Renal alpha-adrenergic receptors and genetic hypertension.
The hypothesis has been proposed that an increase in the number of renal alpha-adrenergic receptors may contribute to the pathogenesis of genetic hypertension. Herein we review recent findings regarding expression of renal alpha 1 (alpha 1a, alpha 1b)- and alpha 2 (alpha 2a, alpha 2b)-adrenergic subtypes and we provide an updated revision of the above-stated hypothesis. Enhancement in receptor number or in post-receptor components responsible for alpha 1- and alpha 2-adrenergic-mediated sodium reabsorption in proximal tubule may contribute to sodium retention and an elevation in blood pressure. Perhaps such changes contribute to the increase in blood pressure in genetically determined hypertension in humans, although direct tests of this notion have not yet been performed.
Jackson
C A
CA
Department of Pharmacology, University of California, San Diego, La Jolla 92093-0636.
Insel
P A
PA
D000818:Animals; D006801:Humans; D006973:Hypertension / Q000235:genetics* / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism; D018341:Receptors, Adrenergic, alpha-2 / Q000378:metabolism
D011942:Receptors, Adrenergic, alpha; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2