Effect of subchronic administration of captopril on alpha1-adrenoceptor agonist'induced contraction of isolated aorta in rat

Angiotensin II is a major endocrine hormone that affects directly both vascular smooth muscle and endothelial cells. Since vascular reactivity to angiotensin II changes in more physiological and pathophysiological conditions, the present study was performed to investigate the effect of intraperitoneal administration of angiotensin-converting enzyme inhibitor and captopril [30 and 50 mg kg 1, once daily for 8 weeks] on contractile response of rat aorta. After 8 weeks, the treated rats were anesthetized, their thoracic aortas were excised and placed in a Petri dish filled with Krebs solution for recording of contraction and relaxation response. The obtained results showed that captopril did not modify body weight gain and food or water intake but contractile response of aortic rings to phenylephrine in treated rats with 30 and 50 mg kg 1 captopril, in the presence of endothelium, decreases about 11-22% and 29-32% [P<0.05-P<0.01], respectively, when compared to the controls. Denuded aortic rings from 30 and 50 mg kg 1 captopril-treated rats showed 11-21% and 7-11% decrease in contractile response, respectively. There was a marked endothelium-dependent relaxation response to acetylcholine in 50 mg kg 1 captopril-treated rats compared to the controls [P<0.05]. Endothelium-independent relaxation response to isosorbide dinitrate showed no significant difference in all groups. According to these results, it is suggested that captopril exerts its relaxant effect directly and/or indirectly through endothelium by production and releasing of endothelium-derived relaxing factors

Modification of nifedipine inhibitory effect on calcium spike and L - Type calcium current by ethanol in F1 neuron of helix aspersa

There is strong evidence demonstrating that nifedipine dissolved in ethanol selectively inhibits only L-type Ca2+ current. In addition, acute ethanol exposure reduces voltage-dependent calcium currents. In the present study, we investigated the antagonistic effect of fixed concentration of nifedipine dissolved in different concentration of ethanol on L-type Ca2+ current. In a Na +/- K+ free solution, nifedipine dissolved in 60 and 120 mM ethanol decreased resting membrane potential of Ca2+ spikes and caused a significant reduction in amplitude, duration and an increase in threshold of Ca2+ spikes. Furthermore, Ca2+ current was inhibited by ethanol in a concentration-dependent manner, so that the reduction of L-type Ca2+ current by nifedipine/60 and 120 mM ethanol was statistically significant. Meanwhile, ethanol concentration-dependent response of Ca2+ currents was observed at its late component in more positive potentials. These results may be consistent with ethanol-dependent inhibition of L-type Ca2+ currents and ethanol-dependent enhancment of a Ca2 +/- activated potassium current