(A) Vessel contraction induced by extracellular potassium was reduced to 61% of the WT response (n = 12 WT and n = 8 KO vessels, *P < 0.05). No change in contraction after potassium-induced depolarization was observed after treatment with captopril (n = 8 WT and n = 9 KO vessels). (B) Vessel contraction induced by angiotensin II was significantly blunted in mutant arteries. Pretreatment with captopril significantly improved angiotensin II–induced contractile responses (n = 12 WT and n = 9 KO vessels of untreated animals, ***P < 0.0001, KO untreated vs. WT untreated; n = 8 WT and n = 9 KO vessels of captopril-treated animals, ^#P < 0.05 KO treated vs. KO untreated). (C and D) Isolated arteries stimulated with increasing concentrations of phenylephrine. Arrows indicate applications of phenylephrine. (D) Statistical analysis of phenylephrine and captopril responses. Captopril treatment improved responses of the KO vessels (n = 12 WT and n = 8 KO vessels of untreated animals, *P < 0.05, ***P < 0.001, KO untreated vs. WT untreated; n = 8 WT and n = 0 KO vessels of captopril-treated animals, ^##P < 0.01 KO treated vs. KO untreated). (E) Contractile responses to phenylephrine stimulation of mesenteric arteries. Arterial rings from KO animals showed a significant enhancement in contractility after AT₁ receptor blockade by losartan (n = 7 WT and n = 8 KO vessels from untreated animals, ***P < 0.001, KO untreated vs. WT untreated; n = 10 WT and n = 8 KO vessels from losartan-treated animals, ^##P < 0.01, ^###P > 0.001, KO treated vs. KO untreated). (F) pCa-force relationships in skinned femoral arteries. Maximal Ca²⁺-induced contraction was blunted in KO arteries, and the pEC₅₀ values significantly shifted leftward in KO skinned arteries (n = 12 WT and n = 8 KO vessels, *P < 0.05, **P < 0.01, ***P < 0.001, KO vs. WT). Error bars indicate ± SEM.