Gender differences in mesenteric vasoconstrictor reactivity following chronic hypoxia

Rayna J. Gonzales, Jessica Bryant, Jay Naik, Thomas Resta, Benjimen Walker

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Male rats demonstrate persistent endothelium-dependent attenuation of vasoconstrictor reactivity following chronic hypoxia (CH). Since estrogen may interfere with hypoxia-induced gene expression, we hypothesized that gender differences exist in this response to CH. However, in conscious, instrumented rats, we found that CH resulted in a similar persistent reduction of pressor/total peripheral resistance responses to phenylephrine (PE) in rats of both genders. In contrast, although previous studies show mesenteric vascular responses to PE are reduced in CH males, we found that mesenteric reactivity was maintained in CH females. Since normoxic females demonstrate greater nitric oxide (NO) production, we hypothesized that the failure of CH to further diminish mesenteric reactivity in females was due to the inhibition of NO-dependent vasodilation. To test this hypothesis, constrictor reactivity of mesenteric arteries from male and female rats was examined. NO synthase (NOS) inhibition augmented constrictor responses to PE in arteries from both normoxic and CH males and normoxic females. In contrast, NOS inhibition had no effect in CH female vessels. Endothelial NOS (eNOS) levels were not different in arteries from control and CH females. Endothelial [Ca2+]i was greater in arterioles from CH females. Thus, CH reduces NO-dependent mesenteric dilation in females; this effect is not due to altered eNOS levels or diminished endothelial [Ca2+]i.

Original languageEnglish (US)
Pages (from-to)473-484
Number of pages12
JournalMicrocirculation
Volume15
Issue number6
DOIs
StatePublished - Aug 2008
Externally publishedYes

Keywords

  • Gender
  • Nitric oxide
  • Rat
  • Resistance arteries

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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