Cardiovascular influences of alpha(1b)-adrenergic receptor defect in mice

Article

关键词: VASCULAR SMOOTH-MUSCLE;    SUBCUTANEOUS SMALL ARTERIES;    CELLULAR HYPERTROPHY;    CARDIAC-HYPERTROPHY;    BLOOD-PRESSURE;    HYPERTENSION;    EXPRESSION;    FAILURE;    GROWTH;    CELLS;   

DOI  :  10.1161/01.CIR.0000012750.08480.55

来源: SCIE

【 摘 要 】

Background-The alpha(1)-adrenergic receptors (alpha(1)-ARs) play a key role in cardiovascular homeostasis. However, the functional role of alpha(1)-AR subtypes in vivo is still unclear. The aim of this Study was to evaluate the cardiovascular influences of alpha(1b)-AR. Methods and Results-In transgenic mice lacking alpha(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 H, 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 11 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 alpha(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.

【 授权许可】

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