Impaired nitric oxide-independent dilation of renal afferent arterioles in spontaneously hypertensive rats

Koichi Hayashi, Hiroto Matsuda, Takahiko Nagahama, Keiji Fujiwara, Yuri Ozawa, Eiji Kubota, Masanori Honda, Hirobumi Tokuyama, Takao Saruta

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Sustained hypertension alters vasomotor regulation in various vascular beds. We studied whether nitric oxide (NO) dependent and NO-independent vasodilator mechanisms are altered in renal microvessels in hypertension. To directly visualize the renal microcirculation, the isolated perfused hydronephrotic rat kidney model was used. After pretreatment with indomethacin (100 μmol/l), afferent arterioles were constricted by norepinephrine (NE) or by increasing renal arterial pressure (i.e., myogenic constriction; from 80 to 180 mmHg). Acetylcholine (ACH) was then added, and the renal microvascular response was assessed by computer-assisted video image analysis. A similar protocol was conducted in the presence of nitro-L-arginine methylester (L-NAME; 100 μmol/l). During NE constriction, ACH caused dose-dependent and sustained vasodilation of the afferent arteriole, similar in magnitude in Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). In the presence of L-NAME, ACH (0.01-1 μmol/l) elicited only transient dilation, and the degree of vasodilation was very low in SHR. During myogenic constriction, afferent arterioles from WKY and SHR kidneys responded to ACH with only transient vasodilation, which was unaffected by NO inhibition; the transient vasodilative responses elicited by ACH (0.1-1 μmol/l) were smaller in SHR than in WKY. In conclusion, ACH has both sustained and transient vasodilative effects on the afferent arteriole. Sustained vasodilation is attributed to NO generation, which is similar in WKY and SHR. In contrast, transient vasodilation, mediated by NO-independent vasodilator factors, is impaired in SHR. Deranged vasodilatory mechanisms in hypertension may disturb the renal microcirculation, which may result in renal injury.

Original languageEnglish
Pages (from-to)31-37
Number of pages7
JournalHypertension Research - Clinical and Experimental
Volume22
Issue number1
Publication statusPublished - 1999 Mar

Fingerprint

Arterioles
Inbred SHR Rats
Dilatation
Nitric Oxide
Acetylcholine
Kidney
Vasodilation
Inbred WKY Rats
Constriction
NG-Nitroarginine Methyl Ester
Microcirculation
Hypertension
Vasodilator Agents
Norepinephrine
Computer-Assisted Image Processing
Microvessels
Indomethacin
Blood Vessels
Arginine
Arterial Pressure

Keywords

  • Acetylcholine
  • Afferent arteriole
  • EDHF
  • Hypertension
  • Nitric oxide

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Hayashi, K., Matsuda, H., Nagahama, T., Fujiwara, K., Ozawa, Y., Kubota, E., ... Saruta, T. (1999). Impaired nitric oxide-independent dilation of renal afferent arterioles in spontaneously hypertensive rats. Hypertension Research - Clinical and Experimental, 22(1), 31-37.

Impaired nitric oxide-independent dilation of renal afferent arterioles in spontaneously hypertensive rats. / Hayashi, Koichi; Matsuda, Hiroto; Nagahama, Takahiko; Fujiwara, Keiji; Ozawa, Yuri; Kubota, Eiji; Honda, Masanori; Tokuyama, Hirobumi; Saruta, Takao.

In: Hypertension Research - Clinical and Experimental, Vol. 22, No. 1, 03.1999, p. 31-37.

Research output: Contribution to journalArticle

Hayashi, K, Matsuda, H, Nagahama, T, Fujiwara, K, Ozawa, Y, Kubota, E, Honda, M, Tokuyama, H & Saruta, T 1999, 'Impaired nitric oxide-independent dilation of renal afferent arterioles in spontaneously hypertensive rats', Hypertension Research - Clinical and Experimental, vol. 22, no. 1, pp. 31-37.
Hayashi, Koichi ; Matsuda, Hiroto ; Nagahama, Takahiko ; Fujiwara, Keiji ; Ozawa, Yuri ; Kubota, Eiji ; Honda, Masanori ; Tokuyama, Hirobumi ; Saruta, Takao. / Impaired nitric oxide-independent dilation of renal afferent arterioles in spontaneously hypertensive rats. In: Hypertension Research - Clinical and Experimental. 1999 ; Vol. 22, No. 1. pp. 31-37.
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