The aim of this study was to assess the pressure response of mesenteric arteries isolated from various hypertensive rat models to the 3 pressor agonists norepinephrine, lysinevasopressin and angiotensin II. The isolated mesenteric arterial beds were perfused with a Krebs-solution and then exposed to increasing doses of the 3 different pressor agents. Compared to Wistar Kyoto controls, spontaneously hypertensive rats exhibited a clearly enhanced vascular response to norepinephrine and lysine vasopressin but not to angiotensin II. In animals with hypertension produced by angiotensin II continuously released by an osmotic micropump, the vascular response to lysine vasopressin and angiotensin II was increased while that to norepinephrine was unchanged. Rats rendered hypertensive by the administration of deoxycorticosterone and salt exhibited an increased vascular response exclusively to angiotensin II. In all models taken together, the magnitude of the vascular response to norepinephrine and lysine vasopressin was related to the blood pressure of the intact animal but this was not the case for angiotensin II. These observations are not incompatible with the concept that changes in the vascular response are predominantly due to structural changes of the vascular wall. However, they suggest that more specific alterations of responsiveness of the vascular smooth muscle must also take place.