Gender-specific compensation for the lack of NO in the mediation of flow-induced arteriolar dilation

Yuming Wu, An Huang, Dong Sun, J R Falck, Akos Koller, Gabor Kaley

Research output: Contribution to journalArticle

66 Citations (Scopus)

Abstract

Flow-induced dilation of gracilis muscle arterioles was examined in both genders of control rats and rats chronically treated with Nω-nitro-L-arginine methyl ester (L-NAME). After L-NAME treatment (4 wk), systolic blood pressure was significantly increased compared with control, whereas the plasma concentration of nitrate/nitrite was significantly reduced. Isolated and pressurized arterioles dilated significantly in response to increases in flow (0-25 μl/min). Flow-induced dilation was comparable in arterioles of control and L-NAME-treated rats but was significantly greater in female than in male rats. L-NAME + indomethacin, which abolished flow-induced dilation in arterioles of male control rats, inhibited the dilation by only ∼75% in female control rats. The residual portion of the response was eliminated by additional administration of miconazole, an inhibitor of cytochrome P-450. Indomethacin did not affect the dilation in female L-NAME-treated rats but completely inhibited the response in male L-NAME-treated rats. The indomethacin-insensitive, flow-induced dilation in female L-NAME-treated arterioles was abolished by miconazole, 6-(2-proparglyoxyphenyl)hexanoic acid, or charybdotoxin. Thus an augmented release of endothelial prostaglandins accounts for the preserved flow-induced dilation in arterioles of male rats, whereas a metabolite of cytochrome P-450 is responsible for the maintenance of flow-induced dilation in female rats, suggesting important differences in the adaptation of the endothelium of arterioles from male and female rats to the lack of nitric oxide (NO) synthesis.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume280
Issue number6 49-6
StatePublished - 2001

Fingerprint

Dilatation
Nitric Oxide
NG-Nitroarginine Methyl Ester
Arterioles
Indomethacin
Miconazole
Charybdotoxin
Blood Pressure
Nitrites
Nitrates
Cytochrome P-450 Enzyme System
Prostaglandins
Endothelium
Maintenance

Keywords

  • Cytochrome P-450 metabolites
  • Hyperpolarizing factor
  • NO synthesis
  • Potassium channels

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Gender-specific compensation for the lack of NO in the mediation of flow-induced arteriolar dilation. / Wu, Yuming; Huang, An; Sun, Dong; Falck, J R; Koller, Akos; Kaley, Gabor.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 280, No. 6 49-6, 2001.

Research output: Contribution to journalArticle

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