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Existence of beta(3)-adrenoceptors in rat heart: functional implications
J Barbier1, C Mouas, F Rannou-Bekono
1EA 1274, Laboratory of Physiology and Biomechanics of Muscular Exercise, UFR-APS, University of Rennes 2, Rennes, France. julie.barbier@uhb.fr
Clinical and Experimental Pharmacology & Physiology
|June 30, 2007
Summary
This study confirms beta(3)-adrenoceptors (AR) in rat hearts, demonstrating their role in cardiac function. A specific beta(3)-AR antagonist blocked the negative inotropic effects of a beta(3)-AR agonist, providing functional evidence.
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Beta(3)-adrenoceptors (AR) are known to exist in various species and mediate diverse physiological responses.
- Their presence and function in the intact mammalian heart, specifically the rat heart, require further elucidation.
Purpose of the Study:
- To investigate the presence and functional significance of beta(3)-AR in the intact rat heart.
- To determine the effects of stimulating beta(3)-AR on cardiac contractility and to characterize the receptor's role in these responses.
Main Methods:
- Utilized the selective beta(3)-AR agonist BRL37344 to assess cardiac function in isolated rat hearts.
- Measured left ventricular developed pressure (LVDP), +dP/dt, and -dP/dt to quantify contractility.
- Investigated the effects of beta(1)-/beta(2)-AR antagonist nadolol and beta(3)-AR antagonist SR59230A on BRL37344-induced responses.
Main Results:
- BRL37344 induced dose-dependent negative inotropic effects, significantly reducing LVDP, +dP/dt, and -dP/dt.
- These effects were not influenced by the beta(1)-/beta(2)-AR antagonist nadolol.
- The negative inotropic effects of BRL37344 were completely abolished by the beta(3)-AR antagonist SR59230A.
Conclusions:
- Provided functional evidence for the existence of beta(3)-AR in the rat heart.
- Demonstrated that beta(3)-AR stimulation leads to negative inotropic effects in the rat heart.
- Established that a specific beta(3)-AR antagonist can block these effects, confirming the functional role of beta(3)-AR in cardiac contractility.
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