Vascular noradrenergic transmission and the effect of captopril on this transmission were examined in the blood perfused rat mesenteric vasculature in situ during the development of two-kidney, one clip Goldblatt hypertension. Three groups of rats including sham operated, 6-8 day hypertensive and 4-6 week hypertensive were studied. Mean blood pressures during anaesthesia were 90.0 +/- 2.0, 119.7 +/- 4.7 and 131.8 +/- 6.8 mmHg in the three groups, respectively. Mesenteric vasoconstrictor responses to norepinephrine were significantly potentiated in both of the hypertensive groups relative to the sham group. Mesenteric vasoconstrictor responses to nerve stimulation were similar in the sham and 6-8 day hypertensive groups. However, responses to nerve stimulation were significantly potentiated in the 4-6 week hypertensive group relative to the sham group. Captopril (1 mg/kg, i.v.) lowered mean blood pressure in all groups, equalizing blood pressure in the 6-8 day hypertensive and sham groups. However, the blood pressure in the 4-6 week hypertensive rats remained significantly elevated after 1 mg/kg captopril. An additional dose of captopril did not lower blood pressure further in this group. Mesenteric vasoconstrictor responses to nerve stimulation and norepinephrine in the three groups were minimally affected by captopril, with significant differences between control and captopril-treated responses occurring randomly at a point or two in a dose-response or frequency-response curve for a given group. The differences in vascular responsiveness to nerve stimulation and norepinephrine between the hypertensive and sham groups continued to be evident after captopril.(ABSTRACT TRUNCATED AT 250 WORDS)