is due to the decreased tubular sodium reabsorption, which may be the result of intrarenal hemodynamic changes related to the elevated renal perfusion pressure. The decreased medullary osmolar gradient probably induced by an increase in the medullary blood flow is a possible contributing factor in the enhanced sodium and water excretion, and the renin-aldosterone system does not seem to play an important role.

Aldosterone↗

PubMed2000

Oxytocin is a cardiovascular hormone.

Oxytocin (OT), a nonapeptide, was the first hormone to have its biological activities established and chemical structure determined. It was believed that OT is released from hypothalamic nerve terminals of the posterior hypophysis into the circulation where it stimulates uterine contractions during parturition, and milk ejection during lactation. However, equivalent concentrations of OT were found in the male hypophysis, and similar stimuli of OT release were determined for both sexes, suggesting other physiological functions. Indeed, recent studies indicate that OT is involved in cognition, tolerance, adaptation and complex sexual and maternal behaviour, as well as in the regulation of cardiovascular functions. It has long been known that OT induces natriuresis and causes a fall in mean arterial pressure, both after acute and chronic treatment, but the mechanism was not clear. The discovery of the natriuretic family shed new light on this matter. Atrial natriuretic peptide (ANP), a potent natriuretic and vasorelaxant hormone, originally isolated from rat atria, has been found at other sites, including the brain. Blood volume expansion causes ANP release that is believed to be important in the induction of natriuresis and diuresis, which in turn act to reduce the increase in blood volume. Neurohypophysectomy totally abolishes the ANP response to volume expansion. This indicates that one of the major hypophyseal peptides is responsible for ANP release. The role of ANP in OT-induced natriuresis was evaluated, and we hypothesized that the cardio-renal effects of OT are mediated by the release of ANP from the heart. To support this hypothesis, we have demonstrated the presence and synthesis of OT receptors in all heart compartments and the vasculature. The functionality of these receptors has been established by the ability of OT to induce ANP release from perfused heart or atrial slices. Furthermore, we have shown that the heart and large vessels like the aorta and vena cava are sites of OT synthesis. Therefore, locally produced OT may have important regulatory functions within the heart and vascular beds. Such functions may include slowing down of the heart or the regulation of local vascular tone.

Animals↗

PubMed1991

Responses of atrial natriuretic peptide, vasopressin, aldosterone and renal function to intracerebroventricular infusion of angiotensin II in dogs.

To assess the mechanisms how angiotensin II (Ang II) given intracerebroventricularly (i.c.v.) induces natriuresis, the effects of Ang II (10 ng/kg/min, for 30 min) on the renin-angiotensin-aldosterone system, the release of vasopressin (AVP) and atrial natriuretic peptide (ANP) and on cardiovascular and renal functions were investigated in anesthetized dogs. In control dogs, vehicle alone (artificial cerebrospinal fluid) was infused at a rate of 10 microliters/min. Ang II given i.c.v. produced a gradual increase in urine flow, urinary sodium and potassium excretion and osmolar clearance, but had no effect on plasma ANP, aldosterone, arterial blood pressure, and renal blood flow. However, i.c.v. Ang II increased plasma AVP and decreased heart rate, plasma renin activity, inulin clearance and filtration fraction. In the cotrol group, vehicle treatment had no effect on these parameters except for decreases in inulin clearance and filtration fraction. These results suggest that circulating ANP and blood pressure may not play an important role in i.c.v. Ang II-induced natriuresis, but increased AVP release and decreased renal sympathetic nervous activity may contribute to the natriuresis.

Aldosterone↗

PubMed2004

Role of uroguanylin, a Peptide with natriuretic activity, in rats with experimental nephrotic syndrome.

