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Vol. 300, Issue 1, 43-49, January 2002
2-Adrenoceptor Subtypes
Department of Biochemistry and Molecular Biology, Faculté de
Médecine de Paris-Ouest, Université René Descartes,
Paris, France
This study investigated the importance of the male sex hormone
testosterone on salt-induced hypertension, renal
2-adrenoceptor subtype distribution, and gene expression
in salt-sensitive (SBH) male Sabra rats. Comparisons of blood pressure
and renal
2-adrenoceptor subtype gene expression and
receptor densities have been made among sham-operated rats, and
gonadectomized rats treated or not with testosterone and submitted to
normal or high salt diet for 6 weeks. In intact rats, only
2B-adrenoceptors were detected in this rat strain
independent of the diet. In these rats, high salt diet increases blood
pressure and up-regulates gene expression and density of
2-adrenoceptors. Gonadectomy abolishes the hypertensive response to salt overload, decreases gene expression and density of
2B-adrenoceptors, and prevents their salt-induced
up-regulation. After gonadectomy, increased gene expression and a
detectable density of
2A-adrenoceptors are observed at
similar levels in normal and high salt diet. In gonadectomized rats,
testosterone replacement restores salt-induced hypertension, density of
renal
2B-adrenoceptors, and gene expression to the
intact levels observed both under normal and high salt diet.
Furthermore, the
2A-adrenoceptor subtype is not detected
in these conditions. If the increase in renal
2B-adrenoceptor subtypes is indicative of the
hypertensive phenotype, the presence of the
2A-adrenoceptor appears associated with a state of salt
resistance in male SBH rats. In conclusion, testosterone is needed for
the full expression of salt-induced hypertension in male salt-sensitive
Sabra rats. Renal densities of
2-adrenoceptor subtypes
are under control of the testicles and are differentially regulated by testosterone.
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