application) Numerous studies suggest that increases in sodium chloride (NaCl) intake increase arterial pressure in several hypertensive models in part by activating the sympathetic nervous system. However, whether salt exerts a similar sympathoexcitatory action in normal conscious animals is unclear. Therefore, this proposal tests the general hypothesis that increased dietary NaCl does increase sympathetic activity, but this action is normally counterbalanced by direct and indirect (decreased angiotensin II-induced sympathoexcitation and baroreflex activation) effects of salt to decrease sympathetic activity. To test this general hypothesis, the following specific hypotheses will be examined. 1) Acute increases in NaCl increase sympathetic activity, but this effect is normally counterbalanced by decreases in circulating angiotensin II (AII) and baroreflex activation. 2) Chronic changes in NaCl intake are directly related to changes in sympathetic activity, vasopressin and activity of the hypothalamic-adrenal pituitary axis, but these actions are normally counterbalanced by reciprocal changes in AII. 3) Changes in dietary NaCl influence sympathetic activity in part by activation of osmoreceptors 4) Chronic increases in NaCl influence activity of sympathetic postganglionic neurons by altering expression of tyrosine hydroxylase and the norepinephrine transporter. 5) If the balance between the sympathoexcitatory and sympathoinhibitory effects of NaCl is disrupted, hypertension will be produced. These hypotheses will be tested in conscious rats by examining the acute and chronic effects of changes in NaCl intake, with and without fixing the activity of the renin-angiotensin system, on renal and lumbar sympathetic activity, plasma catecholamines, vasopressin and corticosterone levels and ganglionic mRNA levels for tyrosine hydroxylase and the norepinephrine transporter.
