PMID- 8304422
OWN - NLM
STAT- MEDLINE
DCOM- 19940310
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 266
IP  - 1 Pt 1
DP  - 1994 Jan
TI  - Ca2+ stores in smooth muscle cells: Ca2+ buffering and coupling to AVP-evoked 
      inositol phosphate synthesis.
PG  - C276-83
AB  - Cytosolic Ca2+ concentrations ([Ca2+]cyt) and [3H]inositol phosphates ([3H]InsP) 
      were correlated while decreasing the Ca2+ content of sarcoplasmic reticulum (SR) 
      stores in cultured A7r5 cells at rest and after activation with 8-arginine 
      vasopressin (AVP). Decreasing Ca2+ influx by reducing extracellular Ca2+ or by 
      treatment with verapamil had no effect on resting [Ca2+]cyt but significantly 
      inhibited the AVP-evoked Ca2+ transients (delta Ca2+). Neither treatment affected 
      basal [3H]InsP, but both treatments increased AVP-evoked synthesis of [3H]InsP. 
      Likewise, basal [3H]InsP were unaffected by brief (10-30 s) exposures to 
      thapsigargin (TG), while AVP-induced [3H]InsP synthesis was significantly 
      augmented. Similar treatment with TG rapidly increased resting [Ca2+]cyt and 
      decreased SR Ca2+ by 9-25% as manifested by decreased delta Ca2+. By contrast, 
      ryanodine induced slow increases in [Ca2+]cyt that stabilized within 30 min; 
      subsequent AVP-induced delta Ca2+ were attenuated by 50%. Ryanodine had no effect 
      on either basal or stimulated [3H]InsP levels. Agents that elevate adenosine 
      3',5'-cyclic monophosphate (cAMP) such as caffeine, 8-bromo-cAMP, and forskolin 
      inhibited AVP-evoked [3H]InsP formation. These observations provide further 
      characterization of a communication pathway between the AVP-sensitive Ca2+ stores 
      in the SR and the plasmalemmal enzyme system involved in the synthesis of 
      inositol 1,4,5-trisphosphate. This pathway is manifested by an inverse 
      relationship between the Ca2+ content of an AVP-sensitive, ryanodine-insensitive 
      SR Ca2+ store and evoked [3H]InsP synthesis and may represent an important 
      component in the tonic regulation of resting [Ca2+]cyt and vasoconstrictor- and 
      hormone-evoked SR Ca2+ release.
FAU - Berman, D M
AU  - Berman DM
AD  - Department of Physiology, University of Maryland School of Medicine, Baltimore.
FAU - Sugiyama, T
AU  - Sugiyama T
FAU - Goldman, W F
AU  - Goldman WF
LA  - eng
GR  - HL-43091/HL/NHLBI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
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  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Buffers)
RN  - 0 (Inositol Phosphates)
RN  - 0 (Terpenes)
RN  - 113-79-1 (Arginine Vasopressin)
RN  - 15662-33-6 (Ryanodine)
RN  - 3G6A5W338E (Caffeine)
RN  - 67526-95-8 (Thapsigargin)
RN  - E0399OZS9N (Cyclic AMP)
SB  - IM
MH  - Arginine Vasopressin/*pharmacology
MH  - Buffers
MH  - Caffeine/pharmacology
MH  - Cyclic AMP/metabolism
MH  - Extracellular Space/metabolism
MH  - Inositol Phosphates/*biosynthesis
MH  - Muscle, Smooth, Vascular/cytology/*metabolism
MH  - Osmolar Concentration
MH  - Ryanodine/pharmacology
MH  - Terpenes/pharmacology
MH  - Thapsigargin
EDAT- 1994/01/01 00:00
MHDA- 1994/01/01 00:01
CRDT- 1994/01/01 00:00
PHST- 1994/01/01 00:00 [pubmed]
PHST- 1994/01/01 00:01 [medline]
PHST- 1994/01/01 00:00 [entrez]
AID - 10.1152/ajpcell.1994.266.1.C276 [doi]
PST - ppublish
SO  - Am J Physiol. 1994 Jan;266(1 Pt 1):C276-83. doi: 10.1152/ajpcell.1994.266.1.C276.