We have demonstrated decreased microvascular sensitivity to norepinephrine during endotoxin shock possibly related to reduced sympathetic receptor activity (Baker et al.: Circ Shock 12:165-176, 1984). The response to other vascular controls such as arginine vasopressin (AVP) may also be altered. Reactivity of the left cremaster muscle microvessels of pentobarbital anesthetized Wistar rats was studied using videomicroscopy and videodensitometry. Femoral arterial pressure (Pm), dose response curves of vessel diameters to topical arginine vasopressin (10(-15) to 10(-6) M), FITC-albumin mean transit times, and plasma velocities were obtained. Escherichia coli endotoxin (6 mg/kg i.v., LD100) was infused over a 1-hr period. Parameter measurements were repeated at 30 min and 90 min post-endotoxin. Both Pm and plasma velocities progressively decreased. Arteriolar constriction and the mean transit times of FITC-labeled albumin progressively increased. The threshold dose for AVP averaged 10(-9) M at control and decreased to 10(-14) M post-endotoxin. Venular diameters were not altered by AVP. The AVP antagonist did not alter the microvascular diameter response to endotoxin but did block the responses to topical and endogenous AVP since arterial pressure and flow velocity decreased at a significantly greater rate than in rats without antagonist. Plasma AVP levels were significantly increased by endotoxin. Reduced alpha adrenergic sensitivity may unmask the responsiveness to AVP or increase the sensitivity of AVP receptors. Increased endogenous AVP may require a smaller exogenous concentration of AVP for constriction.