Renal nerves in the pathogenesis of hypertension: a review

1. Renal nerve discharge may contribute to renal arteriolar hyperplasia and hypertrophy but the kidney is not the major site of increased vascular resistance in hypertension. 2. Natriuretic and diuretic responses to dietary salt are dissociated in some SS hypertensives. Experiments with perfused rat kidneys indicate that this dissociation is due to circulating catecholamines and not to increased renal nerve activity. 3. Reduced tubular dopamine production may be involved in SS hypertension but decreased dopaminergic nerve activity is not apparent. 4. Increased salt intake initiates a generalized increase in vascular resistance in SS hypertensives. The small amount of salt retained over 5-7 days could not produce the observed increase in blood pressure by altering ECF volumes or transmembrane ion gradients which suggests that a systemic vasoconstrictor, such as renin, is involved. In these patients, inappropriate renal nerve activity could shift the balance between salt intake, blood pressure and renin release since low level renal nerve activity raises the blood pressure required to inhibit renin release. Reversal of SS hypertension with ACE inhibitors is consistent with this hypothesis.