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PubMed2003

Prophylactic management of excessive natriuresis with hydrocortisone for efficient hypervolemic therapy after subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Hyponatremia caused by excessive natriuresis is common in patients with aneurysmal subarachnoid hemorrhage (SAH). Natriuresis decreases the total blood volume through osmotic diuresis and increases the risk of symptomatic cerebral vasospasm. In such patients, hypervolemic therapy is difficult to achieve without causing hyponatremia because sodium replacement provokes further natriuresis and osmotic diuresis. We examined the effects of hydrocortisone, which promotes sodium retention, in patients with SAH. METHODS: Twenty-eight SAH patients were randomized into 2 groups after direct surgery: group 1 patients without hydrocortisone treatment (n=14) and group 2 patients with hydrocortisone treatment (1200 mg/d for 10 days; n=14). Both groups underwent hypervolemic therapy by aggressive sodium and water replacement. The goal of the hypervolemic therapy was to maintain the serum sodium level >140 mEq/L and the central venous pressure (CVP) within 8 to 12 cm H2O. RESULTS: Group 2 demonstrated a lower sodium excretion (P<0.05) and higher serum sodium level (P<0.05) compared with group 1. Hyponatremia developed in 6 patients (43%) in group 1 and 0 patients in group 2 (P<0.05). Group 2 also demonstrated a lower urine volume, lower infusion volume (P<0.05) required for hypervolemic therapy, and higher CVP (P<0.05). Failure to maintain CVP was observed in 12 patients (86%) in group 1 and 3 patients (21%) in group 2 (P<0.05). Hydrocortisone caused no serious side effects. CONCLUSIONS: Hydrocortisone clearly attenuates excessive natriuresis. Prophylactic hydrocortisone administration appears to have a therapeutic value in inducing hypervolemia efficiently after SAH.

Adult↗
PubMed1995

Subtype 2 of angiotensin II receptors controls pressure-natriuresis in rats.

Angiotensin II recognizes two receptor subtypes, AT1 and AT2, both of them having been recently cloned. Although AT2 receptors represent 5-10% of angiotensin II receptors in the kidneys of adult rats, their function remains unknown. In the present work, we examined the possible contribution of AT2 receptors to the regulation of pressure-natriuresis in anesthetized rats infused either with the specific AT2 antagonist PD 123319, or with CGP 42112B, an AT2 ligand with agonistic properties. The effects of PD 123319 were examined in a preparation with stable levels of angiotensin II, and in which AT1 receptors were blocked by the specific antagonist losartan. The effects of CGP 42112B were studied in rats deprived of endogenous angiotensin II. AT2 receptor blockade with PD 123319 did not change the renal blood flow while it increased the diuresis and natriuresis. These effects persisted even after full AT1 receptor blockade with losarfan. CGP 42112B did not modify the renal blood flow, but dose-dependently decreased urine flow and natriuresis. These results show that, contrary to AT1 receptors, renal AT2 receptors have no effect on total renal blood flow, but blunt the pressure-natriuresis, thus demonstrating that this receptor subtype is involved in a function of importance for body fluid and blood pressure regulation.

Angiotensin I↗
PubMed2000

Involvement of the renal kallikrein-kinin system in furosemide-induced natriuresis in rats.

This study examined whether the renal kallikrein-kinin system (KKS) is involved with furosemide-induced natriuresis in rats. Intravenous administration of furosemide (10 mg/kg) to anesthetized rats infused with physiological saline (saline) increased renal KK excretion as well as urine volume and urinary excretions of sodium, chloride and potassium. The change in the increase of renal KK excretion by furosemide at a dose of 1.0 mg/kg relative to the control was larger than that of urine volume. Pretreatment with a B2-receptor antagonist, 8-[3-[N-[(E)-3-(6-acetamidopyridin-3-yl)acryloylglycyl]-N-methylamino]-2,6-dichlorobenzyloxy]-2-methylquinoline (FR173657, 100 mg/kg), significantly inhibited the furosemide-induced natriuresis by 58.6%. The effect of FR173657 on the furosemide-induced natriuresis was also examined in hypotonic saline-loading rats. Similar to the saline-loading rats, urinary excretion of sodium collected during the first 8 h in metabolic cages significantly reduced by 22.4% when FR173657 (100 mg/kg) was given concurrently with furosemide (100 mg/kg) and hypotonic saline (5% of body wt.). These results indicate that furosemide increased renal KK excretion through a mechanism different from a washout mechanism and induced natriuresis partly through an augmentation of the renal KKS following the increase in renal KK excretion in both the saline- and hypotonic saline-loading rats.

