Neural Control of Na Balance in Hypertension during Exercise

Hypertension afflicts a great number of individuals and is a major cardiovascular risk factor. Dynamic exercise decreases high blood pressure but the mechanisms are not fully understood. Neural mechanisms act to regulate acute changes in arterial pressure, whereas renal mechanisms play a greater role in long term control of pressure. The renal sympathetic nerves modulate renal Na reabsorption and so impact volume and blood pressure. Thus, neural and renal mechanisms function in an integrated and concerted manner to regulate arterial pressure.

We are currently using a model of hypertension with an activated renin-angiotensin-aldosterone system and increased sympathetic activity.  We hypothesize that voluntary dynamic exercise training will decrease efferent renal sympathetic nerve activity (RSNA) by enhancing nitric oxide-induced GABAergic inhibition at the paraventricular nucleus (PVN). In turn, the decrease in efferent RSNA will increase urinary Na excretion by blunting the expression and function of the epithelial Na channel (ENaC) in the distal nephron.  We use a combination of classic physiologic and pharmacologic approaches as well as in vivo transfer of dominant negative constructs for nitic oxide to ascertain the effect of sedentary or exercise training paradigms on  blood pressure, heart rate, and renal sympathetic nerve activity. In addition, we are evaluating the effects on abundance of ENaC in the kidney, and the impact exercise has on renal function and urinary sodium excretion.

This page was created and maintained by Christine Cupps
updated: 09/15/2004