Carotid sinus hypotension produces alpha-adrenoceptor-mediated changes in the kidney that increase renin release, with a subsequent step sensitive to beta-blockade.
These animal data should not change practice; they leave open translation of adrenergic renin control to human baroreflex physiology.
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.
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Powis et al. (1979) studied this question.
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