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N Nushiro

Publications and source records attributed to N Nushiro.

At least 19 recordsLinked to original sources
PubMed1992

The effects of intrarenal infusion of recombinant human erythropoietin on mean arterial pressure and renal hemodynamics in anesthetized rabbits.

The effects of recombinant human erythropoietin (rHuEPO) on mean arterial pressure (MAP) and renal hemodynamics were studied in anesthetized rabbits without renal failure. Intrarenal infusion of rHuEPO at a rate of 100 U/min for 30 min resulted in no change in MAP, renal blood flow, or renal vascular resistance. rHuEPO also produced no significant change in glomerular filtration rate filtration fraction, or arterial hematocrit. These results demonstrate that rHuEPO has no direct effects on MAP or renal hemodynamics in anesthetized rabbits without renal failure.

Anesthesia↗
PubMed1992

[Tissue renin content in superficial, midcortical, and juxtamedullary afferent arterioles in rabbits].

Tissue renin content within the kidney decreases from outer to inner cortex. However, it is not known whether this gradient is due to a decrease in the number of afferent arterioles from the outer to inner cortex or the decrease in renin content per afferent arteriole. Furthermore, it is still controversial whether sodium depletion increases or decreases this gradient. According to Taugner et al., sodium depletion induces the extension of renin positive part of afferent arterioles from vascular pole toward interlobular artery. Since the length of extension may differ among superficial, midcortical, and juxtamedullary afferent arterioles, the observed gradient may vary depending on whether the entire afferent arteriole or only the vascular pole is examined. In the present study, we microdissected the entire afferent arterioles from superficial, middle, and juxtamedullary cortex of rabbit kidney, and examined tissue renin content. We studied: 1. whether tissue renin content per afferent arteriole decreases from the outer to inner cortex. 2. whether sodium depletion affects the gradient of tissue renin content within the cortex. In result, we reached the conclusions, as follows: 1. Tissue renin content per afferent arteriole decreases steeply from superficial to midcortical to juxtamedullary afferent arterioles. 2. The absolute difference in renin content among the three types of afferent arterioles becomes greater during sodium depletion. The internephron heterogeneity of tissue renin content may contribute to functional heterogeneity.

Animals↗
PubMed1992

[Renin release from microdissected superficial, midcortical, and juxtamedullary afferent arterioles in rabbits].

Though renin release from a single superficial afferent arteriole has been studied extensively, there is no report on renin release from a single midcortical or juxtamedullary afferent arteriole. In the present study, we microdissected the entire afferent arterioles from superficial, middle, and juxtamedullary cortex of rabbit kidney, and examined renin release from a single afferent arteriole. In result, we got the following conclusions. 1. Basal renin release per afferent arteriole decreases steeply from superficial to midcortical to juxtamedullary afferent arterioles during both normal and low sodium intake. 2. Isoproterenol (1.6 x 10(-4)M) significantly stimulates renin release from all three types of arterioles on either diet; however, only in the superficial arterioles is the increase (delta) greater with dietary sodium restriction. These findings indicate substantial heterogeneity of basal and isoproterenol-stimulated renin release, and response to chronic sodium depletion.

Animals↗
PubMed1992

[Beta-blockers].

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Adrenergic beta-Antagonists↗
PubMed1991

Endothelium-derived relaxing factor modulates endothelin action in afferent arterioles.

Endothelin is a potent vasoconstrictor, whereas endothelium-derived relaxing factor (EDRF) is a potent vasodilator. Both are produced by the endothelium. Although they have been studied extensively in large vessels, little is known about their actions in renal microvessels. Using microdissected rabbit afferent arterioles, we studied the vascular response to synthetic endothelin and its interaction with EDRF and the effect of endothelin on renin release. Afferent arterioles were either microperfused in vitro at 60 mm Hg to measure luminal diameter or incubated without microperfusion to assess renin release. When added to the bath, 10(-10) or 10(-9) M endothelin decreased the diameter by 32 +/- 8% (n = 7, p less than 0.01) or 76 +/- 7% (p less than 0.0001), respectively. Pretreatment with Nw-nitro L-arginine, which inhibits synthesis of EDRF, decreased basal diameter by 15 +/- 1% (p less than 0.001) and augmented endothelin-induced constriction; decrease in diameter with 10(-10) M endothelin was 78 +/- 10% (n = 4, p less than 0.01 versus nontreated). In afferent arterioles preconstricted by endothelin, acetylcholine at concentrations of 10(-8) to 10(-5) M increased the diameter in a dose-dependent manner. Basal renin release was 0.62 +/- 0.15 ng angiotensin I/hr/afferent arterioles/hr (n = 13) and was not affected by endothelin (10(-10) to 10(-6) M). Increase in renin release by isoproterenol was the same in afferent arterioles pretreated with vehicle or endothelin (10(-7) M; delta, 0.49 +/- 0.21 versus 0.42 +/- 0.19; n = 13).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Renin release from microdissected superficial, midcortical, and juxtamedullary afferent arterioles in rabbits.

