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PubMed1985

Accelerated natriuresis induced by synthetic atrial natriuretic polypeptide in spontaneously hypertensive rats.

Effects of synthetic alpha human atrial natriuretic polypeptide (alpha-hANP) on diuresis, natriuresis and mean arterial blood pressure (MAP) were compared between 4-5 month-old male spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) under ether anesthesia. In both groups, the peptide injected (0.5 micrograms/100g body weight, i.v.) caused potent (about ten fold), rapid and short-acting (for 15 min) increases in sodium (Na+) and chloride excretions and also an increase in urine flow and potassium excretion with lesser magnitude. Although ratios of the maximum response to basal value were much the same, net increases in urine flow and Na+ output were significantly greater in SHR than in WKY. As to the effect on MAP, a rapid (within 2 min) fall observed in the two groups. These results suggest that the atrial natriuretic peptide may be involved in the altered regulatory mechanism of fluid and electrolyte balance in SHR models with genetic hypertension.

Animals↗

PubMed1987

Atrial natriuretic peptide and the natriuresis due to acute beta-blockade in conscious hypertensive rats.

Acute beta-adrenoceptor blockade in rats is known to produce a natriuresis of hitherto uncertain cause. To investigate this phenomenon plasma atrial natriuretic peptide (ANP) concentrations were measured in groups of conscious metoprolol-treated and control rats. In the active treatment group the blood pressure decreased slowly, as expected, settling at a lower level after 2 hours, and the mean sodium excretion doubled 1 hour after metoprolol administration. This natriuretic effect was maximal after 40-60 minutes and thereafter slowly declined towards basal values. The period of enhanced sodium excretion was associated with a significant rise (68%) of the mean ANP plasma concentration. It suggested that this increase in plasma ANP concentration can mediate the acute natriuretic effect beta-adrenoceptor blockade.

Animals↗

PubMed1988

Atrial natriuretic peptide in volume expansion-induced natriuresis in man.

The role of atrial natriuretic peptide (ANP) in the extracellular volume expansion (ECVE) induced natriuresis was examined in normal man under basal conditions and following dopamine blockage. Hypotonic ECVE was induced by drinking of 20 ml/kg tap water and subsequent intravenous infusion of 2 1 0, 9% saline over a period of 4 hours. This maneuver caused an increase in the plasma concentrations of ANP from 25.8 +/- 3.4 (means +/- SEM) to 59.7 +/- 6.7 fmol/ml. There was a dissociation between ANP response and urinary sodium excretion. A transient rise in glomerular filtration rate (GFR), plasma dopamine and a continuous decrease in plasma renin activity, aldosterone, vasopressin, and noradrenaline were observed. The natriuretic response to ECVE was blunted during dopamine blockade by metoclopramide, but plasma ANP, renin activity, catecholamine and vasopressin levels were not affected. However, plasma aldosterone rose. Our data are compatible with the concept that intrarenal dopamine and raised plasma concentration of ANP contribute to the natriuretic response to ECVE, but these hormonal changes do not completely explain the underlying mechanisms.

Adult↗

PubMed1992

An impairment of renal tubular DA-1 receptor function as the causative factor for diminished natriuresis to volume expansion in spontaneously hypertensive rats.

It has been demonstrated that endogenous kidney dopamine (DA) contributes to the natriuretic response to acute volume expansion (VE). Several studies suggest that a defect in renal DA-ergic mechanism may play a role in genetic hypertension in humans and rats. The present study was designed to determine the role of renal DA and tubular DA-1 receptors in the natriuretic response to VE in age-matched spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats of 10-12 weeks of age. In pentobarbital-anesthetized rats, VE was carried out by intravenously infusing isotonic sodium chloride (5% body weight) over a period of 60 min. This maneuver evoked pronounced increases in urine output, urinary sodium excretion and urinary DA excretion. However, the natriuretic and diuretic response to VE was significantly reduced in SHR, although the increase in urinary DA excretion was similar in both SHR and WKY rats. During VE no significant changes in glomerular filtration rate or blood pressure were noted in either strain of animals, indicating the involvement of renal tubular mechanisms in the natriuretic response. In a separate group of SHR and WKY rats, pretreatment with DA-1 receptor antagonist SCH 23390 caused significant attenuation of the natriuretic and diuretic response to VE in WKY rats but not in SHR, suggesting that unlike WKY rats kidney DA was not contributing to the natriuretic response to VE in SHR. In another group of animals, the renal effects of exogenously administered DA-1 receptor agonist fenoldopam were examined. Fenoldopam (1 microgram/kg/min) produced significant increases in urine output and urinary sodium excretion without causing any alterations in blood pressure or glomerular filtration rate in both SHR and WKY rats. However, the interesting observation was that fenoldopam-induced diuresis and natriuresis were significantly attenuated in SHR compared to the WKY rats. These results show that SHR are not able to eliminate an acute increase in sodium load as efficiently as WKY rats, which may be at least in part due to a defect in renal tubular DA-1 receptor function.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1983

