Biomedical subjects

N Nushiro

Publications and source records attributed to N Nushiro.

26 records · Page 2Linked to original sources

PubMed1988

Interaction between ANP and amiloride in renal tubular sodium handling in anesthetized rabbits.

To examine whether amiloride, an inhibitor of a conductive sodium channel in the distal tubule, modifies a possible tubular action of atrial natriuretic peptide (ANP), alpha-human ANP (0.05 micrograms.kg-1.min-1) was infused intravenously with or without pretreatment of amiloride (5 mg/kg + 0.04 mg.kg-1.min-1) in anesthetized rabbits. No significant changes in arterial pressure and renal blood flow were observed between two groups after ANP infusion. However, increases in filtered sodium load (FNa) and net tubular sodium reabsorption (RNa) induced by ANP were attenuated after the amiloride pretreatment. These attenuations in FNa and RNa could be due to the failure of increase in glomerular filtration rate, although the reason is not clear. Amiloride pretreatment abolished the ANP-induced kaliuresis, whereas ANP-induced increases in urinary sodium and fractional sodium excretion were additive after amiloride pretreatment. Thus, ANP elicited a further natriuretic effect even when the amiloride-sensitive component was blocked. This suggests that there is another mechanism by which ANP induces natriuresis, in addition to any ANP effects mediated by interference with sodium conductive channels.

Amiloride↗

PubMed1988

Nifedipine enhances the vasodepressor and natriuretic effects of atrial natriuretic peptide.

We examined a possible interaction between the calcium entry blocker nifedipine and atrial natriuretic peptide on blood pressure and natriuresis in anesthetized rabbits. The administration of atrial natriuretic peptide (0.05 micrograms/kg/min) produced a significant decrease in mean arterial pressure. Similar reductions in blood pressure were obtained during the administration of nifedipine (1.0 micrograms/kg/min). Atrial natriuretic peptide produced a consistent increase in glomerular filtration rate that was higher than the increase in renal blood flow; hence, the filtration fraction was significantly elevated. Atrial natriuretic peptide also elicited a significant increment in urine volume and urinary sodium excretion, while nifedipine was devoid of any significant effects on renal hemodynamics and renal excretory function during the experimental period. The administration of atrial natriuretic peptide superimposed on an ongoing infusion of nifedipine resulted in a greater fall of blood pressure than that seen during the administration of atrial natriuretic peptide or nifedipine alone. Sodium excretion was also potentiated, but there were no changes in renal hemodynamics or in the filtration fraction. These results suggest that calcium entry blockers potentiate the vasodepressor and the natriuretic effects of atrial natriuretic peptide but prevent its renal hemodynamic effects.

Animals↗

PubMed1988

The effects of atrial natriuretic peptide and amiloride on renal haemodynamics and the renal kallikrein-kinin system.

Anaesthetized rabbits were used to examine the effects of amiloride (an inhibitor of a conductive sodium channel in the distal tubule) and atrial natriuretic peptide (ANP), both singly and in combination, on renal function and the renal kallikrein-kinin system. The administration of ANP (0.05 microgram/kg per min) produced a natriuresis with increases in renal blood flow and glomerular filtration rate. The administration of ANP superimposed on amiloride infusion (5 mg/kg + 0.04 mg/kg per min) showed an additive effect on the natriuresis, although the renal haemodynamic changes were now absent. The infusion of ANP alone increased the urinary excretion of kallikrein and kinins. Prior infusion of amiloride prevented the expected increases in the urinary excretion of kallikrein and kinins after infusion of ANP was superimposed. These results suggest that the observed renal haemodynamic changes could be mediated through renal kallikrein and kinins. The additive effect on sodium excretion might be elicited by the results of alterations in the tubular handling of sodium, although distal tubular function is not modified by ANP. It seems that the renal kallikrein-kinin system is not causally involved in the increased sodium excretion by ANP.