Animals↗
PubMed1990

Effects of piroxicam on natriuresis and kaliuresis in hypertensives and healthy volunteers.

The effects of short-term piroxicam (P) treatment on natriuresis and kaliuresis were evaluated in 22 diuretic-treated hypertensives and 8 healthy subjects. Each hypertensive patient participated in three experimental periods, i.e., P 20 mg q.d. for 3 days and two control phases. Each healthy volunteer completed the six treatment phases, i.e., P 20 mg q.d. for 3 days, furosemide 40 mg orally in a single dose, P 20 q.d. for 3 days with furosemide 40 mg on the third day and three control phases. In healthy volunteers, P induced no change in 24-hour natriuresis and kaliuresis, but it reduced furosemide-stimulated natriuresis. In hypertensives with creatinine clearance (CCr) greater than 60 ml/min, P had no anti-natriuretic and anti-kaliuretic effects. In contrast, P induced a significant reduction in 24-hour natriuresis and kaliuresis in those with CCr less than 60 ml/min. Physicians should be aware of the potential risk of P-induced sodium retention and hyperkalemia, especially in patients with renal insufficiency, even though P was administered for only 3 days.

Adult↗
PubMed1996

Effect of low dietary calcium intake on blood pressure and pressure natriuresis response in rats: a possible role of the renin-angiotensin system.

Dietary Ca is an important modulator of blood pressure in humans and rats. Since the kidney plays a key role in the pathogenesis of hypertension, the effects of a low Ca diet (0.01% Ca) on blood pressure and pressure natriuresis response were studied in normotensive Sprague-Dawley rats. In addition, a possible role of the renin-angiotensin system in the development of hypertension and an altered pressure natriuresis response resulting from low dietary Ca intake was examined. In the low Ca diet group, systolic blood pressure measured by the tail-cuff method was significantly higher than in the normal Ca diet group (1,1% Ca) 1 week after the diet (1 13.0 +/- 7.1 vs. 105.0 +/- 9.5mmHg, p < 0.05). After 4 weeks, the hypertension was more pronounced. Low dietary Ca intake significantly inhibited the water and sodium excretory responses to acute elevation of renal perfusion pressure by tightening an infrarenal aortic constriction. Treatment with an inhibitor of angiotensin-converting enzyme, captopril (30 mg/kg/day), completely abolished the elevation of blood pressure and attenuated the reduced pressure natriuresis response observed in Ca-deficient rats. Although plasma renin activity was not different between the low and normal Ca diet groups after the 2-week dietary regimen, the pressor response to angiotensin II was enhanced by 30% in the low Ca diet group and there was a significant difference in the pressor response between the two groups. These results suggest a possible involvement of the renin-angiotensin system in the development of hypertension and an inhibitory effect on the pressure natriuresis response caused by low dietary Ca intake, via an enhanced sensitivity to angiotensin II.

Analysis of Variance↗
PubMed1999

Improved efficiency of hypervolemic therapy with inhibition of natriuresis by fludrocortisone in patients with aneurysmal subarachnoid hemorrhage.