Natriuresis and kaliuresis in saline-expanded, long-term hypophysectomized rats.

The ability of unanesthetized, long-term hypophysectomized (HPX) rats to excrete a saline challenge was evaluated. HPX rats were hypophysectomized 1-2 months prior to experiments. Saline was administered either by intragastric gavage or by intravenous infusion. For 3 hr following gastric saline loading, HPX rats excreted significantly less sodium and potassium than did intact rats. When saline was administered intravenously, both intact and HPX rats excreted similar amounts of sodium during 3 hr of continued volume expansion. On the other hand, potassium excretion was again markedly lower in saline expanded HPX rats than in intact rats. Saline expanded HPX rats in both series of studies had lower excretion rates of creatinine and had lower plasma aldosterone and corticosterone concentrations than expanded intact rats. Urine osmolalities were not significantly different between intact and HPX rats, either before or after volume expansion, indicating that there was at least partial recovery of posterior pituitary function in the HPX animals. These results suggest that adequate anterior pituitary function is required for supporting the kaliuresis but not the natriuresis associated with saline expansion.

Aldosterone↗

PubMed1985

Reduction of blood pressure and increased diuresis and natriuresis during chronic infusion of atrial natriuretic factor (ANF Arg 101-Tyr 126) in conscious one-kidney, one-clip hypertensive rats.

Conscious one-kidney, one-clip hypertensive rats and their normotensive controls were infused during 7 days with synthetic ANF (Arg 101-Tyr 126) at 100 ng/hr/rat (35 pmol/hr/rat) by means of osmotic minipumps. The basal blood pressure of 193 +/- 6 mmHg gradually declined to 145 +/- 6 mmHg at day 4 after the infusion was started. No changes in blood pressure were observed in ANF-infused normotensive rats. A significantly higher diuresis and natriuresis was observed in ANF-infused hypertensive rats when compared to the non-treated hypertensive group. No such changes were observed in ANF-treated normotensive animals. No differences in PRA were seen in any group. Atrial immunoreactive ANF was significantly lower in one-kidney, one-clip rats than in the normotensive animals, but whether this is the reflection of an increased release in the circulation remains to be elucidated. It is suggested that the hypotensive response of one-kidney, one-clip animals to ANF may be secondary to a dual mechanism, vasodilatation and volume depletion.

Animals↗

PubMed1986

Exaggerated natriuresis in experimental hypertension.

The exaggerated natriuretic response to intravenous isotonic saline volume expansion in conscious spontaneous hypertensive rats (SHR), compared to normotensive Wistar-Kyoto rats (WKY), is associated with an exaggerated inhibition of renal nerve activity. Following bilateral renal denervation, the natriuresis was significantly attenuated in SHR but unaffected in WKY. Thus, the exaggerated natriuretic response to intravenous isotonic saline in SHR is dependent on their enhanced inhibition of renal nerve activity. Conscious Dahl salt-sensitive rats, on either low or high salt diet, did not exhibit an exaggerated natriuretic response to intravenous isotonic saline volume expansion which may be explained by their known impairment of cardiopulmonary baroreceptor reflex mediated suppression of efferent sympathetic nerve activity during intravenous volume expansion. Conscious hypertensive DOCA-NaCl rats exhibited an exaggerated natriuretic response to oral but not to intravenous isotonic saline volume expansion, suggesting differences in gastrointestinal absorption of isotonic saline. It is concluded that enhanced inhibition of efferent renal sympathetic nerve activity via cardiopulmonary baroreceptor reflex activation contributes to the exaggerated natriuretic response to intravenous isotonic saline volume expansion in certain models of experimental hypertension.

