Sympathetic Control of Myocardial Oxygen Balance in Dogs Mediated by Activation of Coronary Vascular α2-Adrenoceptors

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Abstract
Recent observations on sympathetic constriction of the poststenotic coronary bed without dilatory reserve indicate the involvement of postsynaptic α2-adrenoceptors, which are commonly regarded as noninnervated, hormonal receptors. Therefore, we characterized the vascular α-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 β-blockade (4 mg/kg nadolol. n = 21). In experiments without β-blockade (n = 18). the saturation response was similar. Under β-bloekade. α-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 < 0.01) of the control response and to 0.30 ± 0.06 (p < 0.001). respectively, whereas α1-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 > p > 0.05). Without β-blockade. similar attenuations to 0.36 + 0.07 (p < 0.001) by 0.3 mg/ kg rauwolscine and to 0.80 + 0.09 (NS) by 0.12 mg/kg prazosin were observed. Though presynaptic augmentation of sympathetic transmission by α2-blockade during stimulation at lower frequencies was demonstrated, the response in saturation to these stimulations was attenuated more by α2- than by α1-blockade. demonstrating that sympathetic vasoconstriction in the unrestricted coronary bed is mediated mainly by activation of postsynaptic vascular α2-adrenoeeptors.