Published online before print March 25, 2002, doi: 10.1161/01.CIR.0000012750.08480.55
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(Circulation. 2002;105:1700.)
© 2002 American Heart Association, Inc.
Basic Science Reports |
Cardiovascular Influences of 
1b-Adrenergic Receptor Defect in Mice
From the I.R.C.C.S. Neuromed (C.V., L.F., A.N., R.P., G.F., V.T., B.T., G.L.), Pozzilli (IS), Italy; Internal Medicine Department of Medical and Surgical Sciences (D.R., E.P., D.G., E.A.-R.), University of Brescia, Italy; Department of Pharmacology (M.J.M.), University of Aarhus, Aarhus, Denmark; Institut de Pharmacologie et Toxicologie (S.C.), Université de Lausanne, Switzerland; and Department of Experimental Medicine and Pathology (G.L.), La Sapienza University of Rome, Italy.
Correspondence to Giuseppe Lembo, MD, PhD, Department of Experimental Medicine and Pathology, La Sapienza University of Rome, c/o I.R.C.C.S. Neuromed, Località Camerelle, 6077 Pozzilli (IS), Italy. E-mail lembo{at}neuromed.it
Background— The 
1-adrenergic receptors (1-ARs) play a key role in cardiovascular homeostasis. However, the functional role of 1-AR subtypes in vivo is still unclear. The aim of this study was to evaluate the cardiovascular influences of 1b-AR.
Methods and Results— In transgenic mice lacking 1-AR (KO) and their wild-type controls (WT), we evaluated blood pressure profile and cardiovascular remodeling induced by the chronic administration (18 days via osmotic pumps) of norepinephrine, angiotensin II, and subpressor doses of phenylephrine. Our results indicate that norepinephrine induced an increase in blood pressure levels only in WT mice. In contrast, the hypertensive state induced by angiotensin II was comparable between WT and KO mice. Phenylephrine did not modify blood pressure levels in either WT or KO mice. The cardiac hypertrophy and eutrophic vascular remodeling evoked by norepinephrine was observed only in WT mice, and this effect was independent of the hypertensive state because it was similar to that observed during subpressor phenylephrine infusion. Finally, the cardiac hypertrophy induced by thoracic aortic constriction was comparable between WT and KO mice.
Conclusions— Our data demonstrate that the lack of 1b-AR protects from the chronic increase of arterial blood pressure induced by norepinephrine and concomitantly prevents cardiovascular remodeling evoked by adrenergic activation independently of blood pressure levels.
Key Words: receptors, adrenergic, alpha • remodeling • norepinephrine
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