Renal afferent and efferent arteriolar dilation by nilvadipine

Studies in the isolated perfused hydronephrotic kidney

Yuri Ozawa, Koichi Hayashi, Takahiko Nagahama, Keiji Fujiwara, Shu Wakino, Takao Saruta

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Although calcium antagonists are believed to exert preferential vasodilator action on the renal preglomerular afferent arteriole, we recently demonstrated that efonidipine, a novel calcium antagonist, vasodilates both afferent and efferent arterioles. Nilvadipine also is reported to increase renal blood flow and reduce filtration fraction, suggesting indirectly afferent and efferent arteriolar vasodilation. No direct investigation, however, has been conducted examining the renal microvascular action of nilvadipine. We therefore characterized the renal microvascular reactivity to nilvadipine, by using the isolated perfused rat hydronephrotic kidney. The administration of angiotensin II (0.3 nM) caused marked vasoconstriction of afferent (from 13.5 ± 0.6 to 9.2 ± 0.6 μm, p < 0.01, n = 6) and efferent arterioles (from 11.5 ± 1.0 to 7.4 ± 0.7 μm, p < 0.01; n = 5). The subsequent addition of nilvadipine (10 nM, 100 nM, and 1 μM) caused 37 ± 5%, 91 ± 4%, and 95 ± 8% reversal of afferent arteriolar constriction, respectively. Similarly, efferent arterioles manifested 59 ± 12% reversal by 1 μM nilvadipine. Thus unlike nifedipine, which we previously reported to cause modest efferent arteriolar dilation (21 ± 1% reversal at 1 μM), nilvadipine possesses the greater ability to dilate efferent arterioles (p < 0.01 vs. nifedipine), although both antagonists cause similar magnitudes of afferent arteriolar vasodilation. Variable effects on the efferent arteriole suggest the heterogeneity in the calcium antagonist with regard to the renal microvascular action of this agent.

Original languageEnglish
Pages (from-to)243-247
Number of pages5
JournalJournal of Cardiovascular Pharmacology
Volume33
Issue number2
DOIs
Publication statusPublished - 1999 Feb

Fingerprint

nilvadipine
Arterioles
Dilatation
Kidney
Nifedipine
Calcium
Vasodilation
Renal Circulation
Vasoconstriction
Vasodilator Agents
Constriction
Angiotensin II

Keywords

  • Afferent arteriole
  • Calcium antagonists
  • Efferent arteriole
  • Nilvadipine
  • Renal microcirculation

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

Renal afferent and efferent arteriolar dilation by nilvadipine : Studies in the isolated perfused hydronephrotic kidney. / Ozawa, Yuri; Hayashi, Koichi; Nagahama, Takahiko; Fujiwara, Keiji; Wakino, Shu; Saruta, Takao.

In: Journal of Cardiovascular Pharmacology, Vol. 33, No. 2, 02.1999, p. 243-247.

Research output: Contribution to journalArticle

Ozawa, Yuri ; Hayashi, Koichi ; Nagahama, Takahiko ; Fujiwara, Keiji ; Wakino, Shu ; Saruta, Takao. / Renal afferent and efferent arteriolar dilation by nilvadipine : Studies in the isolated perfused hydronephrotic kidney. In: Journal of Cardiovascular Pharmacology. 1999 ; Vol. 33, No. 2. pp. 243-247.
@article{4b4880e1772e4b5089584342142f3098,
title = "Renal afferent and efferent arteriolar dilation by nilvadipine: Studies in the isolated perfused hydronephrotic kidney",
abstract = "Although calcium antagonists are believed to exert preferential vasodilator action on the renal preglomerular afferent arteriole, we recently demonstrated that efonidipine, a novel calcium antagonist, vasodilates both afferent and efferent arterioles. Nilvadipine also is reported to increase renal blood flow and reduce filtration fraction, suggesting indirectly afferent and efferent arteriolar vasodilation. No direct investigation, however, has been conducted examining the renal microvascular action of nilvadipine. We therefore characterized the renal microvascular reactivity to nilvadipine, by using the isolated perfused rat hydronephrotic kidney. The administration of angiotensin II (0.3 nM) caused marked vasoconstriction of afferent (from 13.5 ± 0.6 to 9.2 ± 0.6 μm, p < 0.01, n = 6) and efferent arterioles (from 11.5 ± 1.0 to 7.4 ± 0.7 μm, p < 0.01; n = 5). The subsequent addition of nilvadipine (10 nM, 100 nM, and 1 μM) caused 37 ± 5{\%}, 91 ± 4{\%}, and 95 ± 8{\%} reversal of afferent arteriolar constriction, respectively. Similarly, efferent arterioles manifested 59 ± 12{\%} reversal by 1 μM nilvadipine. Thus unlike nifedipine, which we previously reported to cause modest efferent arteriolar dilation (21 ± 1{\%} reversal at 1 μM), nilvadipine possesses the greater ability to dilate efferent arterioles (p < 0.01 vs. nifedipine), although both antagonists cause similar magnitudes of afferent arteriolar vasodilation. Variable effects on the efferent arteriole suggest the heterogeneity in the calcium antagonist with regard to the renal microvascular action of this agent.",
keywords = "Afferent arteriole, Calcium antagonists, Efferent arteriole, Nilvadipine, Renal microcirculation",
author = "Yuri Ozawa and Koichi Hayashi and Takahiko Nagahama and Keiji Fujiwara and Shu Wakino and Takao Saruta",
year = "1999",
month = "2",
doi = "10.1097/00005344-199902000-00010",
language = "English",
volume = "33",
pages = "243--247",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Renal afferent and efferent arteriolar dilation by nilvadipine