Animals↗

PubMed1988

A high-salt meal produces natriuresis in humans without elevating plasma atriopeptin.

The effects of a high-sodium meal on plasma atrial natriuretic peptide (atriopeptin) and renal sodium excretion were studied in eight normal human subjects. As expected, sodium excretion and urine osmolality increased following the meal. Plasma atriopeptin levels did not increase, however, after the high-sodium meal. In a control experiment, consumption of a low-sodium meal by six of the same subjects did not increase either urinary sodium excretion or plasma atriopeptin concentration. We conclude that the natriuresis elicited by a high-salt meal is not mediated by the atrial peptides.

Adult↗

PubMed2001

Divergent natriuretic action of calcium channel antagonists in mongrel dogs: renal haemodynamics as a determinant of natriuresis.

This study examined the effects of different types of calcium channel antagonists on renal haemodynamics and natriuresis. The intravenous infusion of nifedipine (L-type blocker), efonidipine (L/T-type blocker) or mibefradil (predominant T-type blocker) into anaesthetized dogs elicited similar, albeit modest, reductions in blood pressure. Nifedipine (1 microgram.min(-1).kg(-1)) increased renal plasma flow (RPF) (23+/-6%; P<0.05) and glomerular filtration rate (GFR) (25+/-5%; P<0.05) (all values are means+/-S.E.M., n=7). Efonidipine (0.33 microgram .min(-1).kg(-1)) also elevated RPF (18+/-6%; P<0.05), and tended to increase GFR (17+/-8%; P=0.08). These antagonists exerted contrasting actions on the filtration fraction (FF), with an increase being elicited by nifedipine, whereas efonidipine had no effect. Furthermore, mibefradil (0.01-1 microgram.min(-1).kg(-1)) slightly elevated RPF (between 5+/-3% and 8+/-3%), but failed to alter GFR, resulting in a decrease in FF. Nifedipine slightly increased urinary sodium excretion (U(Na)V) (29+/-16% increase at 1 microgram .min(-1).kg(-1)) and fractional sodium excretion (FE(Na)) (18+/-14%), whereas efonidipine (0.33 microgram .min(-1).kg(-1)) elicited marked elevations in U(Na)V (110+/-38%; P<0.05) and FE(Na) (102+/-44%; P<0.05). Mibefradil (1 microgram .min(-1).kg(-1)) exerted a moderate natriuretic action [U(Na)V, +60+/-32% (P=0.1); FE(Na), +67+/-20% (P<0.05)]. Furthermore, although a positive correlation was observed between U(Na)V and urinary nitrate/nitrite excretion, no differences were noted between the various calcium channel antagonists. Collectively, this study demonstrates that the glomerular haemodynamic and natriuretic actions of these calcium channel antagonists, which possess diverse blocking activities on L/T-type channels, vary. Based on the divergent actions on FF (i.e. increase, no change and decrease by nifedipine, efonidipine and mibefradil respectively), the natriuretic action of calcium channel antagonists is possibly attributed to the inhibition of tubular sodium reabsorption associated with increased post-glomerular blood flow, rather than increased GFR.

Animals↗

PubMed2000

[Role of paraventricular nucleus in natriuresis and diuresis induced by volume expansion in rabbits].

In sham-lesioned and paraventricular nucleus (PVN) lesioned rabbits, the peak increases of urine volume (UV) induced by volume expansion (VE) were 0.59+/-0.09 and 0.31+/-0.03 ml/min (P<0.01) respectively, whereas the peak increases of U(Na)V were respectively 66.76+/-6.74 and 36.05+/-3.44 micromol/min (P<0.01). No significant differences were found in the two increases induced by VE between rabbits with intact and those with sham-lesioned PVN. In rabbits with vagotomy there were no changes in the two increases after PVN lesion (P>0.05). In rabbits with renal denervation there was no significant change in natriuretic response after PVN lesion (P>0.05), but lesion of PVN significantly attenuated diuretic response (P<0.02). There were no significant differences in glomerular filtration rate (GFR) and renal plasma flow (RPF) before or after VE between the rabbits with intact and lesioned PVN (P>0.05). These results suggest that PVN is involved in the regulation of natriuresis and diuresis induced by VE, which are mediated by vagal afferent nerve, whereas the renal sympathetic efferent nerve may be involved in natriuretic response.

