Regulation of Receptor‐Operated and Depolarization‐Operated Ca²⁺ Influx in Anterior Pituitary Tissue

Abstract

Calcium-mobilizing receptors appear to induce calcium movements from both intracellular and extracellular sites.' The mechanism of the Ca2+ influx component remains enigmatic, being probably independent from voltage-sensitive Caz+ channels because it occurs in both excitable and nonexcitable cell types. Several hypotheses for the mechanism have been proposed, including actions of inositol tetrakis-and tris-phosphates, Ca2+-activated Ca2+ channels, and the Na+ /Ca2+One further possibility is that the concomitant activation of protein kinase C (PKC) by such receptors may have a role in signaling Ca2+ influx.Luteinizing hormone-releasing hormone ( LHRH) and thyrotrophin-releasing hormone (TRH) both act through this class of receptor, causing calcium mobilization and phosphoinositide hydrolysis. The Ca-influx processes activated by these hormone receptors in anterior pituitary tissue can be measured by a rapid "Ca2+ influx assay, involving quenching, filtration, and washing with EGTA-containing medium.' The 4sCa2+ influx induced by LHRH, TRH, or K + was maximal by 30 seconds and was concentration dependent, with peak increases over basal "Ca2+ accumulation of 83 2 8% (100 nM LHRH), 162 * 14% (300 nM TRH), and 232 2 30% (60 mM

Biological activity of some thyrotrophin-releasing hormone analogues substituted at the 2 position

“…Since the first hypothalmic releasing factor, pyroglutamylhistidyl proline amide ( pGlu-His-Pro-amide; thyroid hormone-releasing hormone, TRH), was identified [ 1, 21, there have been a number of reports that this tripeptide occurs in other regions of the central nervous system [3] and in certain peripheral tissues [4, 51. Recently, a peptide with a related structure, pGlu-Glu-Pro amide, was identified in rabbit prostate [6] and it was shown to occur also in rabbit and human semen 17, 81. Since rat portal blood has been reported to contain three TRH-immunoreactive components (91, of which only one corresponded chromatographically to TRH, it has become of interest to investigate whether TRH-related peptides such as pGlu-Glu-Pro amide occur in brain.…”

Proceedings of the Physiological Society, 5‐6 January 1990, Liverpool Meeting: Communications

“…It is possible that not only diacylglycerols, but also AA may be important in the physiological activation of certain PKC isoforms. Luteinizing hormone-releasing hormone (LHRH) and thyrotrophin-releasing hormone (TRH) both induce 45Ca2" influx into rat anterior pituitary tissue, but utilize different routes, which are regulated differentially by protein kinase C (Mitchell et al 1989b). The 45Ca2" influx induced by LHRH is largely sensitive to nimodipine (suggesting that it may occur indirectly through voltage-sensitive Ca2+ channels), whereas the response to TRH is resistant to blockers of the known voltagesensitive Ca21 channels or of the Na+/Ca2+ exchanger (Mitchell et al 1989b).…”

“…Luteinizing hormone-releasing hormone (LHRH) and thyrotrophin-releasing hormone (TRH) both induce 45Ca2" influx into rat anterior pituitary tissue, but utilize different routes, which are regulated differentially by protein kinase C (Mitchell et al 1989b). The 45Ca2" influx induced by LHRH is largely sensitive to nimodipine (suggesting that it may occur indirectly through voltage-sensitive Ca2+ channels), whereas the response to TRH is resistant to blockers of the known voltagesensitive Ca21 channels or of the Na+/Ca2+ exchanger (Mitchell et al 1989b). Receptor-activated Ca2+ entry (perhaps such as the response to TRH here) may involve a synergistic action of inositol 1,3,4,5-tetrakisphosphate (InsP4) and inositol 1,4,5-trisphosphate (InsP3) (A. P. The rapid influx of 45Ca2+ into prisms of tissue from male rats was measured in 30 s incubations with stimuli, as described previously (Mitchell et al 1989 a).…”