Arterial baroreceptors and brain histamine contribute to bradycardia to peripheral hyperosmolality
Kenney, M.J.; Bealer, S.L.
American Journal of Physiology 265(4 Pt 2): H1149-H1154
1993
ISSN/ISBN: 0002-9513 PMID: 7902004 Document Number: 408703
The purpose of this study was to determine whether the bradycardic response to peripheral hyperosmolality in conscious rats is dependent on afferent baroreceptor mechanisms and whether central histamine H-2 receptors play a role in baroreflex-mediated changes in heart rate (HR). Mean arterial pressure (MAP) and HR were recorded continuously during a 30-min infusion of 2.5 M NaCl (10 mu-l cntdot 100 g-1 cntdot min-1) hypertonic saline (HTS). HTS infusion significantly increased MAP (21 +- 4 mm Hg) and reduced HR (-62 +- 10 beats/min) in rats with intact arterial baroreceptors. In sinoaortic-denervated rats, HR remained unchanged from control despite a significant increase in MAP. After intracerebroventricular (lateral ventricle) administration of cimetidine or ranitidine (H-2-receptor antagonists) in intact rats, HTS infusion significantly increased MAP (19 +- 2 and 17 +- 2 mm Hg, respectively) but the bradycardia was abolished (-12 +- 10 and -10 +- 10 beats/min, respectively). In contrast, central H-2-receptor blockade did not alter reflex HR responses to the intravenous administration of phenylephrine and nitroprusside or to the central administration of histamine or angiotensin II. These results indicate that the bradycardic response to HTS infusion is mediated through the arterial baroreceptor reflex and involves in part a selective histaminergic pathway.