| dc.description.abstract | The anti-hypertensive drug prazosin brings about a blockage of alpha adrenoceptors which is thought to be different from that caused by conventional alpha adrenoceptor blocking agents. Similarly unlike conventional alpha adrenoceptor blocking agents, prazosin does not cause tachycardia or rennin release in dogs. In this work, the possible mechanism of action of prazosin was further investigated by studying the effect of the drug on isolated tissue preparations like the guinea-pig atria, trachea and ileum, the rabbit sorts, the rat was deferens and the rat mesenteric arteries.
At low concentrations (1.7 x 10¯⁸M ‒ 1.4 x 10¯⁷M) prazosin caused an increase in the rate and force of contraction of the atria. At higher concentrations (1.3 x 10¯⁵ ‒ 2.1 x 10¯⁴M), the rate and force of atria were decreased. Prazosin also antagonized the positive inotropic and chronotropic effects of isoprenaline. The drug lacked beta adrenoceptor blocking activity both in the atria and trachea but possessed slight quinidine-like effect.
Prazosin had no pre-synatic alpha adrenoceptor blocking activity in the guinea-pig ileum and the rat was deferens. Its action was specific at the post – synaptic alpha adrenoceptor sites. Like other alpha adrenoceptor blockers for example, phentolesine and phenoxybenzamins, prazosin blockage is at the µ -adrenoceptor site and not at a point distal to the receptor as suggested by earlier studies. | en_US |
