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-hydroxylase to
altered arteriolar reactivity with high-salt diet and
hypertension
1 Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226; and 2 Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas 75235
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 nitroprusside (SNP),
ANG II, and elevated O2 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 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 -hydroxylase contribute to the altered reactivity of
skeletal muscle arterioles to vasoconstrictor and vasodilator stimuli
in RRM-HT.
microcirculation; skeletal muscle; 20-hydroxyeicosatetraenoic acid; 17-octadecynoic acid; N-methylsulfonyl-12,12-dibromododec-11-enamide; acetylcholine; sodium nitroprusside; angiotensin II; oxygen
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