NaCl does not affect hypothalamic noradrenergic input in deoxycorticosterone acetate/NaCl and dahl salt-sensitive rats

Abstract

Previous studies from our laboratories demonstrated that dietary NaCl supplementation in NaCl-sensitive spontaneously hypertensive rats elevates blood pressure, increases peripheral sympathetic nervous system activity, and depresses endogenous norepinephrine stores and turnover in the anterior hypothalamus. These findings suggest that reduced noradrenergic input to sympathoinhibitory neurons in anterior hypothalamus contributes to NaCl-sensitive hypertension in spontaneously hypertensive rats. The current study tested the hypothesis that dietary NaCl supplementation depresses endogenous norepinephrine stores and turnover in anterior hypothalamus of two other NaCl-sensitive models of hypertension, the Dabi saltsensitive rat and the deoxycorticosterone acetate/NaCl hypertensive rat, thus increasing blood pressure by reducing noradrenergic input to the anterior hypothalamus. Dahl salt-sensitive rats were fed a high (8%) NaCl diet, and deoxycorticosterone acetate/NaCl rats drank 1% NaCl solution ad libitum for 2 or 4 weeks. Age-matched Dahl salt-sensitive rats fed a basal 1% NaCl diet and uninephrectomized Sprague-Dawley rats drinking tap water were controls. Regional brain catecholamines were determined by high-performance liquid chromatography with electrochemical detection. Norepinephrine turnover in hypothalamus (anterior, posterior, and ventral regions) and brain stem (pons and medulla) was assessed using the dopamine β-hydroxylase inhibitor 1-cyclohexyl-2-mercapto-imidazole. High NaCl treatment caused significant elevations in blood pressure in Dahl salt-sensitive and deoxycorticosterone acetate/ NaCI rats, but endogenous norepinephrine levels and turnover rates were not significantly different in anterior hypothalamus or any other brain region studied between the NaCl-supplemented and control groups. Noradrenergic input to the anterior hypothalamus is not reduced in Dahl salt-sensitive and deoxycorticosterone acetate/NaCl rats on a high NaCl intake, suggesting that the neural mechanisms of NaCl sensitivity are different in the Dahl salt-sensitive, deoxycorticosterone acetate/NaCl, and spontaneously hypertensive rat models of hypertension. Thus, the abnormalities in anterior hypothalamic norepinephrine handling observed in NaCl-supplemented, NaCl-sensitive hypertensive rats are strain-specific and not secondary to the NaCl-induced increase in blood pressure.