Hypertension, Vol 8, 83-88, Copyright © 1986 by American Heart Association
H Gavras
Existing data in the literature indicate that alpha 2-adrenergic receptor
agonists have a profound hypotensive action, that sodium attenuates the
affinity of alpha 2-adrenergic receptors for agonists, that the location of
these receptors in the central nervous system is mainly at the sites of
cardiovascular regulation, and that these sites exert a constant tonic
inhibition of sympathetic vasoconstrictor tone. This article proposes the
theory that sodium exerts its hypertensive action by decreasing the state
of affinity of the alpha 2-adrenergic receptors of the central nervous
system for locally occurring agonist neurotransmitters, which results in
disinhibition of sympathoinhibitory neurons and leads to the
hyperadrenergic state characteristic of salt- induced hypertension.
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How does salt raise blood pressure? A hypothesis
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