Stroke, Vol 16, 482-489, Copyright © 1985 by American Heart Association
T Sasaki, NF Kassell, JC Torner, W Maixner and DM Turner
Pharmacological differences between canine and monkey basilar arteries were
studied in vitro. The constrictor response of canine basilar artery to
either norepinephrine or an alpha 1-adrenoceptor agonist phenylephrine was
partly inhibited by an alpha 2-adrenoceptor antagonist yohimbine but not by
an alpha 1-adrenoceptor antagonist prazosin. The contraction elicited by an
alpha 2-adrenoceptor agonist clonidine was inhibited by neither prazosin
nor yohimbine. These results suggest that the receptors in canine basilar
artery which mediate norepinephrine-induced contraction are different from
classical alpha 1 or alpha 2-adrenoceptors, although they more closely
resemble the alpha 2- rather than the alpha 1-subtype. Using monkey basilar
artery, phenylephrine produced the same amplitude of maximum contractile
response as norepinephrine, though a much higher concentration of
phenylephrine than norepinephrine was needed in order to elicit that
maximum response. Clonidine did not elicit contractions. The contraction
induced by norepinephrine was markedly suppressed by both prazosin and
yohimbine in a noncompetitive fashion. The constrictor response of monkey
basilar artery to norepinephrine, therefore, appears to be mediated by
alpha 1-like adrenoceptors. Comparison of ED50 values for thromboxane A2
revealed that the monkey basilar artery was more sensitive to thromboxane
A2 than that of the canine. Prostaglandin F2 alpha produced a larger
maximum contraction in monkey basilar arteries than in canine basilar
arteries, although the ED50 values for monkey basilar arteries were larger
than those for canine basilar arteries. The ED50 values for serotonin in
canine basilar arteries were a little less than those for monkey basilar
arteries, although both arteries produced nearly identical maximum
contractions.
ARTICLES
Pharmacological comparison of isolated monkey and dog cerebral arteries
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