Key result
Histamine is taken up by and released from perivascular adrenergic nerves by periarterial nerve stimulation, causing endothelium-dependent vasodilation in rat mesenteric arteries.
p-value: p=<0.05
Histamine is taken up by perivascular adrenergic nerves and released upon stimulation to induce endothelium-dependent vasodilation in rat mesenteric arteries.
Does not alter clinical vasomotor management; leaves open histamine's role in human perivascular control.
The present study investigated whether histamine was taken up by perivascular adrenergic nerves and released by periarterial nerve stimulation (PNS) to induce vascular responses. In rat mesenteric vascular beds treated with capsaicin to eliminate calcitonin gene-related peptide (CGRP)ergic vasodilation and with active tone, PNS (1 - 4 Hz) induced only adrenergic nerve-mediated vasoconstriction. Histamine treatment for 20 min induced PNS-induced vasoconstriction followed by vasodilation without affecting CGRP-induced vasodilation. Chlorpheniramine, guanethidine, combination of histamine and desipramine, and endothelium-removal abolished PNS-induced vasodilation in histamine-treated preparations. These results suggest that histamine taken up by and released from adrenergic nerves by PNS causes endothelium-dependent vasodilation in rat mesenteric arteries.
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Haruki et al. (2012) studied this question. Histamine treatment and periarterial nerve stimulation (PNS) vs. Control responses without histamine treatment was evaluated on Vasodilation response to PNS (p=<0.05). Histamine is taken up by and released from perivascular adrenergic nerves by periarterial nerve stimulation, causing endothelium-dependent vasodilation in rat mesenteric arteries.
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