Uroguanylin induces natriuresis and diuresis in vivo as well as in vitro and is found mainly in the intestine and the kidney. However, the roles of uroguanylin in nephrotic syndrome, which is associated with sodium and water retention, have not been determined. Therefore, changes in the urine and plasma concentration of immunoreactive uroguanylin (ir-uroguanylin) and its mRNA expression in the kidney and intestine were examined using rats with puromycin aminonucleoside (PAN)-induced nephrosis. Male Sprague-Dawley rats were separated into control and nephrotic groups, and then the urinary excretion of sodium, protein, and ir-uroguanylin was examined over time. The plasma levels and renal and intestinal mRNA expression of uroguanylin at the periods of sodium retention and remarkable natriuresis also were evaluated. The sequential changes of urinary ir-uroguanylin excretion in the nephrotic group were similar to those of urinary sodium excretion. When the urinary excretion of ir-uroguanylin and sodium peaked, the plasma level of ir-uroguanylin also increased compared with that of the control group. Uroguanylin mRNA expression in the kidney increased during the period of sodium retention and then decreased during the period of remarkable natriuresis. Uroguanylin mRNA expression in the small intestines of control and nephrotic rats were identical. However, in a unilateral PAN-induced proteinuria, uroguanylin expression significantly increased in the PAN-perfused kidney compared with that in the opposite kidney. Considering the natriuretic effect of uroguanylin, these results suggested that uroguanylin plays an important role as a natriuretic factor in nephrotic syndrome via both the circulation and the kidney itself.

Animals↗

PubMed1993

Low-dose atrial natriuretic factor and furosemide in experimental acute congestive heart failure.

This study was designed to address three objectives in an experimental model of acute congestive heart failure (CHF) in the dog produced by rapid ventricular pacing. The first objective was to characterize cardiorenal and humoral responses before and during 2 h of acute CHF. The second objective was to determine the modulating action of iv furosemide upon these biologic responses to acute CHF, testing the hypothesis that furosemide-mediated natriuresis is associated with activation of the renin-angiotensin-aldosterone system (RAAS) compared with the control group. The third objective was to determine the modulating action of continuous low-dose atrial natriuretic factor (ANF) administration during acute CHF upon these biologic responses, testing the hypothesis that exogenous low-dose ANF would prevent activation of the RAAS and enhance the natriuretic action of furosemide. In the control group (Group 1; N = 6), plasma ANF increased after the onset of CHF; GFR and sodium excretion were maintained without activation of this RAAS despite arterial hypotension. In Group 2 (N = 6), furosemide in acute CHF increased sodium excretion but in association with a decrease in GFR and activation of the RAAS. Low-dose exogenous ANF and furosemide (Group 3; N = 6) in acute CHF were associated with a maintenance of GFR, no activation of the RAAS, and potentiation of furosemide-induced natriuresis. In summary, these studies demonstrate that furosemide potently increases sodium excretion in acute CHF, but with a decrease in GFR and activation of the RAAS. Low-dose ANF in acute CHF with furosemide maintains GFR, attenuates activation of the RAAS, and potentiates natriuresis.

Acute Disease↗

PubMed1987

Selective renal dopamine-1 receptor stimulation in man.

The selective dopamine-1 (DA-1) receptor agonist, fenoldopam, was studied during intravenous administration to ten normal male subjects on a diet of 150 mEq sodium and 60 mEq potassium per day to determine the mechanism of dopamine-induced natriuresis. During DA-1 receptor stimulation, urine flow rate and renal plasma flow manifested a biphasic increase. Urine flow rate increased from a control of 13 +/- 1 to 17 +/- 1.2 ml/min and again to a peak of 16 +/- 1. Renal plasma flow increased from 344 +/- 39 to 481 +/- 44 ml/min and then to 497 +/- 38. Sodium excretion (UNaV) and fractional sodium excretion (FENa) demonstrated a sustained increase. UNaV rose from a control of 0.21 +/- 0.03 to 0.32 +/- 0.05 mEq/min. FENa rose from a control of 1.6 +/- 0.1 to 2.7 +/- 0.6%. Fenoldopam did not alter glomerular filtration rate. The association of changes in renal plasma flow and in UNaV and FENa demonstrate in man that DA-1 receptor stimulation causes natriuresis by direct renal tubular action. The renal tubular effect appears to be a major determinant of the degree of natriuresis.

Adult↗

PubMed1993

Renal responses to acute volume expansion in young spontaneously hypertensive rats.