Amiloride↗

PubMed1987

Interaction of calcium ion and atrial natriuretic peptide on blood pressure, natriuresis and the renal kallikrein-kinin system in anesthetized rabbits.

To examine whether hemodynamic and natriuretic effects of alpha-human atrial natriuretic peptide (ANP) were modulated by calcium (Ca) ion, Ca entry blocker nifedipine (Nif) was administered prior to ANP infusion in anesthetized rabbits. We also examined the effect of Nif and ANP on the renal kallikrein-kinin system. Both Nif. (1.0 micrograms/kg/min) and ANP (50 ng/kg/min) increased urinary sodium excretion (UNaV) without change in renal hemodynamics, although mean arterial pressure (MAP) decreased. Fractional excretion of sodium (FENa) was also increased significantly by both Nif and ANP. Nif infusion alone decreased MAP, the additional infusion of ANP on Nif pretreatment induced a further decrease in MAP and caused an increase in UNaV and FENa without renal hemodynamics changes. The administration of ANP increased urinary excretion of kallikrein and kinin. The additional infusion of ANP on Nif pretreatment induced a further increase in urinary kallikrein and kinin. These results suggest that Ca ion does not participate in ANP-induced natriuresis. Renal kallikrein-kinin may partly involve in natriuresis induced by ANP.

Animals↗

PubMed1987

Effect of atrial natriuretic factor on renin release in isolated afferent arterioles.

This study was designed to examine the effect of alpha-human atrial natriuretic polypeptide (alpha-hANP) on renin release in the absence of tubules, glomeruli and macula densa. Rabbit afferent arterioles were microdissected and incubated for two consecutive, 20 minute periods. Hourly renin release rate from a single arteriole was calculated. Basal renin release rate was 0.97 +/- 0.13 ng AI.hr-1.Af-1/hr (X +/- SEM, N = 18) and remained stable throughout the incubations. When afferent arterioles were exposed to alpha-hANP (0.01, 0.1 or 1 microM), renin release rate did not change significantly. Isoproterenol (5 microM) increased renin release rate from 0.92 +/- 0.28 to 1.50 +/- 0.46 ng AI.hr-1.Af-1/hr (N = 7, P less than 0.01). After pretreatment of afferent arterioles with alpha-hANP (1 microM), isoproterenol still increased renin release rate from 0.98 +/- 0.24 to 1.64 +/- 0.37 ng AI.hr-1.Af-1/hr (N = 7, P less than 0.01). The increases in renin release rate induced by isoproterenol were not different between the two groups. Pretreatment of rabbits with furosemide for two days before experiments resulted in greater basal renin release rates from microdissected afferent arterioles (1.70 +/- 0.35 ng AI.hr-1.Af-1/hr, N = 14). However, exposure to alpha-hANP (1 microM) did not alter this elevated renin release rate. It is concluded that atrial natriuretic factor may not have a direct action on juxtaglomerular cells.

Animals↗

PubMed1987

The effects of intravenous injection of alpha-human atrial natriuretic polypeptide on blood pressure, renal hemodynamics and urinary kinin excretion in anesthetized rabbits.

