Evidence for lack of innervation of beta-2 adrenoceptors in the blood vessels of the gracilis muscle of the dog.

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Abstract
Cardiac .beta.-1 adrenoceptors respond to sympathetic nerve stimulation (SNS), but it is not clear that SNS evokes .beta.-2 adrenoceptor-mediated vasodilation. Sensitivity of .beta. adrenoceptors to catecholamines and to SNS was evaluated in dogs. Norepinephrine (NE) and epinephrine (E) were equipotent vasoconstrictors (femoral artery blood flow or gracilis autoperfusion pressure) before .alpha.-adrenoceptor blockade with dibozane (DIB). After DIB, NE was 1/100 as potent a vasodilator as E, which was equipotent with isoproterenol (ISO). SNS evoked gracilis muscle vasoconstriction before DIB and vasodilation after. Dilation induced by SNS or acetylcholine (ACH) after DIB was blocked by atropine (AT), but that caused by NE was not. Dilation evoked by NE, E or ISO after DIB and AT was blocked by propranolol (PROP). Vasoconstrictor responses to NE, E or SNS in dogs without DIB were not augmented by PROP at a dose that blocked the dilator effect of ISO. NE and E were equipotent and both 1/10 as potent as ISO as positive inotropic and chronotropic agents. Cardiac responses to NE, E, ISO and SNS were antagonized by PROP. Subclassification of adrenoceptors that subserve cardiac stimulation as .beta.-1 and that subserve vasodilation as .beta.-2 was substantiated. Cardiac .beta.-1 adrenoceptors responded to SNS and to circulating E and NE. Vascular .beta.-2 adrenoceptors responded to circulating E, to ISO and to high doses of NE but not to SNS. .beta.-2 Adrenoceptors in blood vessels appear not to be innervated and may function as hormone receptors sensitive primarily to E released from the adrenal medulla, rather than to NE released from adrenergic nerves.