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(Hypertension. 1995;25:954-961.)
© 1995 American Heart Association, Inc.

Articles

Treatment in Hypertensive Cardiac Hypertrophy, I

Neuropeptide Y and ß-Adrenoceptors

Michael Böhm; Claudia Gräbel; Andreas Knorr; Erland Erdmann

From the Klinik III für Innere Medizin der Universität zu Köln and Bayer AG (A.K.), Wuppertal, Germany.

Abstract In the present study, we investigated serum and myocardial neuropeptide Y concentrations as measures of sympathetic activity as well as myocardial ß-adrenoceptors and ß-adrenoceptor–stimulated adenylyl cyclase activity in spontaneously hypertensive rats (SHR). SHR and control rats at 10 weeks of age were kept on oral treatment with captopril, nitrendipine, or both for 20 weeks. Treatment only slightly reduced but did not normalize blood pressure and cardiac hypertrophy in SHR. The elevated serum concentration of neuropeptide Y, the reduced number of ß-adrenoceptors, and the depressed ß-adrenoceptor–stimulated adenylyl cyclase activity were partly normalized compared with the values observed in control rats. We conclude that antihypertensive treatment, at doses that failed to normalize systolic pressure and to reverse cardiac hypertrophy completely, is able to reduce sympathetic activity in SHR, thereby resensitizing the depressed ß-adrenoceptor–adenylyl cyclase system.

Key Words: hypertension, essential • cardiac hypertrophy • heart failure, congestive • rats, inbred SHR • adenylyl cyclase • receptors, adrenergic • sympathetic nervous system • angiotensin-converting enzyme inhibitors • calcium channel blockers

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