We examined the possibility that changes of the mesenteric resistance play a role in the development of hypertension in spontaneously hypertensive rats (SHRs). Genetically hypertensive (Okamoto) and normotensive Wistar rats (WKYs) were studied after oral treatment for 6 weeks with 100 mg of captopril dissolved in 500 ml water daily. The paired control groups received water. During this treatment, the systolic blood pressure was measured non-invasively with a W+W/BP recorder after preheating of the conscious animals. After these procedures, the rats were anaesthetized, the baseline mesenteric blood flow (MBF, volts) was recorded with a pulsed Doppler flow-meter and the mean arterial blood pressure (MAP) heart rate and mesenteric vascular resistance were also measured. The captopril treatment failed to alter the body weight of SHRs and WKY. In the normotensive group, the MAP was not altered, but the MBF was moderately increased. In contrast, the MAP of the SHRs was markedly decreased, and the MBF was significantly increased. The basal MBF of the SHRs was significantly lower than that of the WKYs. These data suggest that the renin-angiotensin system may exert a tonic vasoconstrictor action on the mesenteric vasculature in SHRs. The increased mesenteric vascular resistance therefore plays an important role in the increased total peripheral resistance in the development of hypertension in SHRs.