MODULATION OF ENDOGENOUS NORADRENALINE RELEASE BY PREJUNCTIONAL α‐ADRENORECEPTORS: COMPARISON OF A CEREBRAL AND PERIPHERAL ARTERY

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Abstract
Stimulation‐evoked fractional release/pulse of noradrenaline (NA) is markedly different in the rabbit basilar artery as compared to the rabbit ear artery. Therefore, using both agonists and antagonists of prejunctional α‐adrenoreceptors, the hypothesis that there are differences in prejunctional mechanisms between these functionally different arteries was tested. Clonidine (10−6M) had similar effects on NA release in both vessels, decreasing release at 2 Hz, but increasing release at 8 Hz. However, 10−5M clonidine had different effects in the two vessels. α‐Adrenoreceptor antagonists, phentolamine (10−6M), yohimbine (10−5M), and phenoxybenzamine (10−5M), all increased NA release to a similar extent in both vessels. However, the effect of phenoxybenzamine was considerably greater than that of the other two antagonists, suggesting that it may have additional sites of action. When the effects of modest drug concentrations were considered, no major qualitative or quantitative differences in the effects of agonists and antagonists on NA release from the two vessels were seen. Thus, the difference in fractional NA release between the basilar and ear arteries cannot be accounted for by differences in prejunctional α‐adrenoreceptor modulation.

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