Studies were performed in anesthetized rabbits to examine the effects of alpha-human atrial natriuretic polypeptide (alpha-hANP) on blood pressure, renal hemodynamics and urinary kinin excretion. Intravenous bolus injection of alpha-hANP at a dose of 5 micrograms resulted in a transient increase in renal blood flow from 26.6 +/- 2.2 to 33.7 +/- 2.2 ml/min (p less than 0.05) and a decrease in mean arterial pressure from 113 +/- 1.8 to 107 +/- 2.2 mmHg (p less than 0.01). The calculated renal vascular resistance decreased from 4.50 +/- 0.34 to 3.28 +/- 0.20 mmHg/ml/min (p less than 0.05). This vasodilatory effect of alpha-hANP was immediate and lasted for 30 min. These hemodynamic alterations were not associated with the changes in glomerular filtration rate estimated by creatinine clearance. Intravenous injection of alpha-hANP also produced marked increases in urine volume from 1.99 +/- 0.43 to 5.7 +/- 1.20 ml/10 min (p less than 0.01), urinary sodium from 42.2 +/- 7.6 to 243 +/- 54 mu Eq/10 min (p less than 0.01), urinary potassium from 37.5 +/- 5.5 to 74.8 +/- 10.3 mu Eq/10 min (p less than 0.01), and urinary kinin excretion from 3.44 +/- 0.49 to 5.26 +/- 0.82 ng/10 min (p less than 0.05). The observed natriuretic effect of alpha-hANP lasted only for 30 min, whereas diuretic and kaliuretic effects were sustained for 120 min. Hematocrit levels did not change significantly throughout the experiment. These results indicate that alpha-hANP is a potent vasodilator substance and that the natriuretic effect induced by the bolus injection of alpha-hANP is mediated mainly through its renal vasodilatory action. It is also suggested that the renal kinin, at least in part, contributes to the natriuretic effect of alpha-hANP.

Animals↗

PubMed1987

The effects of atrial natriuretic peptide on renal function and the renin-aldosterone system in anesthetized rabbits.

To determine the effects of alpha-human atrial natriuretic peptide (ANP) on renal function and the renin-aldosterone system in anesthetized rabbits, ANP (0.05 micrograms/kg/min) or 5% dextrose solution in vehicle control was infused intravenously. The infusion of ANP resulted in a significant decrease in mean arterial pressure with an increase in renal blood flow (RBF). ANP also produced significant increases in urine volume and urinary sodium excretion. ANP tended to increase glomerular filtration rate, filtered sodium load and net tubular reabsorption of sodium. However, there were no significant differences in these parameters compared with control group. Fractional sodium excretion was increased significantly by ANP. Plasma renin activity (PRA) was suppressed only at 30 min after the infusion of ANP, while a significant fall in plasma aldosterone concentration (PAC) lasted even in the recovery period. These results indicate that ANP produces a diuresis and natriuresis through the increased RBF in anesthetized rabbits. It is also suggested that ANP suppresses PAC independent of the inhibition of PRA.

Aldosterone↗

PubMed1986

Role of the renal kinin-prostaglandin system in diltiazem-induced natriuresis.

Intravenous infusion of the Ca2+ entry blocker diltiazem (10 micrograms . kg-1 . min-1 for 30 min) induced an increase in urinary excretion of sodium (UNaV) from 209 +/- 42 to 922 +/- 311 mueq without significant alterations in renal hemodynamics in anesthetized rabbits. Urinary excretion of kinin (UkinV) and prostaglandin E (UPGEV) were also increased by diltiazem, from 14.3 +/- 2.5 to 25.9 +/- 4.8 ng and 1.33 +/- 0.20 to 2.44 +/- 0.34 ng, respectively. Moreover, there was a significant correlation between UkinV and UNaV (r = 0.81, P less than 0.05). A significant relationship between UPGEV and UNaV (r = 0.83, P less than 0.05) was also observed. However, no correlation between urinary excretion of kallikrein (UkallV) and UNaV was found after infusion of diltiazem. Further, to examine a possible contribution of renal kinins and prostaglandins in diltiazem-induced natriuresis, aprotinin (50,000 KIU/kg bolus + 1,000 KIU . kg-1 . min-1 infusion) and indomethacin (8 mg/kg) were used. Aprotinin pretreatment attenuated diltiazem-induced natriuresis, accompanied by suppression of UkallV, UkinV, and UPGEV. However, indomethacin pretreatment did not affect this drug-induced natriuresis, although UPGEV was significantly decreased. Furthermore, under the indomethacin pretreatment, a significant increase in UkinV was produced by diltiazem. These results suggest that renal kinins rather than renal prostaglandin E, at least in part, play a role in diltiazem-induced natriuresis.

Animals↗