05 May

Progesterone-Mediated Calcium Influx: DISCUSSION(2)


Unlike sper-matogenic cells, spermatozoa are not amenable to electro-physiological experiments, thus precluding characterization of the Ca2+ influx pathway on the basis of its biophysical properties. An added complication of trying to identify the involvement of VOCC in the P4-activated Ca2+ influx is the absence of pharmacological tools with sufficient selectivity and potency. Recently, however, a new pharmacological inhibitor, mibefradil, with VOCCT selectivity has been described. Using mibefradil and a different class of VOCCT inhibitor, pimozide, we sought to characterize the P4-activated Ca2+ influx pathway. birth control yasmin

Our results demonstrated a dose-dependent inhibition of the P4-activated Ca2+ influx by both mibefradil and pimozide (Fig. 4) but opposing effects on the P4-initiated AR (Figs. 6 and 7). Moreover, a third class of pharmacological agent (a calmodulin antagonist), calmidazolium, produced a more potent inhibition of the P4-activated Ca2+ influx (Fig. 4) but was without effect on the P4-initiated AR. Therefore, while these three structurally dissimilar drugs are potent inhibitors of the P4-ac-tivated Ca2+ influx, we cannot conclude from these data whether a T-type channel is involved in this Ca2+ influx pathway or the P4-initiated AR. Interpretations of the data that support or refute the involvement of VOCCT are discussed below.

Categories: Progesterone
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