Sympathetic control of myocardial oxygen balance in dogs mediated by activation of coronary vascular alpha 2-adrenoceptors.

Recent observations on sympathetic constriction of the poststenotic coronary bed without dilatory reserve indicate the involvement of postsynaptic alpha 2-adrenoceptors, which are commonly regarded as noninnervated, hormonal receptors. Therefore, we characterized the vascular alpha-adrenoceptor activated during the competition between sympathetic constriction and metabolic dilation of the nonstenosed coronary bed by analyzing myocardial oxygen balance. In 39 anesthetized, spinalized open-chest dogs with bilateral cervical vagotomy, the left decentralized stellate ganglion was stimulated while mean aortic pressure was kept constant. Stimulation at 1 and 10 Hz lowered coronary venous oxygen saturation by 2.5 +/- 0.3 (SEM) and by 11.1 +/- 0.8 saturation %, respectively, in experiments under beta-blockade (4 mg/kg nadolol, n = 21). In experiments without beta-blockade (n = 18), the saturation response was similar. Under beta-blockade, alpha 2-blockade by rauwolscine (0.03 and 0.3 mg/kg) attenuated the decline in saturation induced by 10 Hz stimulation to 0.56 +/- 0.08 (p less than 0.01) of the control response and to 0.30 +/- 0.06 (p less than 0.001), respectively, whereas alpha 1-blockade by prazosin (0.012 and 0.12 mg/kg) modified this response only to 0.94 +/- 0.06 (NS) and to 0.75 +/- 0.08 (0.1 greater than p greater than 0.05). Without beta-blockade, similar attenuations to 0.36 +/- 0.07 (p less than 0.001) by 0.3 mg/kg rauwolscine and to 0.80 +/- 0.09 (NS) by 0.12 mg/kg prazosin were observed.(ABSTRACT TRUNCATED AT 250 WORDS)