Key result
Vasopressin triggers greater blood pressure spikes and reduced ventilation in hypertensive versus normotensive rats.
Why the study?
Limited evidence suggests vasopressin contributes to respiratory regulation, and both increased vasopressinergic activity and enhanced arterial chemoreflex occur in hypertension, but cardiorespiratory responses to vasopressin and the involvement of carotid bodies and V1a receptors remained unclear.
Does intravenous vasopressin alter cardiorespiratory responses in spontaneously hypertensive rats compared to normotensive rats?
Does intravenous vasopressin alter cardiorespiratory responses in spontaneously hypertensive rats compared to normotensive rats?
Vasopressin exerts enhanced cardiovascular and unique respiratory regulatory effects in spontaneously hypertensive rats, mechanisms that appear primarily mediated by V1a receptors and carotid bodies.
Caution advised before extrapolating vasopressin responses to hypertensive patients; leaves open V1a and carotid body roles in human cardiorespiratory control.
Background: Vasopressin (AVP) and its V1a receptor (V1aR) are involved in the regulation of the cardiovascular system. Limited evidence suggests that AVP may also contribute to respiratory regulation. Arterial chemoreflex is the main reflex involved in cardiorespiratory regulation and is triggered from the carotid bodies (CBs), specialized organs that detect changes in arterial blood content. Both increased activity of the vasopressinergic system and enhanced arterial chemoreflex have been found in hypertension. Here, we aimed at determining cardiorespiratory responses to AVP in normo- and hypertensive rats and the involvement of CBs and V1aRs. Methods: Experiments were performed in urethane-anesthetized adult male spontaneously hypertensive (SHR) and normotensive Wistar Kyoto (WKY) rats. Arterial blood pressure (MABP), heart rate (HR), femoral artery blood flow (FABF), minute ventilation (MV), respiratory rate (RR), and end-tidal carbon dioxide (ETCO2) were recorded. We evaluated cardiorespiratory responses to arterial chemoreflex activation with potassium cyanide, intravenous AVP, V1aR antagonist, and CB denervation. Results: In comparison to normotensive animals, SHR rats had significantly greater resting MABP, HR, MV, and enhanced pressor and ventilatory components of arterial chemoreflex. CB denervation caused insignificant changes in cardiorespiratory parameters. Intravenous administration of AVP resulted in a significant increase in MABP in both groups, which was greater in SHR rats, and in ventilatory inhibition, which was present only in SHR rats. CB denervation reduced the pressor response to AVP in normotensive rats and abolished the inhibitory effect of AVP on ventilation in SHR rats. Intravenous administration of the V1aR antagonist caused a significantly greater decrease in MABP in the hypertensive group. Only SHR rats responded with an increase in ventilation after the V1aR antagonist. Effects of AVP were abolished after blockade of V1aRs in both groups. Conclusions: Our study indicates that (i) SHR rats show augmented cardiorespiratory response to AVP, (ii) cardiorespiratory effects of AVP depend on V1aRs; and (iii) respiratory effects of AVP in the hypertensive rats appear to be primarily mediated by CBs.
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Proczka et al. (2025) studied Hypertension (n=24). Intravenous Vasopressin (AVP) vs. Normotensive WKY rats (or baseline) was evaluated on Change in mean arterial blood pressure (MABP) and minute ventilation (MV) in response to intravenous AVP (p=<0.0001). Intravenous vasopressin elicited a significantly greater increase in mean arterial blood pressure and a decrease in pulmonary ventilation in spontaneously hypertensive rats compared to normotensive controls.
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