title: How does salt raise blood pressure? A hypothesis.
abstract: 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.
mesh_terms: D000320:Adrenergic Fibers / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001933:Brain Stem / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D009638:Norepinephrine / Q000097:blood; D051381:Rats; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects* / Q000502:physiology; D012462:Saline Solution, Hypertonic / Q000494:pharmacology; D012965:Sodium Chloride / Q000494:pharmacology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology
chemical_list: D011942:Receptors, Adrenergic, alpha; D012462:Saline Solution, Hypertonic; D012965:Sodium Chloride; D009638:Norepinephrine