T2 - Studies in the isolated perfused hydronephrotic kidney

AU - Ozawa, Yuri

AU - Hayashi, Koichi

AU - Nagahama, Takahiko

AU - Fujiwara, Keiji

AU - Wakino, Shu

AU - Saruta, Takao

PY - 1999/2

Y1 - 1999/2

N2 - Although calcium antagonists are believed to exert preferential vasodilator action on the renal preglomerular afferent arteriole, we recently demonstrated that efonidipine, a novel calcium antagonist, vasodilates both afferent and efferent arterioles. Nilvadipine also is reported to increase renal blood flow and reduce filtration fraction, suggesting indirectly afferent and efferent arteriolar vasodilation. No direct investigation, however, has been conducted examining the renal microvascular action of nilvadipine. We therefore characterized the renal microvascular reactivity to nilvadipine, by using the isolated perfused rat hydronephrotic kidney. The administration of angiotensin II (0.3 nM) caused marked vasoconstriction of afferent (from 13.5 ± 0.6 to 9.2 ± 0.6 μm, p < 0.01, n = 6) and efferent arterioles (from 11.5 ± 1.0 to 7.4 ± 0.7 μm, p < 0.01; n = 5). The subsequent addition of nilvadipine (10 nM, 100 nM, and 1 μM) caused 37 ± 5%, 91 ± 4%, and 95 ± 8% reversal of afferent arteriolar constriction, respectively. Similarly, efferent arterioles manifested 59 ± 12% reversal by 1 μM nilvadipine. Thus unlike nifedipine, which we previously reported to cause modest efferent arteriolar dilation (21 ± 1% reversal at 1 μM), nilvadipine possesses the greater ability to dilate efferent arterioles (p < 0.01 vs. nifedipine), although both antagonists cause similar magnitudes of afferent arteriolar vasodilation. Variable effects on the efferent arteriole suggest the heterogeneity in the calcium antagonist with regard to the renal microvascular action of this agent.

AB - Although calcium antagonists are believed to exert preferential vasodilator action on the renal preglomerular afferent arteriole, we recently demonstrated that efonidipine, a novel calcium antagonist, vasodilates both afferent and efferent arterioles. Nilvadipine also is reported to increase renal blood flow and reduce filtration fraction, suggesting indirectly afferent and efferent arteriolar vasodilation. No direct investigation, however, has been conducted examining the renal microvascular action of nilvadipine. We therefore characterized the renal microvascular reactivity to nilvadipine, by using the isolated perfused rat hydronephrotic kidney. The administration of angiotensin II (0.3 nM) caused marked vasoconstriction of afferent (from 13.5 ± 0.6 to 9.2 ± 0.6 μm, p < 0.01, n = 6) and efferent arterioles (from 11.5 ± 1.0 to 7.4 ± 0.7 μm, p < 0.01; n = 5). The subsequent addition of nilvadipine (10 nM, 100 nM, and 1 μM) caused 37 ± 5%, 91 ± 4%, and 95 ± 8% reversal of afferent arteriolar constriction, respectively. Similarly, efferent arterioles manifested 59 ± 12% reversal by 1 μM nilvadipine. Thus unlike nifedipine, which we previously reported to cause modest efferent arteriolar dilation (21 ± 1% reversal at 1 μM), nilvadipine possesses the greater ability to dilate efferent arterioles (p < 0.01 vs. nifedipine), although both antagonists cause similar magnitudes of afferent arteriolar vasodilation. Variable effects on the efferent arteriole suggest the heterogeneity in the calcium antagonist with regard to the renal microvascular action of this agent.

KW - Afferent arteriole

KW - Calcium antagonists

KW - Efferent arteriole

KW - Nilvadipine

KW - Renal microcirculation

UR - http://www.scopus.com/inward/record.url?scp=0032935843&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032935843&partnerID=8YFLogxK

U2 - 10.1097/00005344-199902000-00010

DO - 10.1097/00005344-199902000-00010

M3 - Article

VL - 33

SP - 243

EP - 247

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 2

ER -