Powis D A, Donald D E
Am J Physiol. 1979 Apr;236(4):H580-5. doi: 10.1152/ajpheart.1979.236.4.H580.
In anesthetized vagotomized dogs with renal arterial pressure constant, carotid sinus hypotension (BCO) caused a reflex rise in systemic arterial pressure, a fall in renal blood flow, and a similar increase in renin release from both kidneys. Unilateral alpha-adrenoceptor blockade with phenoxybenzamine resulted in an increase in basal renal blood flow, a depression of basal renin release, and an abolition of the responses to BCO in the treated kidney. The untreated kidney responsed to BCO as before. Nonblocked and alpha-blocked kidneys released similar amounts of renin when renal blood flow was mechanically reduced by aortic constriction. Administration of propranolol to the nonblocked kidney prevented the release of renin but not the hemodynamic changes resulting from BCO. The experiments demonstrated that under certain conditions carotid sinus hypotension produced alpha-adrenoceptor-mediated changes in the kidney sufficient to cause increased renin release. A step in the renin release mechanism subsequent to the alpha-adrenoceptor-mediated changes in sensitive to propranolol.
在肾动脉血压恒定的麻醉去迷走神经犬中,颈动脉窦低血压(BCO)引起全身动脉压反射性升高、肾血流量下降,且双侧肾脏的肾素释放均有类似增加。用酚苄明进行单侧α-肾上腺素能受体阻断导致基础肾血流量增加、基础肾素释放受抑制,且处理侧肾脏对BCO的反应消失。未处理的肾脏对BCO的反应如前。当通过主动脉缩窄机械性减少肾血流量时,未阻断和α-阻断的肾脏释放的肾素量相似。对未阻断的肾脏给予普萘洛尔可阻止肾素释放,但不能阻止BCO引起的血流动力学变化。实验表明,在某些情况下,颈动脉窦低血压会在肾脏产生α-肾上腺素能受体介导的变化,足以导致肾素释放增加。α-肾上腺素能受体介导的变化之后的肾素释放机制中的一个步骤对普萘洛尔敏感。