SUMMARY The purpose of this study was to determine if any changes occurred in the basal and stimulated rates of oxygen consumption and lactate production of thoracic aortas from spontaneously hypertensive rats (SHR) and renal and deoxycorticosterone acetate (DOCA)-salt hypertensive rats, and, if so, whether these changes were similar in these three models of hypertension. Rings of thoracic aorta were placed in an isothermic (37°C) muscle bath, and isometric tension development, oxygen consumption, and lactate production were measured. The results indicated that under basal conditions oxygen consumption, but not lactate production, was higher in aortas from all three hypertensive models; the elevation above control was greatest in the renal model (95%) and smallest in SHR (34%). On stimulation with 60 mM KCI, a significant increase in oxygen consumption above basal value occurred in all aorta samples (p < 0.05); however, lactate production was increased above basal only in aortas from hypertensive animals. Only in aortas from renal and DOCA-salt models was the rate of oxygen consumption during stimulation significantly greater than that of their normotensive controls (p < 0.05). Developed active stress in response to KCI was the same in all groups, and when the change in lactate production or oxygen consumption was expressed relative to the amount of active stress developed, no differences were observed. These results suggest that, 1) compared to values in aortas from normotensive animals, only the basal rate of oxygen consumption is higher; 2) this higher level of basal metabolic activity is not associated with an alteration in the metabolic cost of force development; and 3) there are quantitative differences between the models with regard to their metabolic characteristics. ( Received July 24, 1984; accepted July 22, 1985. aortas from renal hypertensive rats. These studies suggested that an increase of metabolic activity occurred in association with hypertension; however, a limitation of these studies was that the contractile state of the tissue was not determined when the metabolic parameters were measured and, therefore, the observed elevation in metabolic rate may have been due to a higher level of contractile activity in the tissue from the hypertensive animals. Arner and Hellstrand 3 and McMahon and Paul 4 improved these measurements by using an isolated tissue bath in which force, oxygen consumption, and lactate production were measured simultaneously to study aortas from spontaneously hypertensive rats (SHR) and aldosterone-salt hypertensive rats, respectively.A comparison of these two studies 3 4 indicates that the metabolic changes associated with these two hypertensive models may not be the same.