The renal responses to acute volume expansion (VE) were measured from intact and denervated kidneys in 5 week old spontaneously hypertensive rats (SHR). Urine flow and sodium excretion were measured before, during and after VE from innervated and denervated kidneys in anesthetized (Inactin--0.1 g/kg, ip) age and sex matched SHR and normotensive Wistar Kyoto (WKY) rats. Mean arterial pressure was 23 mm Hg higher in SHR than in WKY. During VE the increment in urinary flow rate and sodium excretion from both innervated and denervated kidneys were greater in SHR than WKY. In another group of SHR, renal perfusion pressure was maintained at a level similar to the arterial pressure in the WKY group (84 mm Hg). When renal perfusion pressure was controlled at the lower level in the SHR there was no longer the increase in diuresis and natriuresis in response to acute VE. Examining differences within a strain, the SHR demonstrate a greater increase in diuresis and natriuresis in response to VE in the absence of renal nerves, unlike the WKY. In conclusion, these results suggest that there is a greater diuresis and natriuresis in the young SHR due to increased renal perfusion pressure and the renal nerves produce a greater retention of water and sodium in SHR compared to WKY.

Animals↗

PubMed1986

Involvement of the adrenal glands in the action of the atrial natriuretic factor.

Adrenalectomized, medullectomized and sham operated rats were treated with either a chronic infusion or a bolus injection of the synthetic atrial natriuretic factor (ANF). ANF did not enhance natriuresis and diuresis in sham operated conscious animals during chronic infusion, but it had a potent action when injected as a bolus into anesthetized rats. The absence of the whole adrenal glands, but not adrenal medulla profoundly modified the renal response to ANF: a) following chronic administration of ANF, the baseline natriuresis paradoxically decreased in adrenalectomized rats, and b) in response to a bolus injection of ANF the natriuretic and diuretic actions of the peptide were attenuated in these animals. The medullectomy-induced decreased natriuresis and dopamine excretion were corrected by ANF infusion. Furthermore, ANF suppressed the compensatory increase of norepinephrine excretion secondary to adrenalectomy. The data suggest that the presence of the adrenal cortex is necessary for the natriuretic and diuretic actions of ANF. The decrease in urinary DA excretion may reflect diminished dopaminergic activity and contribute to the post-medullectomy antinatriuresis, a phenomenon which can be corrected by ANF infusion. ANF may also have a depressing activity on the increased sympathetic tone.

Adrenal Glands↗

PubMed1988

Natriuretic effect of atrial natriuretic peptide in diabetes insipidus rats.

Washout of the solute concentration gradient in the renal medullary interstitium has been suggested to play a role in mediating the natriuretic response to atrial natriuretic peptide (ANP). The purpose of this study was to determine the effects of ANP 8-33 on sodium excretion in Brattleboro diabetes insipidus (DI) rats, in which medullary tonicity is known to be decreased as compared to Long-Evans (LE) control rats. Basal urine osmolality (Uosm) was significantly lower in DI rats as compared to LE rats (123 +/- 6 vs 673 +/- 38 mOsm/kg). Infusion of ANP 8-33 at a rate of 4 micrograms/kg/hr for 60 min resulted in a significantly greater increase in UnaV (delta 6.1 +/- 1.2 vs delta 2.9 +/- 0.7 microEq/min) and urine flow (delta 40 +/- 12 vs delta 8 +/- 7 microliter/min) in the LE rats than in the DI rats. The greater natriuresis occurred in the LE rats despite no significant change in Uosm. Fractional lithium reabsorption (an indicator of proximal sodium reabsorption) decreased similarly in both groups. Infusion of ANP had no effect on mean arterial pressure in LE and DI groups. In summary, infusion of ANP in the DI rat resulted in a significant natriuresis, albeit less than in LE rats. The natriuresis in the LE rats occurred despite no significant change in Uosm. These data suggest that mechanisms other than medullary washout are responsible for the natriuretic effects of ANP.

Animals↗

PubMed2004

Neurohumoral mechanism in the natriuretic action of intracerebroventricular administration of renin.

