ARTERIAL BARORECEPTORS AND BRAIN HISTAMINE CONTRIBUTE TO BRADYCARDIA TO PERIPHERAL HYPEROSMOLALITY

The purpose of this study was to determine whether the bradycardic res ponse to peripheral hyperosmolality in conscious rats is dependent on afferent baroreceptor mechanisms and whether central histamine H-2 rec eptors 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 mul.100 g-1.min-1) hypertonic salin e (HTS). HTS infusion significantly increased MAP (21 +/- 4 mmHg) and reduced HR (-62 +/- 10 beats/min) in rats with intact arterial barorec eptors. In sinoaortic-denervated rats, HR remained unchanged from cont rol despite a significant increase in MAP. After intracerebroventricul ar (lateral ventricle) administration of cimetidine or ranitidine (H-2 -receptor antagonists) in intact rats, HTS infusion significantly incr eased MAP (19 +/- 2 and 17 +/- 2 mmHg, respectively) but the bradycard ia was abolished (-12 +/- 10 and -10 +/- 10 beats/min, respectively). In contrast, central H-2-receptor blockade did not alter reflex HR res ponses to the intravenous administration of phenylephrine and nitropru sside 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 p art a selective histaminergic pathway.