Renal renin content and release decrease from outer to inner cortex; this may be due to a cortical-to-medullary gradient in glomerular density and/or renin content per afferent arteriole. Although low sodium diets have been reported to decrease the tissue renin gradient, little information is available on renin release by different areas of the renal cortex or the effect of a low sodium diet. In the present study, we examined basal- and isoproterenol-stimulated renin release and content in microdissected superficial, midcortical, and juxtamedullary afferent arterioles from rabbits on normal and low sodium diets. Renin content was 25.8 +/- 3.6, 1.4 +/- 0.32, and 0.27 +/- 0.09 ng angiotensin I (Ang I)/hour/arteriole in the superficial, midcortical and juxtamedullary arterioles, respectively. Dietary sodium restriction significantly increased it to 60.1 +/- 7.3, 13.8 +/- 3.1, and 1.48 +/- 0.6, respectively. Renin release was 0.64 +/- 0.13, 0.15 +/- 0.04, and 0.025 +/- 0.013 ng Ang I/hour/arteriole/hour incubation of arteriole in the superficial, midcortical and juxtamedullary arterioles, respectively. With sodium restriction it increased significantly for the superficial, (1.77 +/- 0.27) and midcortical (0.62 +/- 0.11) but not the juxtamedullary arterioles (0.038 +/- 0.02). With either diet, renin release and content among the three types of arterioles were significantly different. Isoproterenol (1.6 x 10(-4) M) significantly stimulated renin release from all three types of arterioles whether rabbits were fed a normal or low sodium diet; however, only in the superficial arterioles was the increase (delta) greater with dietary sodium restriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Role of bradykinin in the regulation of blood pressure and renal blood flow in DOCA-salt hypertensive rats.

We examined the role of bradykinin in the onset and/or the maintenance of blood pressure and renal blood flow in deoxycorticosterone acetate (DOCA)-salt hypertensive rats by using a competitive antagonist of bradykinin [Arg-Pro-Hyp-Gly-Thi-Ser-Dphe-Thi-Arg; Hyp, L-4-hydroxyproline; Thi, beta-(2-theinyl-L-alanine)]. The intravenous injection of the bradykinin antagonist (25, 50 and 100 micrograms) produced an increase in mean arterial pressure in all rats treated with tap water, 1% NaCl and DOCA + 1% NaCl. However, the magnitude of the increase in mean arterial pressure was significantly lower in the DOCA-hypertensive rats than in the two groups of rats drinking tap water and 1% NaCl after 4 and 6 weeks, but there was no significant difference after 2 weeks. The bradykinin antagonist induced a decrease in renal blood flow in all rats. However, the extent of the fall in renal blood flow was reduced in the DOCA-hypertensive rats compared with the control rats drinking tap water. These results suggest that endogenous bradykinin is depressed in the established phase of hypertension in DOCA-hypertensive rats. It is also suggested that endogenous bradykinin may counteract the elevation of vascular resistance in the early stages of this model.

Animals↗
PubMed1990

Interaction of endothelin and Ca++ entry blockers on renal circulation in anesthetized rabbits.

We examined an interaction of endothelium-derived vasoconstrictor endothelin and Ca++ entry blockers on renal blood flow in anesthetized rabbits. A bolus intrarenal arterial injection of endothelin at doses of 10, 25 and 50 ng produced a decrease in renal blood flow with a dose-dependent fashion, while there was no change in systemic arterial pressure. A similar extent of the decrease in renal blood flow was produced at doses of endothelin 50 ng(2.0 x 10(-11)M), angiotensin II 10 ng (9.7 x 10(-12)M) and norepinephrine 250 ng (1.5 x 10(-9)M), although the decrease in renal blood flow by endothelin was sustained in contrast to angiotensin II or norepinephrine. Pretreatment with Ca++ entry blocker nifedipine (1.0 microgram/kg/min) or diltiazem (20 micrograms/kg/min) attenuated the decrease in renal blood flow and reduced the duration time. These results suggest that exogenous endothelin produces a renal vasoconstriction in vivo. However, it seems that endothelin is less potent than angiotensin II in renal circulation in anesthetized rabbits. It is also indicated that the decrease in renal blood flow by endothelin could be mediated through a common Ca++ channel pathway in renal vasculatures.