OBJECT: To reduce the risk of ischemic complications in patients with subarachnoid hemorrhage (SAH), hypervolemic therapy is generally advocated. However, such conventional treatment cannot always ensure the maintenance of an effective intravascular volume expansion, because excessive natriuresis and osmotic diuresis occur after SAH. In this prospective study the authors examined the effects of inhibition of natriuresis with fludrocortisone acetate on intravascular volume expansion during hypervolemic therapy. METHODS: Thirty patients with SAH were randomized and divided into two groups: controls (Group 1, 15 patients) and patients treated with 0.3 mg/day of fludrocortisone (Group 2, 15 patients). In all patients sodium and fluid intake levels were in excess of maintenance requirements in an attempt to maintain a positive water balance and a central venous pressure (CVP) of 8 to 12 cm H2O. The mean sodium and water intake levels for 14 days after SAH were significantly reduced by fludrocortisone in Group 2 (487+/-34.52 mEq/day and 5159.2+/-249.29 ml/day, respectively; p<0.01) compared with Group 1 (634.2+/-42.86 mEq/day and 6611.7+/-365.67 ml/day). Fludrocortisone significantly reduced the urinary sodium excretion (p<0.01) and urine volume (p<0.01) in parallel, and effectively prevented a negative shift in the sodium as well as water balance (p<0.01). The serum sodium level tended to decrease in Group 1, reaching 135 mEq/L on average, but not in Group 2 (p<0.01). Hyponatremia in Group 1 was always observed at the optimal range of CVP values. A decrease in serum potassium level within the range of 2.8 to 3.5 mEq/L was transiently noted in 11 patients (73.3%) of Group 2, but was easily corrected. Possible side effects of fludrocortisone, such as pulmonary edema, were not encountered. CONCLUSIONS: Intravascular volume expansion in the presence of excessive natriuresis requires a large sodium and water intake and is often associated with hyponatremia. Inhibition of natriuresis with fludrocortisone can effectively reduce the sodium and water intake required for hypervolemia and prevent hyponatremia at the same time.

Adult↗
PubMed1992

The role of atrial natriuretic peptide in natriuresis of fasting.

OBJECTIVE: To examine the relation between plasma atrial natriuretic peptide (ANP) and the natriuresis of fasting. DESIGN: ANP, aldosterone and renin were examined during natriuresis of fasting in 25 obese essential hypertensive patients and nine overweight normotensive subjects placed on a supervised 500-KCal diet composed of 50% carbohydrates, 30% fat and 20% protein, and unlimited salt. Twenty-four-hour urinary electrolytes were measured on days 0, 4, 7 and 10 of the diet. RESULTS: Urinary sodium concentration nearly doubled in the patients on day 4, and increased 1.4-fold in the normotensive controls. Plasma ANP rose nearly threefold in the hypertensives on day 4 and nearly doubled in the normotensives. Patients and controls showed similar patterns of natriuresis and ANP secretion during the diet. CONCLUSIONS: We conclude that there is a clear association between ANP levels and natriuresis of fasting.

Adolescent↗
PubMed1991

Natriuresis secondary to carotid chemoreceptor stimulation with almitrine bismesylate in the rat: the effect on kidney function and the response to renal denervation and deficiency of antidiuretic hormone.

Almitrine bismesylate simulates the effects of arterial hypoxia in producing a specific and long-lasting excitation of the peripheral arterial chemoreceptors. Previous work has shown that almitrine produces a diuresis and natriuresis when given intravenously to anaesthetised rats in a stable mannitol induced diuresis. This response is abolished by glossopharyngeal nerve section implying that it is afferently mediated via the carotid body chemoreceptors. We have studied further the efferent limb of this response. The diuresis and natriuresis occurs without significant detectable changes in effective renal plasma flow and glomerular filtration rate suggesting that it is produced mainly by inhibition of renal tubular sodium and water reabsorption. Almitrine produces a diuresis and natriuresis in rats after bilateral nephrectomy and transplantation of a kidney from a donor rat. This effect is not therefore efferently mediated by the renal nerves and probably involves a humoral agent. Almitrine produces a diuresis and natriuresis in rats after bilateral adrenalectomy and in rats with congenital hypothalamic diabetes insipidus indicating that neither adrenal hormones nor changes in antidiuretic hormone levels are implicated.

Almitrine↗
PubMedDate not supplied

Water immersion induced alterations of plasma atrial natriuretic peptide (ANP), diuresis and natriuresis in kidney transplant patients.

