Risks associated with dietary sodium reduction in the spontaneous hypertensive rat model of hypertension.

Sodium balance is maintained by a complex set up of hemodynamic, hormonal and neural mechanisms that affect intake, reabsorption and excretion. The focus of the following research was on the cardiovascular and neuroeffector effects of dietary Na reduction primarily in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) raised from 4 to 15 weeks on a control Na diet (CNa: 12 mmol per 100 g food) or various low Na diets (LNa: 0.5 to 3 mmol per 100 g food). With regards to hemodynamics and volume regulation, the lowest Na diet reduced blood pressure 15% and raised resting heart rate (20%) in SHRs but not WKYs. Blood volume, hematocrit, plasma electrolytes, extracellular volume, and cardiac output were not different between diets or strains. However, both LNa strains were abnormally sensitive to blood loss and showed attenuated pressor responses to both acute and chronic stress situations. Cardiac function was not altered by LNa treatment in either rat strain although structural compensations occurred. LNa treatment significantly attenuated the pressor reduction in mesenteric blood flow during stress which was primarily due to reduction in noradrenergic transmitter release and not due to altered receptor sensitivity, density, or Na/K ATPase activity. Compensatory sympathetic activity was increased as was sodium conservation through humoral mechanisms which maintained homeostasis. However, further neurohumoral compensation was markedly reduced. The data suggests that the hygienic sodium intake in humans should be experimentally defined before generalized measures are taken to reduced dietary sodium use throughout society.