Contribution of cytochrome P-450 ω-hydroxylase to altered arteriolar reactivity with high-salt diet and hypertension
American Journal of Physiology. Heart and Circulatory Physiology
Contribution of cytochrome P-450 -hydroxylase to altered arteriolar reactivity with high-salt diet and hypertension. Am J Physiol Heart Circ Physiol 278: H1517-H1526, 2000.-The present study evaluated the contribution of cytochrome P-450 -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
... h, sodium nitroprusside (SNP), ANG II, and elevated O 2 were measured via television microscopy under control conditions and following cytochrome P-450 -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 -hydroxylase inhibition. In RRM-HT rats, cytochrome P-450 -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 O 2 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 -hydroxylase contribute to the altered reactivity of skeletal muscle arterioles to vasoconstrictor and vasodilator stimuli in skeletal muscle; acetylcholine; sodium nitroprusside; angiotensin II; oxygen The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.