This experiment was designed to determine the microvascular responses to the two known naturally occurring vasoconstrictors, norepinephrine (NE) and vasopressin, at known levels of central vasomotor activity before, during and after halothane anesthesia. The responses to topical application of NE and vasopressin were studied in the microvasculature of the mesentery and cremaster muscle, using microscopic methods. Neural (CNS) stimulation was accomplished through electrodes chronically implanted in vasoactive sites of the forebrain and midbrain. The increase in blood pressure in response to CNS stimulation was decreased during halothane anesthesia (32.4 +/- 5.4 per cent before and 24.7 +/- 6.1 per cent during; P less than 0.001). There was no significant change in the steady-state diameter of the microvasculature under study during or after halothane anesthesia. Marked abatement of arteriolar vasoconstriction in response to CNS stimulation was seen prior to halothane. However, the same target vessel showed increased constriction in response to topically applied NE (from 32.3 +/- 4.7 to 53.2 +/- 7.8 per cent; P less than 0.01) during halothane anesthesia. By contrast, the response to vasopressin decreased (from 42.4 +/- 5.7 to 1.0 +/- 6 per cent; P less than 0.001) with halothane. The precise mechanism(s) underlying the described hypersensitivity to NE and hyposensitivity to vasopressin in the same vascular structure during halothane anesthesia remains undetermined.