Soman (pinacolyl methylphosphonofluoridate) not only increases acetylcholine levels by inhibiting cholinesterases, it also alters the levels of some other neurotransmitters including norepinephrine, dopamine, and serotonin. Soman also causes an alteration in the activities of the enzymes metabolizing norepinephrine when it is administered to animals. Because these alterations may result from indirect effects on the enzymes, the effects of in vitro application of soman on catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) activities in rabbit tissues were investigated. Enzyme activities were determined in rabbit lung, liver, cerebellum, cerebrum, brain stem, mesenteric artery, pulmonary artery, renal artery, central ear artery, thoracic aorta, and diaphragm. MAO and COMT activities were not affected by soman in any tissues tested, except the lung and liver, where the activity of COMT was increased (p less than 0.05). Thus, reported effects of soman in vivo on norepinephrine, dopamine, or serotonin concentrations, and MAO and COMT activities do not seem to result from direct effects on the activities of these amine-metabolizing enzymes.

Ricin is a toxic lectin that inhibits protein synthesis. Because ricin decreases arterial pressure and causes cardiovascular collapse, its effects on the vascular neuroeffector system were investigated. Rabbits were given either of two doses of ricin, and then norepinephrine (NE) release from aorta to transmural stimulation, NE uptake into aorta, NE content of aorta, monoamine oxidase activity, and catechol-O-methyl transferase activity in aorta were determined 18 hours, 4 days or 7 days later. Norepinephrine uptake and enzyme activities in the aorta were not altered by ricin administration. Norepinephrine release and content of aorta were increased at most time periods following ricin administration, significantly so for NE content at 4 days and for release at 18 hours following the lower dose of ricin. We conclude that the mechanisms involved in the release of NE from sympathetic nerves in the vasculature are not impaired by ricin administration, but rather show changes that indicate increased compensatory activity.

Effects of terbutaline applied in vivo or in vitro on alpha-adrenergic receptors in the rabbit aorta in normal and Ca(2+)-free solution, and on basal, high potassium-, and phenylephrine-stimulated Ca2+ uptake into aorta were investigated. Three day terbutaline administration (25 mg/kg, subcutaneously three times daily) to rabbits increased the pKB for phentolamine in aorta rings (control 7.3 +/- 0.2, n = 9; terbutaline 7.8 +/- 0.2, n = 15). It also depressed phenylephrine-stimulated contractions of aorta rings in Ca(2+)-free but not those in normal Krebs solution. It did not significantly depress the basal, or phenylephrine-evoked Ca2+ influx into aorta rings, but decreased high potassium-induced Ca(2+)-influx (control 0.58 +/- 0.05 mumoles/g aorta; n = 3, terbutaline 0.41 +/- 0.06 mumoles/g aorta, n = 3). In vitro application of 50 microM terbutaline did not significantly alter phenylephrine-stimulated contractions of aorta rings in Ca(2+)-free Krebs solution or significantly depress basal or phenylephrine-induced Ca2+ influx into aortas, but did decrease high potassium-stimulated Ca(2+)-influx. Thus, 3-day terbutaline administration increased the affinity of alpha-adrenergic receptors for phentolamine and had a tendency to increase contractions of aorta rings to phenylephrine. It also decreased high potassium-stimulated Ca2+ influx, and depressed phenylephrine-induced contractions in Ca(2+)-free Krebs solution, while in vitro terbutaline application also decreased potassium-induced Ca2+ influx.