Figure 2. (A) Halothane-induced vasoconstriction in a pressurized mesenteric resistance artery over the concentration range of 0.11–2.64 mM (0.25–10 vol% at 37 degrees Celsius). The bars indicate the duration of the halothane application. The halothane-induced constrictions are shown above on an expanded time scale. ID = inside diameter of the vessel; OD = outside diameter of the vessel. (B) The concentration-response relationship for the vasoconstricting effect of halothane. The responses at each concentration represent the peak changes in OD normalized to the maximum in each vessel (n = 8). The mean data (plus/minus SEM) were fit with a Hill equation (solid line) yielding an EC⁵⁰of 0.46 mM (1.5 vol% at 37 degrees Celsius); the cooperativity factor was 1.6. (C) The vasoconstricting responses to halothane (hal, 1.43 mM) and caffeine (caf, 25 mM) are unaffected by the reduction in bath [Calcium²+] from 1.8 mM to 250 nM (low Calcium sup 2+), whereas the vasoconstriction resulting from Potassium sup +-induced membrane depolarization (Potassium sup +, [K sup +]^bath= 40 mM) is nearly abolished. (D) In contrast, ryanodine (ryo, 10 micro Meter) had no effect on the Potassium sup +-induced constriction but, after an initial priming dose of caffeine (see text), completely blocked the vasoconstricting responses to both caffeine and halothane.