Abstract
Autonomic control of the kidney is predominantly sympathetic, and sympathetic neurons densely innervate the kidneys and have varicosities on both vascular and tubular elements. The basal discharge rate of renal sympathetic nerves is 0.5–2Hz, and this causes the continuous release of norepinephrine. Efferent renal sympathetic nerve activity stimulates renin release (threshold, 0.5Hz; β1-adrenoceptor-mediated), increases tubular transport (threshold, 1Hz; α1-adrenoceptor-mediated), and constricts the renal vasculature (threshold, 2.5Hz; α1-adrenoceptor-mediated). Autonomic control of the kidney contributes to blood volume restoration following a positive or negative perturbation in volume status and helps balance the work load between the two kidneys. Renal efferent sympathetic nerve activity impairs sodium excretion and shifts the renal pressure–natriuresis curve to the right such that higher long-term levels of blood pressure are required to maintain sodium excretion in balance with sodium intake. Therefore, efferent renal sympathetic nerve activity contributes to the pathophysiology of hypertension.
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