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

Cardiac /S-l adrenoceptors respond to sympathetic nerve stimulation (SNS), but it is not clear that SNS evokes fi-2 adrenoceptor-mediated vasodilation. Sensitivity of B 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 aadrenoceptor 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 I 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 fi-1 and that subserve vasodilation as fi-2 was substantiated. Cardiac fi-1 adrenoceptors responded to SNS and to circulating E and NE. Vascular fi-2 adrenoceptors responded to circulating E, to ISO, and to high doses of NE, but not to SNS. fi-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. Circ Res 46: 344-352, 1980