Increasing evidence suggests that the renal nerves may contribute to the pathogenesis of several types of experimental hypertension. It has been demonstrated that renal denervation can either attenuate the severity or delay the development of hypertension in spontaneously hypertensive rats (SHR), in DOCA-salt treated rats and in renovascular hypertensive rats. On the other hand, intrarenal administration of catecholamines has been shown to elicit an increase in systemic arterial pressure as long as the infusion is continued. The underlying mechanisms by which renal nerves might participate in the regulation of cardiovascular homeostasis have not been entirely clarified. It is known that efferent renal nerve activity, by exerting a direct influence on renal arteriolar tone, renin release and sodium and water excretion, can interfere with the control of arterial pressure by modifying peripheral resistances, circulating angiotensin II and volume balance. In addition, a role of afferent renal nerve activity in cardiovascular control and, possibly, in the pathogenesis of renovascular hypertension, has recently been proposed after the demonstration of mechano- and chemoreceptors inside the kidney. Indeed, blood pressure is reflexly influenced either by several manoeuvres applied to the kidney or by the electrical stimulation of afferent renal nerve fibres. Afferent and efferent renal nerve activity appear to be closely related since recent experiments by our group have provided further evidence of the existence of neural renorenal reflexes by which one kidney exerts a tonic inhibitory effect on the release of renin from juxtaglomerular cells and on tubular sodium and water reabsorption of the contralateral kidney.
|Journal||Journal of Hypertension, Supplement|
|Publication status||Published - Dec 1985|
ASJC Scopus subject areas
- Internal Medicine