Cardiovascular and metabolic alterations in mice lacking beta1- and beta2-adrenergic receptors.
Targeted disruption of murine beta-adrenergic receptor (beta-AR) genes has helped to clarify the role of specific beta-AR subtypes in regulating cardiovascular development and function. In the mouse, the beta1-AR is primarily responsible for sympathetic regulation of both cardiac chronotropy and inotropy. In contrast, all three beta-ARs play a role in regulating peripheral vascular tone. The impact of ablation of both beta1- and beta2-ARs on cardiac development and on resting cardiovascular and metabolic parameters is remarkably minimal. However, exercise stress reveals additional important contributions of beta1- and beta2-ARs to cardiovascular performance.
Bernstein
Daniel
D
Department of Pediatrics, Stanford University, Palo Alto, CA, USA. danb@stanford.edu
D000818:Animals; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000254:growth & development* / Q000378:metabolism* / Q000503:physiopathology; D015444:Exercise / Q000502:physiology; D006801:Humans; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000254:growth & development / Q000378:metabolism / Q000503:physiopathology; D009200:Myocardial Contraction / Q000187:drug effects; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D018342:Receptors, Adrenergic, beta-1 / Q000172:deficiency*; D018343:Receptors, Adrenergic, beta-2 / Q000172:deficiency*; D013564:Sympathetic Nervous System / Q000254:growth & development / Q000378:metabolism / Q000503:physiopathology
D011943:Receptors, Adrenergic, beta; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2