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Biomedical subjects

N Nushiro

Publications and source records attributed to N Nushiro.

12 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↗
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↗