Animals↗

PubMed1976

Exaggerated natriuresis in the conscious spontaneously hypertensive rat.

In response to an acute saline load, many patients with essential hypertension exhibit an exaggerated natriuresis relative to normotensive controls. In the present study, the urinary responses of conscious,Okamoto-strain, spontaneously hypertensive rats (SHR), and Wistar-Kyoto strain normotensive rats (NTR) to an acute saline load were evaluated to determine if a similar exaggerated natruiresis exists in this form of hypertension. Twelve rats of each strain per group (12 weeks of age) were housed in metabolism cages for 1 week. Systolic blood pressures (tail cuff) were significantly different (206+/- 9 mm. Hg in SHR and 135 +/- 3 mm. Hg in NTR). After a 4-hour control urine collection, 6 ml. of 0.9 per cent sodium chloride were given by gavage. Urine was collected again for 2 hours. Control urinary excretions of sodium, potassium, and creatinine in SHR and NTR were 11.2 +/- 4.8 muEq per hour, 50.1 +/- 7.6 muEq per hour, and 39.9 +/- 5.5 mg. per hour in SHR, and 13.8 +/- 2.4 muEq per hour, 34.9 +/- 5.5 muEq per hour, and 37.5 +/- 7.1 mg. per hour in NTR, respectively. The respective control values for sodium, potassium, and creatinine excretion in the two groups were not significantly different. Following the saline load, sodium and creatinine excretion rates were significantly elevated in both groups of rats. However, the increase in sodium excretion in SHR (60.8 +/- 7.2 MUEq per hour) was more than double and significantly different from that of the NTR (26.6 +/- 3.7 muEq per hour). In contrast, the increments in creatinine excretion in the two groups of rats were not significantly different from each other. In the NTS, urinary potassium excretion was significantly elevated (59.0 +/- 7.9 muEq per hour) whereas in SHR it was not significantly altered (12.0 +/- 8.8 muEq per hour). The change in urinary creatinine excretion as an index of change in glomerular filtration rate suggests that the greater increase in sodium excretion by the SHR was the result of decreased fractional reabsorption of sodium and not the result of a greater increase in glomerular filtration rate. The exaggerated natriuretic response to salt loading in SHR resembles that in hypertensive man except that in SHR, a simultaneous kaliuretic response is absent.

Animals↗

PubMed1992

Acute inhibition of endopeptidase 24.11 in essential hypertension: SCH 34826 enhances atrial natriuretic peptide and natriuresis without lowering blood pressure.

The acute renal, endocrine, and hemodynamic effects of the orally active endopeptidase inhibitor SCH 34826 (400 mg every 6 hours for five doses) were investigated in a group of 6 male patients [with established mild to moderate essential hypertension and left ventricular (LV) hypertrophy] in a balanced random-order double-blind, placebo-controlled cross-over study. Plasma atrial natriuretic factor (ANF) concentrations increased (p < 0.05) to fourfold control values after the first dose of inhibitor, but later postdose increments of ANF were less pronounced. Plasma cyclic GMP also increased significantly (p < 0.05). These effects were associated with a transient modest but significant (p < 0.05) increase in sodium excretion (50 mmol sodium in excess of placebo values) that was complete in 24 h. Mean 24-h urinary excretions of cyclic GMP and immunoreactive ANF were also significantly increased by 55 and 86%, respectively. Other urine indexes (including other electrolytes, volume, creatinine, aldosterone, and cortisol) and renal hemodynamics [including glomerular filtration rate (GFR) and effective renal plasma flow (RPF)] were unchanged. Renin-angiotensin-aldosterone system (RAAS) activity was not significantly altered. Plasma epinephrine increased after the initial three doses of SCH 34826. Systolic blood pressure (SBP) and heart rate (HR) were not altered by SCH 34826. Diastolic BP (DBP) increased slightly (p = 0.044). Acute inhibition of endopeptidase 24.11 by SCH 34826 in essential hypertension caused significant increments in plasma ANF and cyclic GMP together with modest natriuresis. No antihypertensive effect was observed in the first 30 h of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗

PubMed1992

Antidiuresis and natriuresis induced by gastric distension in water-loaded rats.

