Contribution of cytochrome P-450 ω-hydroxylase to altered arteriolar reactivity with high-salt diet and hypertension

Jefferson C. Frisbee, J R Falck, Julian H. Lombard

Research output: Contribution to journalArticle

53 Scopus citations

Abstract

The present study evaluated the contribution of cytochrome P-450 ω- hydroxylase in modulating the reactivity of cremaster muscle arterioles in normotensive rats on high-salt (HS) and low-salt (LS) diet and in rats with reduced renal mass hypertension (RRM-HT). Changes in arteriolar diameter in response to ACh, sodium nitroprusside (SNP), ANG II, and elevated O2 were measured via television microscopy under control conditions and following cytochrome P-450 ω-hydroxylase inhibition with 17-octadecynoic acid (17- ODYA) or N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS). In normotensive rats on either LS or HS diet, resting tone was unaffected and arteriolar reactivity to ACh or SNP was minimally affected by cytochrome P- 450 ω-hydroxylase inhibition. In RRM-HT rats, cytochrome P-450 ω- hydroxylase inhibition reduced resting tone and significantly enhanced arteriolar dilation to ACh and SNP. Treatment with 17-ODYA or DDMS inhibited arteriolar constriction to ANG II and O2 in all the groups, although the degree of inhibition was greater in RRM-HT than in normotensive animals. These results suggest that metabolites of cytochrome P-450 ω-hydroxylase contribute to the altered reactivity of skeletal muscle arterioles to vasoconstrictor and vasodilator stimuli in RRM-HT.

Original languageEnglish (US)
Pages (from-to)H1517-H1526
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume278
Issue number5 47-5
DOIs
StatePublished - May 2000

Keywords

  • 17- octadecynoic acid
  • 20-hydroxyeicosatetraenoic acid
  • Acetylcholine
  • Angiotensin II
  • Microcirculation
  • N-methylsulfonyl-12,12-dibromododec-11- enamide
  • Oxygen
  • Skeletal muscle
  • Sodium nitroprusside

ASJC Scopus subject areas

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

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