PMID- 7956933 OWN - NLM STAT- MEDLINE DCOM- 19941216 LR - 20181130 IS - 0013-7227 (Print) IS - 0013-7227 (Linking) VI - 135 IP - 5 DP - 1994 Nov TI - Differential regulation of Ca2+ homeostasis in ovine large and small luteal cells. PG - 2099-108 AB - This study was undertaken to characterize differences in Ca2+ homeostasis between small and large ovine luteal cells. Although increasing extracellular pH (pHex) resulted in increases in intracellular calcium ([Ca2+]in) in both cell types, the large cells exhibited a greater sensitivity, suggesting that distinct [Ca2+]in regulatory mechanisms with distinct pH optima are operating in the two cell types. The sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase inhibitors thapsigargin (TG) and cyclopiazonic acid (CPA) increased [Ca2+]in in both cell types. Treatment of small cells with CPA resulted in transient increases in [Ca2+]in, whereas CPA produced sustained increases in [Ca2+]in in large cells. In small cells, pretreatment with CPA prevented further increases in [Ca2+]in in response to TG and vice versa. In large cells, TG pretreatment precluded further increases in [Ca2+]in with either prostaglandin F2 alpha (PGF2 alpha) or CPA. In contrast, after CPA pretreatment, PGF2 alpha or TG induced further increases in [Ca2+]in in large cells. This suggests that a TG-sensitive, CPA-insensitive Ca2+ pool is present in large cells but not in small cells. Neither Na+ removal nor KCl addition affected [Ca2+]in in either cell type, indicating that neither the Na+/Ca2+ exchanger nor voltage-dependent Ca2+ channels are involved in Ca2+ homeostasis in these cells. Addition of the calcium antagonist, LaCl3 (La3+), produced a gradual increase in [Ca2+]in in large cells but no changes in [Ca2+]in in small cells. Additionally, treatment with increasing concentrations of 4-bromo-A23187 resulted in titratable increases in [Ca2+]in that are greater in large than small cells, suggesting that small cells possess a higher Ca(2+)-buffering capacity than large cells. Progesterone secretion by large cells was significantly inhibited at alkaline pHex. In the presence of PGF2 alpha, progesterone secretion exhibited a distinct pH optimum of 7.0. In contrast, pHex did not affect secretion of progesterone in small cells under any of the conditions tested. TG, CPA, and La3+ all reduced secretion of progesterone in large, but not small, cells. These results demonstrate that ovine large and small luteal cells differ in regulation of [Ca2+]in homeostasis, and that treatments that increase [Ca2+]in decrease progesterone secretion in large cells but have no effect in small cells.(ABSTRACT TRUNCATED AT 400 WORDS) FAU - Martinez-Zaguilan, R AU - Martinez-Zaguilan R AD - Department of Biochemistry, University of Arizona, Tucson 85724. FAU - Wegner, J A AU - Wegner JA FAU - Gillies, R J AU - Gillies RJ FAU - Hoyer, P B AU - Hoyer PB LA - eng GR - HD-00907/HD/NICHD NIH HHS/United States GR - HD-26778/HD/NICHD NIH HHS/United States GR - HL-07249/HL/NHLBI NIH HHS/United States GR - etc. PT - Comparative Study PT - Journal Article PT - Research Support, U.S. Gov't, Non-P.H.S. PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Endocrinology JT - Endocrinology JID - 0375040 RN - 0 (Calcium Channels) RN - 0 (Carrier Proteins) RN - 0 (Indoles) RN - 0 (Sodium-Calcium Exchanger) RN - 0 (Terpenes) RN - 4G7DS2Q64Y (Progesterone) RN - 67526-95-8 (Thapsigargin) RN - B7IN85G1HY (Dinoprost) RN - SY7Q814VUP (Calcium) RN - X9TLY4580Z (cyclopiazonic acid) SB - IM MH - Animals MH - Calcium/*metabolism MH - Calcium Channels/analysis/physiology MH - Carrier Proteins/physiology MH - Corpus Luteum/*cytology/*metabolism/physiology MH - Dinoprost/pharmacology MH - Female MH - Homeostasis/drug effects/*physiology MH - Hydrogen-Ion Concentration MH - Indoles/pharmacology MH - Progesterone/metabolism MH - Sheep/*physiology MH - Sodium-Calcium Exchanger MH - Terpenes/pharmacology MH - Thapsigargin EDAT- 1994/11/01 00:00 MHDA- 1994/11/01 00:01 CRDT- 1994/11/01 00:00 PHST- 1994/11/01 00:00 [pubmed] PHST- 1994/11/01 00:01 [medline] PHST- 1994/11/01 00:00 [entrez] AID - 10.1210/endo.135.5.7956933 [doi] PST - ppublish SO - Endocrinology. 1994 Nov;135(5):2099-108. doi: 10.1210/endo.135.5.7956933.