Antidiuretic and natriuretic responses were observed following gastric distension in anesthetized, water-loaded rats. An increase of intragastric pressure to 25, 30, 35, and 40 cm H2O of 2-minute duration respectively elicited 11, 35, 45, and 55% inhibition of water diuresis with concomitant, graded increase of sodium excretion by the kidney. These antidiuretic and natriuretic responses to gastric distension persisted and sustained the same intensity after acute bilateral cervical vagotomy, indicating that the sensory input conveyed from the gastric mechanoreceptors to central nervous system during gastric distension should involve afferent fibers other than vagus nerve. Rats with diabetes insipidus (D1) produced by hypothalamic lesions were also tested, but neither antidiuresis nor natriuresis in response to gastric distension was observed in these D1 rats whose neurohypophysis contained little antidiuretic hormone (ADH). In conclusion, gastric distension may induce liberation of ADH and probably other neurohypophysial hormone which affects renal handling of sodium and water in anesthetized, water-loaded rats.

Animals↗

PubMed2004

[High doses of aspirin reduce natriuresis in hypertensive patients treated with enalapril].

Angiotensin converting enzyme inhibitors have been shown to be useful in the treatment of essential hypertension while anti-platelet agents improve the overall cardiovascular risk profile in this population. Our aim was to assess the interaction of two different aspirin (ASA) doses--81 and 325 mg/day--with the antihypertensive effect of enalapril as well as their impact upon the urinary sodium excretion (Na(u)). A total of 22 patients between 35 and 65 years of age were included in a prospective double blind trial with a partial cross-over design. We excluded patients with secondary hypertension and recent use of anti-inflammatory drugs. Patients were placed on enalapril and a low sodium diet--<6 g of NaCl/day--and, sequentially, on two different doses of aspirin separated by a 10 day wash out period. Blood pressure (BP) was measured at weekly visits. Systolic, diastolic and mean BP levels decreased significantly in enalapril-treated patients (p<0.01) and no difference was detected between the two AAS dosages although a non-statistically significant difference towards better BP control was observed when 81 mg of ASA was used. Na(u) was higher at baseline when compared with the two periods under ASA (p<0.01) and Na(u) was higher with 81 mg than with 325 mg. These results suggest that in essential hypertensive individuals treated with enalapril and two ASA doses, low doses of ASA are associated with better blood pressure control and higher natriuresis.

Adult↗

PubMed1979

[Effect of the time of theophylline administration on the intensity of diuresis and natriuresis in the rat].

The present study originates in two experimental data: circadian variations evidence of water, electrolytes and solutes urinary excretion and theophylline diuretic and salidiuretic effects knowledge; we purpose to evidence theophylline-induced water and sodium renal excretion in rats as modified by the time of drug administration. Theophylline single dose is injected in 100 animals (20 lots of 5 rats) at 8 h, 14 h, 20 h or 2 h and urines are collected during a consecutive to injection hours long period: 8 h-14 h (I), 14 h-20 h (II), 20 h-2 h (III) or 2 h-8 h (IV). Diuresis increases in + 40,4 p. cent (I), in + 123,7 p. cent (II), in + 123,3 p. cent (III) in + 65,4 p. cent (IV). So, natriuresis increases in 39,6 p. cent (I), in 223,2 p. cent (II), in 114,3 p cent (III) and in 109,6 p. cent (IV). These results evidence that theophylline diuretic and natriuretic effects change strongly with injection time, being largest if it is injected at 14 h and slightest if injected at 8 h. Such observations prompt to study if the other pharmacological properties of theophylline, especially at pulmonary level, response also with a time-dependant intensity.

Animals↗

PubMedDate not supplied

[The effects of the acute administration of atrial natriuretic peptide on the mechanisms regulating diuresis and natriuresis in the essential hypertension patient].

