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Contractions were elicited by field stimulation and norepinephrine in canine cutaneous arteries in Krebs-bicarbonate and Krebs-Tris media and the effect of angiotensin II, 1 x 10(-7) M, on these responses was determined. The absolute magnitude of the field stimulation responses was much greater in the bicarbonate buffer. Angiotensin caused potentiation in both media of the responses to field stimulation and norepinephrine. In Triss buffer with 5 mM calcium the responses to field stimulation and norepinephrine were greater than in 2.5 mM calcium, however; the degree of potentiation caused by angiotensin was similar at both calcium concentrations. The angiotensin potentiating effect in vitro appears to involve a postsynaptic action of the polypeptide which is not affected by alteration of calcium concentration or the medium.

Sixteen dogs were instrumented for recording mean arterial blood pressure (MAP) and blood flow from the left renal artery (RBF) and for intra-arterial infusions of norepinephrine (NE) and angiotensin II (ANG II). Nine dogs (group 1) were studied while normotensive and also when hypertensive. Seven control dogs (group 2) were studied only when normotensive. In a control session conducted in group 1 and at weekly intervals for up to 6-12 wk after the right renal artery was clipped, infusions of NE and ANG II were given intra-arterially to produce graded decreases in RBF. Group 2 was studied similarly in a control session and 4-7 wk later. Regressions of the values of percent change RBF (arc sin transformation) on the concentrations of NE and ANG II in renal arterial blood estimated the renal vascular reactivity of the hypertensives' contralateral kidney and the normotensives' kidney. In group 1, during the postclipping intervals when MAP and plasma renin activity were increased, the renal vascular reactivity to NE, but not to ANG II was increased. This was based on the significant elevation above the X axis in the postclipping regressions. In group 2, MAP, plasma renin activity, and renal vascular reactivity to NE and ANG II were unchanged over the 4- to 7-wk interval of study. These results indicate that the contralateral kidney develops an increased vascular reactivity to NE but not to ANG II in Goldblatt hypertension.