Cardiovascular influences of α1b-adrenergic receptor defect in mice

Carmine Vecchione, Luigi Fratta, Damiano Rizzoni, Antonella Notte, Roberta Poulet, Enzo Porteri, Giacomo Frati, Daniele Guelfi, Valentina Trimarco, Michael J. Mulvany, Enrico Agabiti-Rosei, Bruno Trimarco, Susanna Cotecchia, Giuseppe Lembo

Research output: Contribution to journalArticlepeer-review


Background - The α1-adrenergic receptors (α1-ARs) play a key role in cardiovascular homeostasis. However, the functional role of α1-AR subtypes in vivo is still unclear. The aim of this study was to evaluate the cardiovascular influences of α1b-AR. Methods and Results - In transgenic mice lacking α1-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 α1b-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.

Original languageEnglish
Pages (from-to)1700-1707
Number of pages8
Issue number14
Publication statusPublished - Apr 9 2002


  • Norepinephrine
  • Receptors, adrenergic, alpha
  • Remodeling

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine


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