Background A new beta 3‐adrenoceptor (β3‐AR) has been shown to mediate peripheral vasodilation. This study was conducted to evaluate effects of the β3‐AR agonist, SR58611 in normal and hypertensive dogs.Materials and Methods In protocol 1, SR58611 was infused in normal dogs after placebo, after β1/β2 blockade with nadolol, after β1/β2/β3 blockade with bupranolol and after combined autonomic blockade (CAB). In protocol 2, perinephritic hypertension was produced in dogs, which received SR58611 at 3 and 6 weeks of hypertension. Effects of SR58611 were evaluated at 7 weeks of hypertension after CAB.Results In normal dogs, SR58611 produced a dose‐dependent decrease in mean aortic pressure (AOP) (from 116 ± 19 to 100 ± 19 mmHg, − 14%; P < 0·05) that was accompanied by baroreflex activation (heart rate increased by 70%; P < 0·01). This hypotensive effect resulting from peripheral vasodilation persisted after nadolol or CAB while baroreflex activation was blunted or abolished. A biphasic response of cardiac output, characterized by a rise and a decline (P < 0·05) reflected a reduction in after‐ and pre‐load. After CAB, SR58611 did not modify cardiac contractility. SR58611 stimulated lipolysis as reflected by a 4‐fold increase in blood free fatty acids (FFA) (P < 0·0005). Under CAB, the rise of FFA was reduced (P < 0·01). In hypertensive dogs, SR58611 produced a dose‐dependent decrease in mean AOP (from 168 ± 32 to 125 ± 35 mmHg; − 26%, P < 0·0001), that was greater than in normal dogs (P < 0·05). Reflex‐mediated tachycardia also occurred but at higher blood pressure values. Blood FFA rose similarly (P < 0·0001). Under CAB, heart rate remained unchanged but SR58611 still induced a decrease (P < 0·0001) in mean AOP concomitantly with a rise of (dP/dt)/DP40 (P < 0·005), an effect not observed in normal dogs.Conclusions β3‐AR stimulation exerts hypotensive effects, increases cardiac contractility and stimulates lipolysis in hypertensive dogs.