UNLABELLED: The present article aimed to study the intactness of the physiological mechanism of ANP secretion in 64 kidney transplant patients treated with cyclosporine A + prednisone (CyA group--35 patients) or azathioprine + prednisone + promethasine respectively (Aza group or--29 patients). The control group comprised 15 healthy persons. ANP plasma levels were assessed before and 1 h and 2 h after neck out water immersion (WI). Higher basal ANP levels were found in patients of the CyA and Aza group than in normals (significantly higher in patients of the CyA group). WI induced an increase of plasma volume (PV) which was of comparable magnitude in all examined groups. It was accompanied by a significant increase of plasma ANP, diuresis and of natriuresis, which was significantly lower in transplanted patients than in normals. Only in healthy persons a significant positive correlation was found between the WI induced increase of plasma ANP and diuresis and natriuresis respectively. CONCLUSIONS: 1) kidney transplant patients are characterized by an intact, although reduced response of ANP secretion, diuresis and natriuresis to central hypervolaemia; 2) WI induced increase of diuresis and natriuresis does not seem to be only dependent upon ANP secretion in kidney transplant patients; 3) kind of immunosuppressive therapy seems to be of importance in the pathogenesis of altered ANP secretion in kidney transplant patients.

Adult↗
PubMed1987

Effects of atrial natriuretic factor on natriuresis and cGMP in patients with essential hypertension.

Human atrial natriuretic factor (h-ANF) or its vehicle only, were infused at rates of 0.8, 1.6 and 3.2 micrograms/min over three successive 30-min periods, into five patients with mild essential hypertension and seven normotensive controls. Baseline (mean +/- s.e.m.) plasma ANF levels were 13 +/- 2 in patients and 8 +/- 1 pg/ml in controls. During the first period, plasma ANF and cyclic guanosine monophosphate (cGMP) levels increased in both groups without significant alteration of blood pressure, heart rate, diuresis, natriuresis or cGMP excretion rate. During the second period of infusion, plasma ANF levels increased up to 179 +/- 39 and 177 +/- 30 pg/ml in patients and controls and plasma cGMP concentrations increased X 5.0 and X 4.9, respectively; natriuresis increased X 2.4 in patients and X 3.1 in controls while urinary cGMP increased X 10.9 in patients and X 10.5 in controls. During the last period, three controls became hypotensive while blood pressure remained stable in the other controls and in the patients with essential hypertension. During this period, the increases in plasma ANF concentration, diuresis, natriuresis and urinary cGMP excretion were similar in both groups. However, the mean plasma cGMP concentration after 90 min infusion was significantly higher in hypertensive patients than in control subjects (30.7 +/- 3.3 versus 15.6 +/- 3.4 pmol/ml, P less than 0.05). The half-life and clearance of plasma ANF, upon discontinuation of the infusion, were similar in both groups. Our data suggest that patients with mild essential hypertension have enhanced increases in plasma cGMP but normal increases in diuresis, natriuresis and cGMP excretion following infusion of h-ANF at pharmacological rates.

Adult↗
PubMed1988

Salicylic acid causes a diuresis and natriuresis in normal and common bile-duct-ligated cirrhotic miniature swine.

In patients with liver disease, or in normal subjects who are sodium-depleted, the administration of either a nonsteroidal anti-inflammatory drug or acetylsalicylate (aspirin) has a detrimental effect on the kidney; profound renal vasoconstriction and the retention of sodium and water may occur. We observed recently that salicylate (SA), in contrast to meclofenamate (MECLO) or aspirin, caused a diuresis and natriuresis in the sodium-depleted dog. To determine if SA would similarly affect the kidneys in a cirrhotic subject, the effects of SA (40 mg/kg) and subsequent MECLO treatment (2 mg/kg) were evaluated in five normal and six common bile-duct-ligated (CBDL) miniature swine. All six CBDL animals showed signs of biliary cirrhosis and four of the six were ascitic at the time of study. SA did not significantly alter renal blood flow or glomerular filtration rate in either the normal or CBDL animals. In both groups, SA caused a significant diuresis and natriuresis. MECLO, given after SA, caused a reduction in renal blood flow in the normal but not in the CBDL animals, but did not alter glomerular filtration rate in either group. In the CBDL animals, when MECLO was given alone a significant decrease in renal blood flow occurred. MECLO abolished the SA-induced diuresis and natriuresis in the normal swine but only affected the SA-mediated natriuresis in the CBDL animals. SA significantly reduced renal prostaglandin E2 excretion in both groups. With MECLO, prostaglandin E2 excretion was reduced further in the normals but not in the CBDL animals. These data demonstrate that SA does not produce detectable renal vasoconstriction in the cirrhotic pig.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Intrarenal mechanisms mediating pressure natriuresis: role of angiotensin and prostaglandins.

