Responses to histamine were investigated in the systemic and hindlimb vascular bed of the rabbit under conditions of constant flow. Injections of histamine iv caused dose-related decreases in systemic arterial pressure, while injections of histamine into the hindlimb perfusion circuit caused dose-related increases in perfusion pressure. Both the systemic vasodepressor response and hindlimb constrictor response were reduced in the presence of the H1 antagonist pyrilamine but were unaffected after the administration of the H2 antagonist cimetidine. These data suggest that the H1 receptor mediates a vasoconstrictor response in the rabbit, and that the H2 receptor plays little if any role in mediating responses to histamine. Responses to histamine in the hindlimb vascular bed were unaltered by the cyclooxygenase inhibitor sodium meclofenamate, the α adrenergic blocker phentolamine, the angiotensin AT1 receptor antagonist candesartan, or the K+ATP channel blocker U-37883A, suggesting that constrictor responses to histamine are not mediated by constrictor products generated from the cyclooxygenase pathway, by alpha 1 receptors, by angiotensin AT1 receptors, or by actions on K+ATP channels, respectively. In summary, these results suggest that histamine produces both a vasodepressor and a vasoconstrictor response in the rabbit, and that these responses are mediated primarily through activation of the H1 receptor.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology