ARTERIAL BARORECEPTORS AND BRAIN HISTAMINE CONTRIBUTE TO BRADYCARDIA TO PERIPHERAL HYPEROSMOLALITY

Citation
Mj. Kenney et Sl. Bealer, ARTERIAL BARORECEPTORS AND BRAIN HISTAMINE CONTRIBUTE TO BRADYCARDIA TO PERIPHERAL HYPEROSMOLALITY, The American journal of physiology, 265(4), 1993, pp. 80001149-80001154
Citations number
20
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
265
Issue
4
Year of publication
1993
Part
2
Pages
80001149 - 80001154
Database
ISI
SICI code
0002-9513(1993)265:4<80001149:ABABHC>2.0.ZU;2-3
Abstract
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.