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Evidence for involvement of central vasopressin V 1b and V 2 receptors in stress‐induced baroreflex desensitization
Author(s) -
MilutinovićSmiljanić Sanja,
Šarenac Olivera,
LozićDjurić Maja,
Murphy David,
JapundžićŽigon Nina
Publication year - 2013
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/bph.12161
Subject(s) - desensitization (medicine) , vasopressin , baroreflex , heart rate , antagonist , medicine , reflex , receptor , receptor antagonist , endocrinology , stimulation , tachycardia , vasopressin receptor , blood pressure , pharmacology , anesthesia
Background and Purpose It is well recognized that vasopressin modulates the neurogenic control of the circulation. Here, we report the central mechanisms by which vasopressin modulates cardiovascular response to stress induced by immobilization. Experimental Approach Experiments were performed in conscious male W istar rats equipped with radiotelemetric device for continuous measurement of haemodynamic parameters: systolic and diastolic BP and heart rate ( HR ). The functioning of the spontaneous baro‐receptor reflex ( BRR ) was evaluated using the sequence method and the following parameters were evaluated: BRR sensitivity ( BRS ) and BRR effectiveness index ( BEI ). Key Results Under baseline physiological conditions intracerebroventricular injection of 100 and 500 ng of selective non‐peptide V 1a or V 1b or V 2 receptor antagonist did not modify BP , HR and BRR . Rats exposed to 15 min long stress by immobilization exhibited increase of BP , HR , reduction of BRS and no change in BEI . Pretreatment of rats with V 1a receptor antagonist did not modulate the BP , HR , BRS and BEI response to stress. Pretreatment of rats with V 1b receptor and V 2 receptor antagonist, at both doses, prevented BRR desensitization and tachycardia, but failed to modulate stress‐induced hypertension. Conclusions and Implications Vasopressin by the stimulation of central V 1b‐ and V 2‐like receptors mediates stress‐induced tachycardia and BRR desensitization. If these mechanisms are involved, BRR desensitization in heart failure and hypertension associated with poor outcome, they could be considered as novel targets for cardiovascular drug development.