The effects of neurotoxic insecticides on central cholinergicallymediated hypertension

Malathion by itself produced a double-phased blood pressure response in the anaesthetized rat. Immediately after intravenous injection of malathion there was a shortlasting hypotension (up to 90 sec), followed by a prolonged hypertension similar to that observed after intravenous injection of phisostigmine to rats. The hypotensive response is probably due to accumulation of acetylcholine after cholinesterase inhibition by malathion. The hypertensive response to malathion is due to secondary activation of adrenergic mechanisms in the central nervous system. Malathion coused dose-dependent inhibition of the central cholinergically mediated hypertension in rats produced by intravenous injection of physostigmine. Both the degree and duration of hypertension were equally depressed. These experiments indicate that development of central cholinergically-mediated hypertension is possible only in the presence of functionally competent cholinesterase. Both lindan and permethrine also depress the central cholinergically mediated hypertension produced by intravenous injection of physostigmine. Thus, all the three neurotoxic insecticides can inhibit transmitter interaction which is the basis of central cholinergically mediated hypertension, but not necessarily by the same mechanisms.