PMID- 8384800
OWN - NLM
STAT- MEDLINE
DCOM- 19930429
LR  - 20220316
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 264
IP  - 3 Pt 1
DP  - 1993 Mar
TI  - Acute hypoxia increases cytosolic calcium in cultured pulmonary arterial 
      myocytes.
PG  - L323-8
AB  - The effects of hypoxia on the cytosolic Ca2+ concentration, [Ca2+]i, were 
      characterized in cultured pulmonary arterial smooth muscle (PASM) cells. Reducing 
      O2 tension (PO2) from 150 to < 25 Torr induced a reversible 100-200% increase in 
      [Ca2+]i that was characterized by two components: an early rise in [Ca2+]i that 
      was dependent on the rate, as well as the magnitude, of decline in PO2 and a 
      later, steady-state increase that was independent of the rate at which PO2 
      changed. Caffeine lowered [Ca2+]i during normoxia and blocked the early component 
      of the response to hypoxia, whereas the steady-state hypoxic response was only 
      partially inhibited. Like hypoxia, thapsigargin (TG) elevated [Ca2+]i, and there 
      was no additional hypoxia-induced elevation in [Ca2+]i at any time after exposure 
      to TG. At steady state, the hypoxic responses were completely reversed by removal 
      of extracellular Ca2+, whereas, on average, verapamil and nifedipine attenuated 
      the hypoxia-induced increases in [Ca2+]i by only 44 and 35%, respectively. These 
      results suggest that hypoxia-induced elevation of [Ca2+]i in PASM cells consists 
      of an early release of Ca2+ from the sarcoplasmic reticulum and a later influx of 
      extracellular Ca2+, in part, through nifedipine- and verapamil-insensitive Ca2+ 
      channels. The results are consistent with the idea that hypoxia and thapsigargin 
      may share common mechanisms for tonically increasing [Ca2+]i.
FAU - Salvaterra, C G
AU  - Salvaterra CG
AD  - Department of Medicine, Baltimore Veterans Affairs Hospital, Maryland.
FAU - Goldman, W F
AU  - Goldman WF
LA  - eng
GR  - HL-43091/HL/NHLBI NIH HHS/United States
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 (Calcium Channels)
RN  - 0 (Terpenes)
RN  - 3G6A5W338E (Caffeine)
RN  - 67526-95-8 (Thapsigargin)
RN  - CJ0O37KU29 (Verapamil)
RN  - EC 7.2.2.10 (Calcium-Transporting ATPases)
RN  - I9ZF7L6G2L (Nifedipine)
RN  - S88TT14065 (Oxygen)
RN  - SY7Q814VUP (Calcium)
RN  - TSN3DL106G (Fura-2)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Caffeine/pharmacology
MH  - Calcium/analysis/*metabolism/pharmacology
MH  - Calcium Channels/drug effects/physiology
MH  - Calcium-Transporting ATPases/antagonists & inhibitors
MH  - Cells, Cultured
MH  - Cytosol/chemistry/*metabolism
MH  - Fura-2
MH  - Hypoxia/*physiopathology
MH  - Male
MH  - Microscopy, Fluorescence
MH  - Muscle, Smooth, Vascular/chemistry/cytology/metabolism
MH  - Nifedipine/pharmacology
MH  - Oxygen/pharmacology
MH  - Pulmonary Artery/*cytology/metabolism/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sarcoplasmic Reticulum/chemistry/metabolism
MH  - Terpenes/pharmacology
MH  - Thapsigargin
MH  - Verapamil/pharmacology
EDAT- 1993/03/01 00:00
MHDA- 1993/03/01 00:01
CRDT- 1993/03/01 00:00
PHST- 1993/03/01 00:00 [pubmed]
PHST- 1993/03/01 00:01 [medline]
PHST- 1993/03/01 00:00 [entrez]
AID - 10.1152/ajplung.1993.264.3.L323 [doi]
PST - ppublish
SO  - Am J Physiol. 1993 Mar;264(3 Pt 1):L323-8. doi: 10.1152/ajplung.1993.264.3.L323.