The ability of the kidney to increase sodium and water excretion in response to increases in perfusion pressure has been recognized for more than 50 years. Because glomerular filtration rate is tightly autoregulated, pressure natriuresis occurs as the result of decreased tubular sodium reabsorption rather than increased filtered load. Micropuncture and microperfusion data support the contention that acute changes in arterial pressure can alter proximal tubule reabsorption; however, studies have failed to show a consistent association between changes in sodium excretion and peritubular, interstitial, or tubular pressures. Thus, the specific intrarenal mechanism for the change in tubular reabsorption in response to an acute change in arterial pressure does not appear to be related to the peritubular physical factors at the level of outer cortical nephrons. The possible roles of angiotensin and prostaglandins as humoral mediators of pressure natriuresis are considered in this report. Although angiotensin II is a powerful modulator of the slope of the pressure natriuresis relationship, the responsiveness of sodium excretion to arterial pressure is actually enhanced by angiotensin-converting enzyme inhibitors. These data suggest that angiotensin does not mediate the basic phenomenon. Recent experiments indicate that intrarenal prostaglandins also modulate the magnitude of the pressure natriuresis relationship, but these hormones do not appear to be essential for its basic manifestation.

Absorption↗
PubMed1994

Modulation of natriuresis and renal dopamine excretion by sympathetic activity and the renin-angiotensin-aldosterone system.

The involvement of the sympathetic nervous system and the renin-angiotensin-aldosterone system in renal dopamine (DA) synthesis and sodium excretion (UNaV) were studied in 11 healthy volunteers. On a low sodium diet (LoSo, 50 mmol Na+) saline infusions were given without pretreatment or after oral intake of 50 mg captopril or 300 micrograms clonidine. On a high sodium diet (HiSo, 250 mmol Na+) saline was infused without or after intake of 300 micrograms clonidine. UNaV, the excretion rates of the DA precursor 3,4-dihydroxyphenylalanine (DOPA; UDOPAV), DA (UDAV), and noradrenaline (NA; UNAV), hormonal parameters, blood pressure (BP), glomerular filtration parameters, blood pressure (BP), glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured. Saline infusion alone during LoSo increased natriuresis without changes in catechol excretion or suppression of plasma renin activity (PRA) or plasma aldosterone (PALD). Sympatho-inhibition by clonidine resulted in marked antinatriuresis, decrease in BP and decrease in UDOPAV and UDAV, whereas plasma DOPA, GFR, and ERPF remained unchanged. PRA and PALD rose as indication of activation of the RAA system, probably by the reduced renal perfusion pressure after clonidine. Captopril significantly stimulated the saline-induced natriuresis without affecting UDOPAV and UDAV. On HiSo, when sympathetic tone is relatively suppressed, saline infusion alone stimulated natriuresis but did not affect catechol excretion or PRA. In the first and second hour after saline infusion PALD was suppressed. Clonidine again reduced BP and natriuresis, while PRA, PALD, and UDOPAV and UDAV were unaffected. These results suggest that sympathetic nerve activity may stimulate the intrarenal DA production.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Volume expansion enhances the recovery of renal function and prolongs the diuresis and natriuresis after release of bilateral ureteral obstruction: a possible role for atrial natriuretic peptide.

