Abstract

Treatment of GH(3) pituitary cells with p-chloromercurybenzenesulfonate (PCMBS) increased the cytosolic Ca(2+) concentration ([Ca(2+)](i)). This effect was reversed by dithiothreitol and blocked by L-type Ca(2+) channel antagonists or Na(+) removal. PCMBS increased membrane conductance and depolarized the plasma membrane. Apart from minor effects on K(+) and Ca(2+) channels, PCMBS increased (6 times at -80 mV) an inward Na(+) current whose properties were similar to those of a background Na(+) conductance (BNC) described previously, necessary for generation of spontaneous electrical activity. In rat lactotropes and somatotropes in primary culture, PCMBS also produced a Na(+)-dependent [Ca(2+)](i) increase, whereas little or no effect was observed in thyrotropes, corticotropes, and gonadotropes. The Na(+) conductance elicited by PCMBS in somatotropes seemed to be the same as that stimulated by the hypothalamic growth hormone (GH)-releasing hormone, which regulates membrane excitability and GH secretion. The BNC studied here could play a physiological role, regulating excitability and spontaneous activity, and explains satisfactorily the [Ca(2+)](i)-increasing actions of the mercurials reported previously in several excitable tissues.

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