EFFECTS OF ADRENALECTOMY AND CHEMICAL SYMPATHECTOMY ON PRESSER AND TACHYCARDIC RESPONSES TO DIPHENYLENEIODONIUM

We have reported that diphenyleneiodonium (DPI), a flavoprotein inhibi tor, caused presser and tachycardic responses by indirectly activating the sympathetic nervous system. In this study, bilateral adrenalectom y and chemical sympathectomy by 6-hydroxydopamine (6-OH-DA) were used to examine the contributions of the adrenal medullae and sympathetic n erve terminals to the presser and tachycardic responses to DPI in pent obarbital-anesthetized rats. Intravenous bolus injections of DPI (0.05 -1.6 mg/kg) caused dose-dependent increases in mean arterial pressure and HR. Neither bilateral adrenalectomy nor pretreatment (26 hr earlie r) with 6-OH-DA (100 mg/kg, i.p.) significantly affected the dose-MAP curve of DPI, although 6-OH-DA but not adrenalectomy slightly and sign ificantly shifted the dose-HR curve to the right without affecting the maximum. The combination of bilateral adrenalectomy and 6-OH-DA reduc ed the maximum mean arterial pressure and HR responses to DPI by 71% a nd 35%, respectively. Intravenous bolus injection of DPI (1.6 mg/kg) c aused increases in plasma norepinephrine, epinephrine and dopamine of more than 2, 2 and 0.1 ng/ml, respectively. Although bilateral adrenal ectomy reduced the DPI-induced increases of norepinephrine, epinephrin e and dopamine by 85%, 100% and 93%, and and 6-OH-DA reduced these inc reases by 67%, 48% and 61%, respectively, the combination of adrenalec tomy and 6-OH-DA abolished the increases in catecholamines. These resu lts show that sympathetic nerve terminals and sympathoadrenals play ov erlapping roles in the presser and tachycardic responses to DPI, with the adrenal medullae as the primary source of plasma catecholamines re leased by DPI.