| First Author | Lateef DM | Year | 2016 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 310 |
| Issue | 7 | Pages | H891-8 |
| PubMed ID | 26801314 | Mgi Jnum | J:232637 |
| Mgi Id | MGI:5779745 | Doi | 10.1152/ajpheart.00963.2015 |
| Citation | Lateef DM, et al. (2016) Bombesin-like receptor 3 regulates blood pressure and heart rate via a central sympathetic mechanism. Am J Physiol Heart Circ Physiol 310(7):H891-8 |
| abstractText | 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, telemeteredBrs3null 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 inBrs3null mice, reaching a similar heart rate and higher mean arterial pressure than control mice. When sympathetic input was blocked with propranolol, the heart rate ofBrs3null 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 inBrs3null and control mice. Intravenous infusion of the BRS-3 agonist MK-5046 increased mean arterial pressure and heart rate in wild-type but not inBrs3null mice, and this increase was blocked by pretreatment with clonidine, a sympatholytic, centrally acting alpha2-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. |