Plasma atrial natriuretic peptide (ANP) levels are elevated in patients with bilateral ureteral obstruction (BUO). To further evaluate the role of ANP in postobstructive diuresis, natriuresis and recovery of renal function, 3 groups of dogs were studied: Group 1, 6 dogs that underwent 48 hours of unilateral ureteral obstruction (UUO); Group 2, 6 dogs that underwent 48 hours of BUO; and Group 3, 6 dogs volume replete with normal saline during 48 hours of BUO. All 3 groups underwent hourly hemodynamic and clearance studies for 15 hours after the release of obstruction. Group 1 experienced no increase in either urine output or sodium excretion from the ipsilateral or contralateral kidney after release of obstruction. Groups 2 and 3 both experienced an initial diuresis and natriuresis after BUO (p < 0.01). However, in Group 2 diuresis and natriuresis after BUO ceased at 5 and 2 hours, respectively, while in Group 3 both persisted for 10 and 9 hours, respectively. Before obstruction the GFR was similar in all three groups. In Group 1 the GFR decreased significantly in the ipsilateral kidney (34.5 +/- 1.4 to 14.48 +/- 1.5 ml. per minute, (p < 0.01)) and increased significantly in the contralateral kidney (32.4 +/- 2.8 to 44.4 +/- 2.0 ml. per minute, (p < 0.05)) and remained so throughout the postobstruction period. The GFR in Groups 2 and 3 decreased to a similar level 1 hour after release (13.3 +/- 1.7 and 17.5 +/- 3.4 ml. per minute, respectively); however, Group 2 remained decreased during the period after release while group 3 increased to 23.4 +/- 3.4 ml. per minute (p < 0.01) at 11 hours after release of obstruction. In Group 2 the control plasma ANP level was 17.9 +/- 3.7 pg./ml. and was not altered by BUO, whereas ANP increased significantly after 48 hour BUO in Group 3, from 30.6 +/- 6.7 to 63.7 +/- 11.7 pg./ml. (p < 0.01). Before and after 48 hours of BUO, the pulmonary capillary wedge pressure was 5.0 +/- 2.0 mm. Hg and 7.0 +/- 1.0 mm. Hg (NS) in Group 2, while it increased from 7.18 +/- 1.5 mm. Hg to 11.6 +/- 1.9 mm. Hg (p < 0.01) in Group 3. We conclude that volume expansion during BUO enhances postobstructive diuresis and natriuresis and allows a greater recovery of GFR after release of the obstruction. This effect may be mediated through elevated plasma levels of ANP as measured in this study.

Animals↗
PubMed1994

Does endothelin work as an intrarenal mechanism to alter pressure natriuresis in spontaneously hypertensive rats?

OBJECTIVE: To study the possible involvement of intrarenal endothelial dysfunction in the modulation of the pressure-natriuresis curve in spontaneously hypertensive rats (SHR). METHODS: We examined the effect of endothelin on pressure natriuresis in isolated perfused kidneys from 16-week-old SHR and Wistar-Kyoto (WKY) rats. Plasma and urinary endothelin levels in intact rats and the rate of endothelin release from isolated kidneys were also determined. RESULTS: Urinary sodium excretion by SHR kidneys was 60% less than by WKY rat kidneys at a given perfusion pressure. Endothelin-1 increased the renal vascular resistance dose-dependently and the change was comparable in SHR and WKY rats. A high perfusate concentration of endothelin-1 markedly reduced urinary sodium excretion, resulting in a significant rightwards shift of the pressure-natriuresis curve. However, endothelin-1 at concentrations below 0.1 nmol/l did not decrease urinary sodium excretion, despite its renal vasoconstrictory activity. In a different in vivo study, plasma endothelin-like immunoreactivity was similar in the two groups, as was the urinary endothelin excretion. However, the rate of endothelin release from isolated SHR kidneys was slightly greater than from WKY rat kidneys. CONCLUSION: Since the difference in endothelin levels is not remarkable, it seems unlikely that increased intrarenal production of endothelin plays a role in the maintenance of hypertension in SHR by modulating the pressure-natriuresis curve.

Animals↗
PubMed1994

[Effect of low calcium diet on blood pressure and pressure natriuresis response in rats: role of the renin-angiotensin system].

