Abstract

alpha 1-adrenoceptor sensitivity to noradrenaline has been studied in some arterial smooth muscles of rats and rabbits infected with T. brucei. In rabbits, a decrease in sensitivity of the arterial smooth muscles to noradrenaline was observed in the thoracic aorta, central ear but not renal arteries. No change in the sensitivity of the smooth muscles to histamine was observed. In rats, noradrenaline potency was reduced in the aorta, renal but not tail arteries. In both species, affinity of noradrenaline for alpha 1-adrenoceptors was significantly (P less than 0.05) reduced in arteries where the potency of noradrenaline was reduced. Prazosin KB values in infected animals were significantly (P less than 0.05) lower than controls. These results are interpreted to suggest either an alteration in the structure of alpha 1-adrenoceptors during an infection, or accumulation of some factor(s) in the receptor microenvironment that modulated binding of agonists and antagonists to the receptors during an infection with T. brucei. The possible role of reduced alpha 1-adrenoceptor affinity in the hypotension observed during an infection with T. brucei is discussed.

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