Blood pressure and neurogenic adaptations to reduced dietary sodium in the SHR model of hypertension.

Sodium (Na) balance is maintained by a complex set of genetic, hemodynamic, hormonal and neural mechanisms that affect intake, reabsorption and excretion. This research focused on the role of a reduction in dietary Na on cardiovascular and neuroeffector function in normotensive (WKY) and spontaneously hypertensive rats (SHR) raised from 5-20 weeks on a control Na diet (12 mmol per 100 g food) or various low Na diets (0.5-2 mmol per 100 g food). For comparison purposes, high Na (140 mmol per 100 g food) results are reported. With regards to hemodynamics and volume regulation, the lowest Na diet reduced blood pressure 15% in SHRs but not in WKYs. Body weights, blood volume, hematocrit, plasma electrolytes, extracellular volume, and cardiac output were not different between diets or strains. However, both SHR and WKY low Na groups were abnormally sensitive to blood loss and showed attenuated pressor responses, mediated by the sympathetic nervous system, to both acute and chronic stress situations. Low Na treatment significantly attenuated the pressor response during stress, which was primarily due to reduction in noradrenergic transmitter release. In spite of depressed function during restriction of dietary Na, compensatory responses were adequate to maintain homeostasis, but the neurohumoral compensatory reserve was thereby markedly curtailed. The data suggest that risks are associated with a reduced intake of dietary Na. These findings imply that the "hygienic" Na intake in man should be carefully experimentally defined before generalized measures are taken to reduce dietary Na in society.