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Gender differences in mesenteric vasoconstrictor reactivity following chronic hypoxia.

Rayna J Gonzales1, Jessica M Bryant, Jay S Naik

  • 1Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico, USA. rjgonzal@arizona.edu

Microcirculation (New York, N.Y. : 1994)
|December 17, 2008
PubMed
Summary

Chronic hypoxia (CH) similarly reduces vasoconstrictor responses in male and female rats. However, CH impairs nitric oxide-dependent mesenteric vasodilation only in females, despite unchanged endothelial NOS levels.

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Area of Science:

  • Cardiovascular Physiology
  • Endocrinology
  • Respiratory Physiology

Background:

  • Chronic hypoxia (CH) induces persistent endothelium-dependent attenuation of vasoconstrictor reactivity in male rats.
  • Estrogen's role in hypoxia-induced gene expression suggests potential gender differences in CH responses.
  • Previous studies indicate reduced mesenteric vascular responses to phenylephrine (PE) in CH males.

Purpose of the Study:

  • To investigate gender differences in pressor and mesenteric vascular responses to CH.
  • To determine if nitric oxide (NO) pathway alterations explain maintained mesenteric reactivity in CH females.
  • To test the hypothesis that CH inhibits NO-dependent vasodilation in female mesenteric arteries.

Main Methods:

  • Conscious, instrumented rats (male and female) were exposed to chronic hypoxia (CH).
  • Pressor and total peripheral resistance responses to phenylephrine (PE) were measured.
  • Mesenteric artery constrictor reactivity was examined in normoxic and CH rats of both genders, with and without nitric oxide synthase (NOS) inhibition.
  • Endothelial NOS (eNOS) levels and endothelial intracellular calcium ([Ca2+]i) were assessed.

Main Results:

  • CH caused a similar persistent reduction in pressor/total peripheral resistance responses to PE in both male and female rats.
  • Mesenteric vascular reactivity to PE was maintained in CH females, unlike CH males.
  • NOS inhibition augmented PE responses in normoxic males and females, and CH males, but not in CH females.
  • eNOS levels were unchanged, but endothelial [Ca2+]i was elevated in CH female arterioles.

Conclusions:

  • CH reduces NO-dependent mesenteric vasodilation in female rats.
  • This effect in females is not attributable to altered eNOS levels or diminished endothelial [Ca2+]i.
  • Gender-specific mechanisms may underlie vascular adaptations to chronic hypoxia.