Key result
Pretreatment with V1b and V2 receptor antagonists prevented stress-induced baroreflex desensitization and tachycardia in rats, but failed to modulate stress-induced hypertension.
Why the study?
Does central vasopressin receptor antagonism prevent stress-induced baroreflex desensitization and tachycardia in conscious rats?
Does central vasopressin receptor antagonism prevent stress-induced baroreflex desensitization and tachycardia in conscious rats?
Central vasopressin V1b and V2 receptors mediate stress-induced tachycardia and baroreflex desensitization, identifying them as potential novel targets for cardiovascular drug development in conditions like heart failure and hypertension.
Supports V1b/V2 antagonism for autonomic stress responses; leaves open translation to human hypertension or heart failure.
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 Wistar 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 V1a or V1b or V2 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 V1a receptor antagonist did not modulate the BP, HR, BRS and BEI response to stress. Pretreatment of rats with V1b receptor and V2 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 V1b- and V2-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.
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Milutinović‐Smiljanić et al. (2013) studied Stress-induced baroreflex desensitization. Selective non-peptide V1a, V1b, or V2 receptor antagonists vs. Baseline/stress without pretreatment was evaluated on Blood pressure, heart rate, and baroreceptor reflex sensitivity. Pretreatment with V1b and V2 receptor antagonists prevented stress-induced baroreflex desensitization and tachycardia in rats, but failed to modulate stress-induced hypertension.
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