The participation of brain NO synthase in blood pressure control of adult spontaneously hypertensive rats |
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Authors: | Silvie Hojná Michaela Kadlecová Zdenka Dobe?ová Věra Valou?ková Josef Zicha Jaroslav Kune? |
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Institution: | (1) Institute of Physiology AS CR, Charles University, Videnska 1083, 142 20 Prague 4, Czech Republic;(2) Institute of Physiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic;(3) Cardiovascular Research Center, Prague, Czech Republic |
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Abstract: | Increased blood pressure (BP) in genetic hypertension is usually caused by high activity of sympathetic nervous system (SNS)
which is enhanced by central angiotensin II but lowered by central nitric oxide (NO). We have therefore evaluated NO synthase
(NOS) activity as well as neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS) protein expression in brainstem
and midbrain of adult spontaneously hypertensive rats (SHR) characterized by enhanced sympathetic vasoconstriction. We also
studied possible participation of brain NO in antihypertensive effects of chronic captopril treatment of adult SHR. NOS activity
was increased in midbrain of SHR compared to Wistar-Kyoto (WKY) rats. This could be ascribed to enhanced iNOS expression,
whereas nNOS expression was unchanged and eNOS expression was reduced in this brain region. In contrast, no significant changes
of NOS activity were found in brainstem of SHR in which nNOS and iNOS expression was unchanged, but eNOS expression was increased.
Chronic captopril administration lowered BP of adult SHR mainly by attenuation of sympathetic tone, whereas the reduction
of angiotensin II-dependent vasoconstriction and the decrease of residual BP (amelioration of structural remodeling of resistance
vessels) were less important. This treatment did not affect significantly either NOS activity or expression of any NOS isoform
in the two brain regions. Our data do not support the hypothesis that altered brain NO formation contributes to sympathetic
hyperactivity and high BP of adult SHR with established hypertension. |
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Keywords: | angiotensin II-dependent vasoconstriction brainstem endothelial NOS genetic hypertension inducible NOS midbrain neuronal NOS NO-dependent vasodilation sympathetic vasoconstriction |
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