Sh. Carlson et al., The role of the central nervous system in NaCl-sensitive hypertension in spontaneously hypertensive rats, AM J HYPERT, 14(6), 2001, pp. 155S-162S
The central and peripheral nervous system is typically considered to be a s
hort-term modifier of sympathetic nervous system activity, but several line
s 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 hype
rtensive rat (SHR). When these rats are fed a high NaCl diet, their arteria
l pressure rapidly increases and is maintained about 30 mm Hg higher than t
hose of pair fed controls. The increase in arterial pressure is associated
with a decrease in norepinephrine release, specifically in the anterior hyp
othalamic nucleus (AHN), resulting in increased sympathetic nervous system
activity, peripheral vasoconstriction, and arterial pressure. Furthermore,
administration of an alpha (2)-adrenergic receptor agonist in this area blo
cks the NaCl-sensitive increase in arterial pressure in the SHR but has no
significant effect on arterial pressure in normotensive controls. We have i
dentified three intermediary steps by which dietary NaCl reduces AHN norepi
nephrine release. First, dietary NaCl causes an increase in plasma NaCl and
a blunting of the plasma NaCl circadian rhythm. Second, alterations in pla
sma NaCl activate osmosensitive neurons in the organum vasculosum of the la
mina terminalis (OVLT). Third, OVLT input to the AHN appears to increase th
e release of atrial natriuretic peptide with a resultant decrease in the lo
cal release of norepinephrine. Finally, our evidence demonstrates that thes
e 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 Na
Cl-sensitive hypertension in SHR. (C) 2001 American Journal of Hypertension
, Ltd.