scholarly journals Thyrotropin-releasing hormone activates Na+/H+ exchange in rat pituitary cells

1987 ◽  
Vol 242 (2) ◽  
pp. 411-416 ◽  
Author(s):  
T J Hallam ◽  
A H Tashjian
Keyword(s):  
Calcium Ionophore ◽  
Thyrotropin Releasing Hormone ◽  
Free Calcium ◽  
Pituitary Cells ◽  
Ph Indicator ◽  
Ph Change ◽  
Cytosolic Ph ◽  
Releasing Hormone ◽  
Rat Pituitary Cells ◽  
Stimulation Of

The effects of thyrotropin-releasing hormone (TRH) and 12-O-tetradecanoylphorbol 13-acetate (TPA) on cytosolic pH (pHi) were studied on GH4C1 pituitary cells loaded with the fluorescent pH indicator bis(carboxyethyl)carboxyfluorescein (BCECF) and the fluorescent Ca2+ indicator quin2. TRH, which was minimally effective at around 10(-9) M, and TPA, 100 nM, produced very small elevations in pHi of about 0.05 pH units from the normal basal resting pHi of GH4C1 cells of around 7.05. The effects were more marked after acid-loading the cells using 1 micrograms of nigericin/ml. Preincubation with amiloride or replacing the extracellular Na+ with choline+ completely blocked the elevations stimulated by TRH or TPA, consistent with an activation of the Na+/H+ antiport mechanism. The effects were completely independent of the cytoplasmic free calcium concentration ([Ca2+]i). The calcium ionophore ionomycin produced an elevation in [Ca2+]i with no concomitant effect on pHi, and amiloride, although completely inhibiting the pH change stimulated by TRH, failed to affect the initial stimulated [Ca2+]i transient. Although the data are consistent with an elevation in pHi by TRH which is caused by stimulation of a protein kinase C and subsequent activation of the antiporter, the rapidity of the onset of the pHi response to TRH could not be mimicked by a combination of TPA and ionomycin. These results, together with previous findings which show that secretion can be mimicked by TPA and ionomycin, suggest that TRH-stimulated Na+/H+ exchange plays no part in the acute stimulation of secretion, but that TRH increases the pH-sensitivity of the antiport system during increased synthesis of prolactin and growth hormone.

scholarly journals Thyrotropin-releasing Hormone Stimulation of Prolactin Release from Clonal Rat Pituitary Cells

1981 ◽  
Vol 67 (6) ◽  
pp. 1769-1776 ◽  
Author(s):  
Marvin C. Gershengorn ◽  
Sylvia T. Hoffstein ◽  
Mario J. Rebecchi ◽  
Elizabeth Geras ◽  
Brian G. Rubin
Keyword(s):  
Thyrotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Releasing Hormone ◽  
Hormone Stimulation ◽  
Rat Pituitary ◽  
Rat Pituitary Cells ◽  
Stimulation Of

scholarly journals Alterations in the frequency and shape of Ca2+ fluctuations in GH4C1 cells induced by thyrotropin-releasing hormone and Bay K 8644

1995 ◽  
Vol 306 (2) ◽  
pp. 399-406 ◽  
Author(s):  
K D Brady ◽  
K A Wagner ◽  
A H Tashjian ◽  
D E Golan
Keyword(s):  
Fold Increase ◽  
Thyrotropin Releasing Hormone ◽  
Spike Frequency ◽  
Bay K 8644 ◽  
Pituitary Cells ◽  
Fall Time ◽  
Releasing Hormone ◽  
Spike Amplitude ◽  
Rat Pituitary Cells ◽  
Ca2 Channels

We have examined statistically the actions of thyrotropin-releasing hormone (TRH) and Bay K 8644, an L-type Ca(2+)-channel agonist, on the frequency and shape of cytosolic Ca2+ spikes in individual GH4C1 rat pituitary cells. TRH induced a brief (0-40 s) suppression of Ca2+ spikes followed by a period (40-200 s) of increased spike frequency. TRH treatment reduced the rate of rise and amplitude of Ca2+ spikes, and increased the rate of fall, relative to spontaneous spikes before treatment. TRH had no significant effect on the correlation between spike amplitude and the spike decay time constant tau, suggesting that the increased rate of fall was due to enhanced Ca2+ extrusion and not to decreased Ca(2+)-induced Ca2+ release. Bay K rapidly (t1/2 = 9-13 s) induced a 2-fold increase in the rate of rise of spikes with no change in the total rise time, leading to an increase in spike amplitude. It increased by 2-fold the fall time of spikes, as predicted solely by the previously observed relationship between spike amplitude and fall time. Bay K therefore appeared to increase the number of Ca2+ channels participating in each spike event without altering the kinetics of channel activation or deactivation, and without influencing Ca2+ extrusion. After addition of Bay K, the interval between spikes gradually (t1/2 approximately 100 s) increased, whereas the rate of rise remained constant and maximal. To explain these actions of TRH and Bay K, we postulate that a fraction of L-type Ca2+ channels are inactivated during each spike and must be re-activated in order to participate in a subsequent spike. We conclude further that the changes in spike frequency and profiles induced by these secretagogues are most consistent with a model in which TRH induces increases in both Ca2+ influx and efflux while Bay K induces a large increase in Ca2+ influx but has little effect on efflux.

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