Abstract
Experiments were performed to get further insights into the erectogenic mechanism of prostaglandin Et (PGEI), which was compared to that of papaverine (PAP). PGEI and PAP were effective in abolishing the contraction induced by N-ethylmaleimide (NEM), an adenylate cyclase blocker. However, preincubation with PGEI but not with PAP markedly attenuated the amplitude of adrenergic nerve mediated contraction following prolonged electrical field stimulation. Preincubation with PGEI was ineffective in counteracting the increase in tension due to exogenous norepinephrine. These data together with previous studies corroborate the hypothesis that in the presence of PGEI a dual erectogenic mechanism takes place in modulating the cyclic-adenosine-monophosphate metabolism of the cavernous smooth muscle cell as well as the release of norepinephrine from the sympathetic terminal.
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