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The central and peripheral nervous system is typically considered to be a short-term modifier of sympathetic nervous system activity, but several lines of evidence suggest that they contribute to chronic elevation of arterial pressure in at least some forms of hypertension. Our studies focus on the mechanisms underlying NaCl-sensitive hypertension in the spontaneously hypertensive rat (SHR). When these rats are fed a high NaCl diet, their arterial pressure rapidly increases and is maintained about 30 mm Hg higher than those of pair fed controls. The increase in arterial pressure is associated with a decrease in norepinephrine release, specifically in the anterior hypothalamic nucleus (AHN), resulting in increased sympathetic nervous system activity, peripheral vasoconstriction, and arterial pressure. Furthermore, administration of an alpha2-adrenergic receptor agonist in this area blocks the NaCl-sensitive increase in arterial pressure in the SHR but has no significant effect on arterial pressure in normotensive controls. We have identified three intermediary steps by which dietary NaCl reduces AHN norepinephrine release. First, dietary NaCl causes an increase in plasma NaCl and a blunting of the plasma NaCl circadian rhythm. Second, alterations in plasma NaCl activate osmosensitive neurons in the organum vasculosum of the lamina terminalis (OVLT). Third, OVLT input to the AHN appears to increase the release of atrial natriuretic peptide with a resultant decrease in the local release of norepinephrine. Finally, our evidence demonstrates that these factors lead to an increased rise in sympathetic nervous system activity during the early wake phase in SHR on a high NaCl diet, contributing to NaCl-sensitive hypertension in SHR.

The Role of the central nervous system in NaCl-sensitive hypertension in spontaneously hypertensive rats