Anesthesia↗
PubMed1989

Role of endogenous bradykinins in the acute depressor effect of angiotensin converting enzyme inhibitor captopril--assessed by a competitive antagonist of bradykinin.

To examine whether a hypotensive effect of converting enzyme inhibitor captopril was mediated partly by a potentiation of endogenous bradykinin, a newly synthesized competitive antagonist of bradykinin (B 4147) was used in anesthetized rats. The injection of B 4147 alone (50 and 100 micrograms) elicited significant increases in blood pressure. Although the administration of captopril (1 mg/kg, i.v.) caused a decrease in mean arterial pressure (MAP), the injection of the kinin antagonist (50 and 100 micrograms) after the captopril produced an increase in MAP by an average of 42 and 47% of the initial fall induced by captopril, respectively. The hypertensive effect of B 4147 was enhanced in magnitude and duration after the captopril. These results suggest that an accumulation of endogenous kinins by captopril contributes partly to the acute hypotensive effect of converting enzyme inhibitors in anesthetized rats.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Interaction of atrial natriuretic peptide and amiloride on renal hemodynamics through renal kallikrein and kinins in anesthetized rabbits.

We investigated the interaction of atrial natriuretic peptide (ANP) and amiloride on renal function and the renal kallikrein-kinin system in anesthetized rabbits. The infusion of ANP alone (50 ng/kg/min) induced a natriuretic action with increments in renal blood flow (RBF) and creatinine clearance (Ccr). The infusion of ANP with amiloride (5 mg/kg + 0.04 mg/kg/min) produced a further increase in natriuresis despite the absence of an increase in RBF and Ccr induced by ANP alone. The urinary excretion of kallikrein and kinins was increased by the administration of ANP. However, the pretreatment with amiloride prevented the increase in the urinary excretion of kallikrein and kinins induced by ANP. These results suggest that the additive effect on sodium excretion might be attributable to changes in the tubular handling of sodium, although ANP did not modify the distal tubular function on sodium reabsorption. It is also suggested that the renal kallikrein-kinin system is not causally involved in the increased sodium excretion by ANP.

Amiloride↗
PubMed1988

Effects of a competitive antagonist of bradykinin on blood pressure and renal blood flow in anesthetized rats.

To examine a possible role of endogenous bradykinin in the regulation of blood pressure (BP) and renal blood flow (RBF), a newly synthesized competitive antagonist of bradykinin (B4147) was studied in anesthetized rats. Also, the question of whether the hypotensive effect of the converting enzyme inhibitor, captopril, is mediated partly by an accumulation of endogenous bradykinin was considered. The intravenous infusion of B4147 (25 micrograms/min) inhibited the depressor effect of exogenous bradykinin (0.5 microgram, i.v.) by 69%. After an intravenous injection of B4147 at doses of 25, 50 and 100 micrograms, BP increased and RBF decreased in a dose-dependent fashion. The increase in BP was not blocked by pretreatment with an angiotensin II antagonist (1-Sar-8-Ile angiotensin II; 20 micrograms/kg per min) or an alpha 1-blocker (prazosin; 0.1 mg/kg). The administration of captopril (1 mg/kg) decreased mean BP from 110 +/- 3.5 to 71 +/- 1.9 mmHg (P less than 0.001). However, the injection of B4147 (50 micrograms) after the administration of captopril elicited an increase in BP of 43% of the initial decrease induced by captopril. These results suggest that the effects of B4147 on BP and RBF are not mediated through angiotensin II or sympathetic alpha 1-stimulation. Endogenous bradykinin could contribute to the maintenance of BP and RBF in anesthetized rats, probably counter-balancing the vasoconstrictor mechanisms. It is also suggested that bradykinin may partly participate in the acute hypotensive effect induced by the converting enzyme inhibitor captopril.

Animals↗
PubMed1988

Contribution of bradykinin to maintenance of blood pressure and renal blood flow in anaesthetized spontaneously hypertensive rats.

We used a newly synthesized competitive antagonist of bradykinin (B 4147) to determine whether bradykinin contributes to the maintenance of blood pressure and renal blood flow in anaesthetized Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). The injection of B 4147 (50 micrograms, intravenously) caused an increase in blood pressure and a decrease in renal blood flow in both strains. However, the magnitude in the change in blood pressure was significantly lower in SHR than in WKY. The reduction of renal blood flow was greater in WKY than in SHR, but there was no significant difference in the basal renal blood flow. These results indicate that bradykinin contributes to the maintenance of blood pressure and renal blood flow in both strains. However, bradykinin antagonist produced a more prominent systemic effect in WKY than in SHR. This suggests that a deficiency in the bradykinin system in SHR contributes to the development or the maintenance of hypertension.

Animals↗
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↗