Chang P C, Grossman E, Kopin I J, Goldstein D S
Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland.
J Hypertens. 1994 Jun;12(6):681-90.
To examine the existence of presynaptic beta-adrenoceptors modulating forearm norepinephrine release in 31 healthy volunteers.
The spillover rate of norepinephrine in forearm venous plasma and the total plasma appearance rate of norepinephrine in the forearm were estimated using intra-arterial infusion of [3H]-norepinephrine. Isoprenaline was infused intra-arterially to stimulate beta-adrenoceptors, terbutaline to stimulate beta 2-adrenoceptors, propranolol to block beta-adrenoceptors, metoprolol to block beta 1-adrenoceptors, isoprenaline combined with metoprolol to stimulate beta 2-adrenoceptors, epinephrine to stimulate alpha- and beta-adrenoceptors, yohimbine to block alpha 2-adrenoceptors and sodium nitroprusside to increase forearm blood flow directly.
No systemic hemodynamic effects or changes in arterial plasma norepinephrine level were noted during the intra-arterial infusions. Metoprolol and propranolol decreased norepinephrine spillover and its rate of appearance in the forearm without affecting forearm blood flow. Isoprenaline and sodium nitroprusside increased and epinephrine decreased forearm norepinephrine spillover. Terbutaline increased forearm norepinephrine spillover and its rate of appearance in the forearm. Terbutaline increased the forearm rate of appearance and spillover of norepinephrine more than did sodium nitroprusside or isoprenaline at the same level of forearm blood flow. Infusion of isoprenaline failed to increase norepinephrine spillover or its forearm appearance rate more than would be expected from the increase in forearm blood flow. Administration of epinephrine increased spillover and forearm appearance rate of norepinephrine during intra-arterial infusion of yohimbine.
The terbutaline, propranolol, metoprolol and yohimbine plus epinephrine results suggest that beta-adrenoceptors enhance release of norepinephrine from vascular sympathetic nerve endings in humans.
检测31名健康志愿者中调节前臂去甲肾上腺素释放的突触前β-肾上腺素能受体的存在情况。
通过动脉内输注[3H]-去甲肾上腺素来估算前臂静脉血浆中去甲肾上腺素的溢出率以及前臂中去甲肾上腺素的总血浆出现率。动脉内输注异丙肾上腺素以刺激β-肾上腺素能受体,特布他林刺激β2-肾上腺素能受体,普萘洛尔阻断β-肾上腺素能受体,美托洛尔阻断β1-肾上腺素能受体,异丙肾上腺素联合美托洛尔刺激β2-肾上腺素能受体,肾上腺素刺激α-和β-肾上腺素能受体,育亨宾阻断α2-肾上腺素能受体,硝普钠直接增加前臂血流量。
动脉内输注期间未观察到全身血流动力学效应或动脉血浆去甲肾上腺素水平的变化。美托洛尔和普萘洛尔降低了前臂去甲肾上腺素的溢出及其出现率,而不影响前臂血流量。异丙肾上腺素和硝普钠增加了前臂去甲肾上腺素的溢出,肾上腺素则降低了前臂去甲肾上腺素的溢出。特布他林增加了前臂去甲肾上腺素的溢出及其在前臂中的出现率。在相同的前臂血流量水平下,特布他林比硝普钠或异丙肾上腺素更能增加前臂去甲肾上腺素的出现率和溢出率。输注异丙肾上腺素未能使去甲肾上腺素的溢出或其在前臂中的出现率增加超过前臂血流量增加所预期的程度。在动脉内输注育亨宾期间给予肾上腺素增加了去甲肾上腺素的溢出和前臂出现率。
特布他林、普萘洛尔、美托洛尔以及育亨宾加肾上腺素的结果表明,β-肾上腺素能受体可增强人类血管交感神经末梢去甲肾上腺素的释放。