The authors investigated the role of atrial natriuretic peptide (alpha-hANP 99-126) in essential hypertension by evaluating some hemodynamic and renal effects of acute peptide infusion (1 micrograms/kg for 1 min + 50 ng/kg for the following 20 min) in fourteen subjects: eight mild to moderate, untreated, essential hypertensives (EH) and six normotensive (N) controls, during 2 hour-clearance periods, the 1st after ANP infusion, the 2nd during placebo (PL) administration. The double-blind study was carried out after the patients had rested and fasted overnight. It showed no significant changes in heart rate (HR); instead, compared with placebo, mean blood pressure (MBP) decreased significantly in both groups, beginning from the 3rd min after ANP infusion was begun (N: PL = 87.04 +/- 1.7 mmHg, ANP = 80.9 +/- 3.7 mmHg, p less than 0.0001; EH: PL = 102.6 +/- 3.2 mmHg, ANP = 97.7 +/- 5.9 mmHg, p less than 0.01). Among the urinary parameters we considered, cyclic GMP (cGMP) increased after ANP infusion in all subjects (N: PL = 129.1 +/- 56.3 pmol/mL, ANP = 199.2 +/- 85.4 pmol/mL; EH: PL = 106.55 +/- 56.2 pmol/mL, ANP = 220.03 +/- 92.7 pmol/mL, p less than 0.05); diuresis showed a prompt and significant increase in EH (N: PL = 837 +/- 368 mL, ANP = 1066 +/- 340 mL; EH: PL = 713 +/- 286 mL, ANP = 1043 +/- 280 mL, p less than 0.005), and so did natriuresis (N: PL = 23 +/- 14.3 mEq/L, ANP = 33 +/- 14.6 mEq/L; EH: PL = 25.6 +/- 8.9 mEq/L, ANP = 41.9 +/- 13.8 mEq/L, p less than 0.01); urinary potassium excretion was significantly reduced in EH (N: PL = 18.7 +/- 12.9 mEq/L, ANP = 14.2 +/- 6.9 mEq/L; EH: PL = 16.5 +/- 7.9 mEq/L, ANP = 10.7 +/- 4.8 mEq/L, p less than 0.005), while no changes were noted in glomerular filtration rate (GFR), estimated as creatinine clearance, urinary magnesium, albumin and aldosterone excretion. To investigate other potential mechanisms involved in renal effects of ANP, the urinary excretion of both prostaglandins 6-cheto PGF1-alpha and thromboxane B2 (TXB2), and dopamine were studied. The results showed only a significant decrease of dopamine urinary excretion in EH after ANP administration (N: PL = 50.4 +/- 28.7 micrograms/L, ANP = 45.0 +/- 29.7 micrograms/L; EH: PL = 47.3 +/- 21.5 micrograms/L, ANP = 27.1 +/- 12.7 micrograms/mL, p less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗

PubMed1990

Dopamine and natriuresis. Mechanism of action and developmental aspects.

The present paper summarizes our studies on the mechanisms of the dopamine induced changes in renal macro- and microcirculation as well as in proximal and distal tubular sodium handling which contributes to the natriuresis induced by the drug. Some aspects of the physiological role of locally generated dopamine in regulating sodium excretion are also reviewed. Finally, by describing the cardiovascular, renal and hormonal effects of dopamine in the preterm human neonate, some of the developmental aspects of the renal effects of the drug are also discussed.

Animals↗

PubMed1989

Bilateral acute heart atrial auriectomy reduced diuresis and natriuresis following hypertonic sodium load in anaesthetized dogs.

Anaesthetized dogs were deprived of a portion of the atrial natriuretic factor producing tissue by bilateral acute heart atrial auriectomy. Their ability to respond by diuresis and natriuresis either to the expansion of extracellular fluid volume with isotonic saline (3% b.w.) or to hyperosmolality induced by hypertonic saline loading (0.13% b.w. of 20% NaCl solution) was subsequently reduced by about 50%. It is thus suggested that atrial natriuretic system may also play a role in osmoregulation by taking part in the promotion of renal sodium excretion.

Animals↗