α- and β-Adrenoceptors in Hypertension. I. Cardiac and Renal α1-, β1, and β2-Adrenoceptors in Rat Models of Acquired Hypertension

Abstract

Summary: To determine whether adrenoceptor changes in genetic hypertension occur primary or secondary to blood pressure elevation, we measured cardiac and renal α₁,- (by [¹²⁵I]Be 2254 binding) and β₁- and β₂-adrenoceptors (by ( – )-[¹²⁵I]iodocyanopindolol binding) densities in various rat models of acquired hypertension (Dahl S rats on a high-sodium diet. 1-clip-1-kidney (1C-IK) renal hypertensive and DOCA-salt hypertensive rats) in comparison with genetically identical age-matched untreated rats. In addition, α₁-adrenoceptors were assessed in spontaneously hypertensive rats (SHR) and in SHR treated with the immunosuppressant cyclosporin A. In heart, no clear pattern of changes in α₁- or β₁ and β₂-adrenoceptors was obtained. In kidney, however. β₁- and β₂-adrenoceptors were increased in all models of hypertension, and a good correlation between renal β-adrenoceptors and systolic blood pressure was found. In contrast, renal β-adrenoceptors were only increased in SHR but not in any form of acquired hypertension. Thus, renal α₁-adrenoceptor increases probably occur secondary to blood pressure elevation, whereas α₁-adrenoceptor increases appear to be associated with genetic hypertension. Because renal α-adrenoceptors are linked to tubular sodium reabsorption. we suggest that an increase in renal α₁,- (and α₂)-adrenoceptors may be a very early step in the development of genetic hypertension.