INTRODUCTION: Intracerebroventricular (i.v.t.) administration of renin (R) decreases urinary volume and increases urinary sodium excretion. We investigated whether i.v.t.-R-induced natriuresis could be associated with the release of atrial natriuretic peptide (ANP), its interaction with renal ANP-A receptors (ANPR-A) and the subsequent increase of urinary cyclic 3-5 guanosine monophosphate (cGMP). METHODS: In i.v.t. cannulated rats, the left carotid artery was catheterised with PE-50 tubing for blood collection, renin was injected i.v.t. and arterial blood samples were collected at 0, 2, 5, 10 and 15 minutes of injection, and urinary sodium and cGMP excretion at 1-, 3- and 6-hour periods of urine collection. Plasma ANP levels and urinary cGMP were determined by radioimmunoassay, and each urine sample was analysed for sodium concentration using a flame photometer. RESULTS: Our results demonstrate that i.v.t.-R administration increases plasma ANP levels after two minutes of injection and urinary cGMP concentration at 1-, 3- and 6 hour period of urine collection. The natriuretic action induced by i.v.t.-R was blunted by peripheral administration of anantin, an ANPR-A antagonist. We assessed the role of brain angiotensin II (Ang II) AT1-receptors on the i.v.t.-induced antidiuresis, natriuresis and cGMP urinary excretion, the last as an indirect index of ANP secretion. Blockade of brain Ang II AT1-receptors with losartan (LOS; 120 microg/3 microl, i.v.t.), inhibited the antidiuretic action and blocked the increased urinary sodium and cGMP excretion induced by i.v.t.-R (7.14 mGU/5 microl). The increase in urinary cGMP was independent of nitric oxide synthase stimulation, since L-NAME pre-treatment did not alter the renal actions induced by i.v.t.-R. CONCLUSIONS: Our results suggest that there is a link between the brain and the kidney. The activation of brain angiotensinergic neurons and stimulation of AT1- receptors may stimulate the release of ANP to the circulation. The released ANP circulates to the kidneys where it acts through renal ANPR-As and the consequent increase in cGMP to produce natriuresis.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2001

[Recent trends in studies of the etiology of hypertension: Renal mechanism of blood pressure regulation].

The kidney plays an important role in the control of systemic blood pressure by regulating the composition of body fluid and electrolyte and by producing and releasing various vasoactive substances such as renin-angiotensin and prostaglandins(PGs). The kidney possesses an intrinsic mechanism called 'pressure-natriuresis' in which an increase in perfusion pressure promotes natriuresis. According to this mechanism, hypertension can be classified as salt-sensitive or non-salt-sensitive based on the response to dietary sodium loading. Thus, a shift of the curve to the right and a decrease in the slope are the two basic abnormalities seen in the pressure-natriuresis relationship in hypertension, with each representing a different pathophysiology. In non-salt-sensitive essential hypertension, glomerular capillary pressure is within the normal range due to elevated preglomerular resistance, while it is elevated in salt-sensitive hypertension. Such differences may be reflected in the rate of progression of renal dysfunction as well as renal pathology. Finally, the mechanism responsible for the altered renal microcirculation involves dysregulation of intrinsic mechanisms(myogenic responses and tubuloglomerular feedback) as well as various local factors, in particular, angiotensin II, nitric oxide, and oxidative stress.

Angiotensins↗

PubMed1992

Effects of manidipine on blood pressure and renal function in salt-loaded, spontaneously hypertensive rats.

The purpose of this study was to investigate the effects of 4-week oral administration of manidipine (40 mg daily), a newly developed calcium channel blocker, on blood pressure and renal function in salt-loaded (8% NaCl) spontaneously hypertensive rats. Systolic blood pressure of spontaneously hypertensive rats increased from 167 +/- 4 to 221 +/- 7 mmHg with salt loading for 4 weeks; manidipine completely prevented this elevation in blood pressure. Urinary excretion of sodium in salt-loaded spontaneously hypertensive rats was twelve-fold compared with those receiving a normal diet (0.38% NaCl). The pressure-natriuresis relationship was obtained during week 4 of the metabolic study. At similar renal perfusion pressures, sodium excretion was significantly higher in salt-loaded rats than in rats fed a normal diet. Glomerular filtration rate and renal plasma flow were similar between the two groups. In salt-loaded spontaneously hypertensive rats, treatment with manidipine improved the pressure-natriuresis relationship toward lower pressures. Further, manidipine attenuated the autoregulation of glomerular filtration rate and renal plasma flow. These results indicate that manidipine normalizes the relation between sodium excretion and renal perfusion pressure in salt-loaded spontaneously hypertensive rats by resetting pressure natriuresis.

Animals↗