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Papers In Press, published online ahead of print February 26, 2002
Endocrinology and Reproduction Research Branch, NICHD, Bethesda, MD 20892-4510
Corresponding Author: stankos{at}helix.nih.gov
It is well established that G protein-coupled receptors stimulate nitric oxide-sensitive soluble guanylyl cyclase by increasing intracellular Ca2+ and activating Ca2+-dependent nitric oxide synthases. In pituitary cells, receptors that stimulated adenylyl cyclase, growth hormone-releasing hormone, corticotropin-releasing factor and thyrotropin-releasing hormone, also stimulated calcium signaling and increased cGMP levels, whereas receptors that inhibited adenylyl cyclase, endothelin-A and dopamine-2, also inhibited spontaneous calcium transients and decreased cGMP levels. However, receptor-controlled up- and down-regulation of cyclic nucleotide accumulation was not blocked by abolition of Ca2+ signaling, suggesting that cAMP production affects cGMP accumulation. Agonist-induced cGMP accumulation was observed in cells incubated in the presence of various phosphodiesterase and soluble guanylyl cyclase inhibitors, confirming that Gs-coupled receptors stimulated de novo cGMP production. Furthermore, cholera toxin, an activator of Gs, forskolin, an activator of adenylyl cyclase, and 8-Br-cAMP, a permeable cAMP analog, mimicked the stimulatory action of Gs-coupled receptors on cGMP production. Basal, agonist-, cholera toxin-, and forskolin-stimulated cGMP production, but not cAMP production, was significantly reduced in cells treated with H89, a protein kinase A inhibitor. These results indicate that coupling of seven plasma membrane-domain receptors to adenylyl cyclase signaling pathway provides an additional, calcium-independent and cAMP-dependent mechanism for modulating soluble guanylyl cyclase activity in pituitary cells.
J. Biol. Chem, 10.1074/jbc.M112439200
Submitted on December 28, 2001
Revised on February 21, 2002
Accepted on February 26, 2002
Calcium-independent and cAMP-dependent modulation of soluble guanylyl cyclase activity by G protein-coupled receptors in pituitary cells
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