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Introduction Upregulation of vasopressinergic system and increased chemoreflex activity contribute to essential hypertension. Vasopressin (AVP) V1a receptors (V1aRs) were found in the brain stem structures involved in the control of breathing and in the carotid bodies (CBs). It has also been shown that in normotensive rats intravenous (i.v.) and local (intra‐carotid, i.a.) AVP administration results in different hemodynamic and respiratory response. Purpose We aimed at finding out how systemic (i.v.) and local (i.a.) administration of AVP affects cardiorespiratory system via V1aRs in normo‐ and hypertensive rats and if V1aRs are expressed in CBs in spontaneously hypertensive (SHR) and normotensive Wistar‐Kyoto (WKY) rats. Methods The study was performed on urethane‐anesthetized adult male WKY (n=7) and SHR rats (n=7). Animals were implanted with vascular catheters into femoral vein (i.v. infusions), femoral artery (hemodynamic parameters) and external carotid artery (local infusions), as well as the tracheal tube (respiratory parameters) and subcutaneous ECG electrodes. After obtaining baseline parameters, the arterial chemoreflex was triggered with i.v. administration of potassium cyanide (KCN) (30 μg/100 μL). Bolus of AVP was given i.v. (10 ng/100 μL) and i.a. (5 ng/50 μL). After stabilization of hemodynamic and respiratory parameters, V1a receptor was blocked by administration of V1aR antagonist (d(CH2)51,Tyr(Me)2,Arg8)‐Vasopressin; 5 μg/100 μL) and AVP and KCN infusions were repeated. After measurements, carotid bodies (CBs) were collected and immunostained for V1aRs and visualized with confocal microscopy. Results Resting mean arterial blood pressure (MABP), heart rate (HR) and minute ventilation (MV) were significantly higher in SHR rats than in WKY control. In both groups hemodynamic and respiratory response to pharmacological trigger of the reflex occurred, however increase in MABP and MV were significantly greater in SHR than in WKY rats. Intravenous AVP administration caused an increase in MABP, but ventilatory inhibition only in SHR rats. Intra‐arterial AVP infusion caused a modest increase in MABP in both groups, but inhibition of ventilation only in SHR rats. Blockade of V1aR abolished the effects of both systemic and local AVP administration. Furthermore, V1aR antagonist decreased the pressor component of the chemoreflex, however it did not influence ventilatory response. Immunostaining revealed V1aRs in CBs in both groups. Conclusions Our findings show that enhanced cardiorespiratory responses to activation of arterial chemoreflex and augmented pressor and ventilatory effects of systemic and local administrations of AVP are present in hypertensive rats and depend on V1aRs. Presence of V1aRs in CBs suggests that AVP may control cardiorespiratory system via arterial chemoreceptors.