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Aim: To observe the expression of Leptin receptors (OB-R) in male rat anterior pituitary, and study the influence of Leptin on the level of intracellular free Ca2+ ([Ca2+]i) in the cultured growth hormone (GH) cell of male rat pituitary., Methods: RT-PCR method was used to observe the expression of Leptin receptors (OB-R) in male rat anterior pituitary. We used grade centrifuging method to get growth hormone (GH) cell, and [Ca2+]i in GH cell was examined by laser scanning confocal system., Results: OB-R mRNA were expressed in male rat anterior pituitary, including OB-R (common form), OB-Ra (short form) and OB-Rb (long form). There were about 70% or 80% GH cell by grade centrifuging. Leptin at 10(-8)mol/L could decrease the level intracellular free Ca2+ ([Ca2+]i) in cultured GH cell., Conclusion: There are three subtypes of Leptin receptors expressions in male rat anterior pituitary, and Leptin could reduce intracellular free Ca2+ level of GH cell markedly.

We found previously that ACh can significantly inhibit the proliferation of cultured human pituitary adenoma cells. In order to make a further investigation of the mechanism of the inhibitory effect of ACh on the proliferation of pituitary adenoma cells, we observed the levels of protein kinase C (PKC), [Ca(2+)](i) and cAMP/cGMP in cultured pituitary adenoma cells after treatment with ACh. The results demonstrate that (1) compared with control, PMA, a PKC activator, increased the activity of cytoplasm, membrane and total PKC in human pituitary adenoma cells. However, after a 15-min treatment with ACh (10 micromol/L), a significant reduction of the activity of cytoplasm, membrane and total PKC in human pituitary adenoma cells was observed, and the reduction effect could be blocked by atropine. (2) The level of [Ca(2+)](i) of single adenoma cells was found to decrease immediately on the addition of ACh (10 micromol/L), which could also be blocked by atropine. (3) ACh increased the amount of cAMP in the cytoplasm of human pituitary adenoma cells, but had no effect on that of cGMP. These data provide an important clue to explore the molecular mechanisms of the inhibitory effect of ACh on the proliferation of pituitary adenoma cells, and suggest that the modulating effect of ACh on the proliferation of pituitary adenoma cells results from the interactions of several cellular signaling pathways.