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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Physiol+Heart+Circ+Physiol
2016 ; 310
(7
): H891-8
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Bombesin-like receptor 3 regulates blood pressure and heart rate via a central
sympathetic mechanism
#MMPMID26801314
Lateef DM
; Xiao C
; Brychta RJ
; Diedrich A
; Schnermann J
; Reitman ML
Am J Physiol Heart Circ Physiol
2016[Apr]; 310
(7
): H891-8
PMID26801314
show ga
Bombesin-like receptor 3 (BRS-3) is an orphan G protein-coupled receptor that
regulates energy expenditure, food intake, and body weight. We examined the
effects of BRS-3 deletion and activation on blood pressure and heart rate. In
free-living, telemetered Brs3 null mice the resting heart rate was 10% lower than
wild-type controls, while the resting mean arterial pressure was unchanged.
During physical activity, the heart rate and blood pressure increased more in
Brs3 null mice, reaching a similar heart rate and higher mean arterial pressure
than control mice. When sympathetic input was blocked with propranolol, the heart
rate of Brs3 null mice was unchanged, while the heart rate in control mice was
reduced to the level of the null mice. The intrinsic heart rate, measured after
both sympathetic and parasympathetic blockade, was similar in Brs3 null and
control mice. Intravenous infusion of the BRS-3 agonist MK-5046 increased mean
arterial pressure and heart rate in wild-type but not in Brs3 null mice, and this
increase was blocked by pretreatment with clonidine, a sympatholytic, centrally
acting ?2-adrenergic agonist. In anesthetized mice, hypothalamic infusion of
MK-5046 also increased both mean arterial pressure and heart rate. Taken
together, these data demonstrate that BRS-3 contributes to resting cardiac
sympathetic tone, but is not required for activity-induced increases in heart
rate and blood pressure. The data suggest that BRS-3 activation increases heart
rate and blood pressure via a central sympathetic mechanism.