The physiology and pharmacology of the renal nerves

The kidney possesses an extensive sympathetic innervation of both vascular and tubular elements and their functional role is only now becoming apparent. There is a graded recruitment of effects when the nerves are stimulated, with neurogenically mediated renin release being initially observed, at higher levels of activation there is a concomitant increase in tubular sodium reabsorption, while at very high frequencies there are marked reductions in renal blood flow and glomerular filtration rate. There is evidence that under normal physiological circumstances the renal nerves have a relatively low activity and it is likely that their primary action is to modulate renin release and sodium and water retention. Reflex neural regulation of kidney function can be exerted by a number of systems; the cardiovascular system, via the carotid sinus baroreceptor reflex, and the receptors of the heart and lungs; the somatosensory system, by receptors in the skin, muscle and joints; via the visceral system, by means of receptors in the gut; as well as mechano- and chemo-receptors within the kidneys themselves. These actions of the renal nerves are mediated by a range of adrenoceptors at the different neuro-effector junctions. There is a good consensus that at the granular renin-containing cells of the juxtaglomerular apparatus, beta 1-adrenoceptors mediate the release of renin. By contrast, at the vasculature alpha 1-adrenoceptors are involved in causing vasoconstriction although there is evidence that post-synaptic alpha 2-adrenoceptors may also contribute. Finally, at the tubular epithelial cells themselves, alpha 1-adrenoceptors are activated to stimulate sodium reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)