Beta-adrenoceptor changes in hypertension: cause or consequence of the elevation in blood pressure?
Cardiac, pulmonary and renal beta-adrenoceptor density and subtype distribution were measured by radioligand binding in three rat models of acquired hypertension. Dahl salt-sensitive (DS) rats on a high-sodium diet, renal hypertensive rats and DOCA-salt rats. The results were compared with previously obtained data from spontaneously hypertensive rats (SHR) of different ages and from SHR treated with the immunosuppressant cyclosporin A. Cardiac and pulmonary beta-adrenoceptor density and subtype distribution were unaltered in any of the three groups compared with their respective controls. However, renal beta-adrenoceptor density was uniformly increased without alterations of the beta 1: beta 2-adrenoceptor ratio. The previously described beta 2-adrenoceptor increase in heart and lung of SHR was not found in any model of acquired hypertension and might be characteristic for the SHR. However, renal beta-adrenoceptor alterations seem generally to occur secondary to blood pressure elevation.
Kanczik
R
R
Medizinische Klinik und Poliklinik, University of Essen, Federal Republic of Germany.
Khamssi
M
M
Michel
M C
MC
Brodde
O E
OE
D000818:Animals; D001794:Blood Pressure; D003900:Desoxycorticosterone / Q000633:toxicity; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology*; D006978:Hypertension, Renovascular / Q000209:etiology / Q000503:physiopathology; D051381:Rats; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D012965:Sodium Chloride / Q000633:toxicity
D011943:Receptors, Adrenergic, beta; D003900:Desoxycorticosterone; D012965:Sodium Chloride