Dietary Ca is an important modulator of arterial blood pressure in humans and rats. Since the kidney plays a key role in the pathogenesis of hypertension, the effect of a low Ca diet (0.01%Ca) on blood pressure and pressure natriuresis response was studied in Sprague-Dawley rats. In addition, a possible role of the renin-angiotensin system in the development of hypertension and an altered pressure natriuresis response resulting from low dietary Ca intake was investigated. In the low Ca diet group, systolic blood pressure determined by the tail-cuff method was significantly higher than in the normal Ca diet group (1.1%Ca) 1 week after the diet (113.0 +/- 7.1 vs. 105.0 +/- 9.5 mmHg, p < 0.05). Furthermore, low dietary Ca treatment significantly inhibited the water and sodium excretory responses to acute elevation of renal perfusion pressure. Treatment with an inhibitor of angiotensin converting enzyme, captopril (30 mg/kg/day), attenuated both the development of hypertension and the reduced pressure natriuresis response observed in Ca-deficient rats. Although plasma renin activity was not different between the low and normal Ca diet groups after the 2-week dietary regimen, the pressor response to angiotensin II injection was significantly greater in the low Ca diet group. These results indicate a possible involvement of the renin-angiotensin system in the development of hypertension and the inhibitory effects of the pressure natriuresis response caused by low dietary Ca intake, via enhanced sensitivity to angiotensin II.

Animals↗
PubMed1996

Nisoldipine and pressure-natriuresis curves in transgenic (mRen2)27 rats.

OBJECTIVES: The mechanism by which antihypertensive drugs influence pressure natriuresis gives insight into their mode of action. We tested the effects of nisoldipine on pressure natriuresis, glomerular filtration rate, and renal blood flow in transgenic (mRen2)27 rats and Sprague-Dawley Hannover control rats. METHODS: The rats were anaesthetized, uninephrectomized with denervation of the remaining kidney, administered noradrenaline, 17-hydroxycorticosterone, vasopressin, and aldosterone to 'clamp' these regulatory systems and nisoldipine (0.5 mg/kg bolus plus 0.017 mg/kg per min). The glomerular filtration rate and renal plasma flow were measured with inulin and PAH. Renal perfusion pressure was varied from approximately 100 to approximately 200 mmHg with clamps above and below the kidney. RESULTS: Nisoldipine shifted not only the pressure-diuresis and pressure-natriuresis curves but also the fractional sodium and water curves leftwards in transgenic (mRen2)27 rats, but not in Sprague-Dawley Hannover rats. Nisoldipine increased the glomerular filtration rate and renal blood flow in transgenic (mRen2)27 rats but not in Sprague-Dawley Hannover rats. CONCLUSIONS: Nisoldipine shifts the pressure-natriuresis curve in transgenic (mRen2)27 rats leftwards; sodium and water excretion is increased for any given perfusion pressure. This effect is intrinsic to the kidney and is associated with inhibition of tubular sodium and water reabsorption and with an increase in renal perfusion.

Animals↗
PubMed1995

[The effect of renal dopamtne receptor blockade on natriuresis induced by volume expansion and intracerebroventricular injection of hypertonic saline in rabbits].

The present study was carried out to study the effects of renal dopamine receptor blockade on natriuresis induced by volume expansion (VE) and intracerebroventricular injection of hypertonic saline (ICHNa) in connexion with the use of dopamine receptor blockers haloperidol (Hal) in anesthetized rabbits. In the VE experiments, Hal group decreases the peak increase of UNa V from control group of 65.0 +/- 15.0 to 19.0 +/- 5.5 mumol/min (P < 0.02). In the ICHNa experiments, the peak increase of UNa V in control and Hal groups were respectively 28.9 +/- 4.6 and 29.0 +/- 5.8 mumol/min (P > 0.50). In the experiments of rabbit with intact renal dopamine receptor, the natriuresis induced by VE+ICHNa was significantly greater than those due to either inducing factor acting alone. Renal dopamine receptor blockade also significantly attenuated the natriuresis induced by VE+ICHNa. These results indicate that renal dopamine receptor blockade significantly attenuated the natriuresis induced by VE or VE+ICHNa, but did not affect the response of ICHNa. In the rabbits with intact renal dopamine receptor, the natriuretic response induced by VE+ICHNa was significantly greater than those response by either inducing factor acting alone.

Animals↗