FASEB J.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Michel, M. C.
Right arrow Articles by Brodde, O. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Michel, M. C.
Right arrow Articles by Brodde, O. E.

The FASEB Journal, Vol 3, 139-144, Copyright © 1989 by The Federation of American Societies for Experimental Biology

REVIEWS

Renal alpha-adrenergic receptor alterations: a cause of essential hypertension?

MC Michel, PA Insel and OE Brodde
Department of Pharmacology, University of California, San Diego, La Jolla 92093.

Based on a review of literature in various fields of research related to hypertension, we develop a new working hypothesis on the pathophysiology of genetically determined increases in blood pressure. According to our hypothesis, the primary defect is located in the kidneys. Renal alpha-adrenergic receptor density is increased in the early stages of the disease, before increases in blood pressure occur. Most renal alpha-adrenergic receptors are located in the proximal tubules and enhance Na+ reabsorption. A genetically determined increase of alpha 1- or alpha 2- or of both alpha-adrenergic receptor subtypes would impair Na+ excretion and, together with increased Na+ intake, would lead to positive Na+ balance. Subsequently, various mechanisms would be activated to restore a neutral Na+ balance, including the secretion of a natriuretic factor that inhibits Na+/K+-ATPase. Inhibition of Na+/K+-ATPase in extrarenal tissues would increase the intracellular concentration of Na+ and, via Na+/Ca2+ exchange, of Ca2+. Elevated intracellular Ca2+ would enhance vascular smooth muscle contractility and neuronal transmitter release, thereby leading to vasoconstriction and to increases in blood pressure. We thus hypothesize that hypertension is a homeostatic response designed to protect blood volume from a genetically determined renal alpha- adrenergic receptor-mediated increase in Na+ retention.


This article has been cited by other articles:


Home page
 J. Pharmacol. Exp. Ther.Home page
R. Büscher, V. Herrmann, K. M. Ring, M. T. Kailasam, D. T. O'Connor, R. J. Parmer, and P. A. Insel
Variability in Phenylephrine Response and Essential Hypertension: A Search for Human alpha 1B-Adrenergic Receptor Polymorphisms
J. Pharmacol. Exp. Ther., November 1, 1999; 291(2): 793 - 798.
[Abstract] [Full Text]

Home page
 Nephrol Dial TransplantHome page
M. C. Michel, C. Plogmann, T. Philipp, and O.-E. Brodde
Functional correlates of {alpha}2A-adrenoceptor gene polymorphism in the HANE study
Nephrol. Dial. Transplant., November 1, 1999; 14(11): 2657 - 2663.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
E. R. Perl
Causalgia, pathological pain, and adrenergic receptors
PNAS, July 6, 1999; 96(14): 7664 - 7667.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1989 by The Federation of American Societies for Experimental Biology.