Key result
Endothelium-dependent, phasic relaxations caused by histamine in monkey cerebral arteries are mediated by nitric oxide released by H1-receptor stimulation.
Why the study?
Does histamine cause endothelium-dependent relaxation via nitric oxide in monkey cerebral arteries?
Does histamine cause endothelium-dependent relaxation via nitric oxide in monkey cerebral arteries?
Histamine induces endothelium-dependent phasic relaxation in monkey cerebral arteries mediated by nitric oxide via H1-receptors, and sustained relaxation via H2-receptors in smooth muscle.
Does not guide human therapy; extends mechanistic insight into H1-NO signaling in primate cerebral arteries.
Monkey cerebral artery strips partially contracted with prostaglandin F2α responded to histamine with biphasic patterns of relaxation. The delayed and sustained relaxation was suppressed by cimetidine, whereas the phasic response was abolished by treatment with chlorpheniramine and NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor. The inhibition by L-NA was reversed by L-arginine. D-NA was without effect. Endothelium denudation abolished the phasic relaxation. We hypothesized that endothelium-dependent, phasic relaxations caused by histamine are mediated by NO that is released by H1-receptor stimulation, whereas the sustained relaxation is associated with the activation of H2-receptors in the smooth muscle of monkey cerebral arteries.
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Ayajiki et al. (1992) studied this question. Histamine was evaluated on Arterial relaxation. Endothelium-dependent, phasic relaxations caused by histamine in monkey cerebral arteries are mediated by nitric oxide released by H1-receptor stimulation.
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