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EXISTENCE OF β 3 ‐ADRENOCEPTORS IN RAT HEART: FUNCTIONAL IMPLICATIONS
Author(s) -
Barbier J,
Mouas C,
RannouBekono F,
Carré F
Publication year - 2007
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2007.04633.x
Subject(s) - nadolol , agonist , antagonist , endocrinology , medicine , inotrope , beta (programming language) , stimulation , chemistry , receptor , biology , propranolol , computer science , programming language
SUMMARY1 β 3 ‐Adrenoceptors (AR) have been reported to be present in numerous species, where they mediate multiple responses. 2 The aim of the present study was to determine whether β 3 ‐AR are present in intact rat heart and the functional implications of β 3 ‐AR stimulation. The response to the cardiac β 3 ‐AR‐selective agonist BRL37344 was expressed as the percentage of values measured at baseline. 3 BRL37344 induced dose‐dependent negative inotropic effects at concentrations ranging from 10 −11 to 10 −7 mol/L. BRL37344 (10 −8 mol/L) induced a decrease of left ventricular developed pressure (LVDP) from 127 ± 5 to 89 ± 16 mmHg (69 ± 15%; P < 0.01) and +dP/dt from 2594 ± 59 to 1885 ± 50 mmHg/s (72 ± 8%; P < 0.01). Moreover, a significant reduction of –dP/dt from 2176 ± 42 to 1458 ± 43 mmHg/s (67 ± 8%; P < 0.01) was observed. The BRL37344 dose–response curves were not altered by nadolol (10 −5 mol/L), a potent β 1 ‐ and β 2 ‐AR antagonist, but were completely suppressed by the addition of SR59230A (10 −5 mol/L), a potent β 3 ‐AR antagonist. 4 The present study provides functional evidence for the presence of β 3 ‐AR in rat hearts and shows, for the first time, that a highly specific β 3 ‐AR antagonist can block the attenuation of LVDP caused by the specific β 3 ‐AR agonist BRL37344 in rat beating hearts.