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Query: UMLS:C0392674 (
exhaustion
)
13,658
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Acidosis has been known to cause "Ca
2+
transients", however, the mechanism is still uncertain. Here, we demonstrated that multiple H
+
sensors, such as ASICs, TRPV1 and proton-sensing G protein coupled receptors (GPCRs) are involved in extracellular acidification-induced intracellular calcium ([Ca
2+
]
i
) elevation. By using calcium imaging measures, we observed that both ASIC and TRPV1 channels inhibitors suppressed the [Ca
2+
]
i
elevation induced by extracellular acidosis in cultured rat cardiac myocytes. Then, both channels mRNA and proteins were identified by RT-PCR, western blotting and immunofluorescence. ASIC-like and TRPV1-like currents were induced by extracellular acidification, suggesting that functional ASIC and TRPV1 channels jointly mediated extracellular calcium entry. Furthermore, either pre-
exhaustion
of sarcoplasmic reticulum (SR) Ca
2+
with thapsigargin or IP
3
receptor blocker 2-APB or PLC inhibitor U73122 significantly attenuated the elevation of [Ca
2+
]
i
, indicating that the intracellular Ca
2+
stores and the PLC-IP
3
signaling also contributed to the acidosis-induced elevation of [Ca
2+
]
i
. By using genetic and pharmacological approaches, we identified that
ovarian cancer G protein-coupled receptor 1
(
OGR1
) might be another main component in acidosis-induced release of [Ca
2+
]
i
. These results suggest that multiple H
+
-sensitive receptors are involved in "Ca
2+
transients" induced by acidosis in the heart.
...
PMID:Multiple H
+
sensors mediate the extracellular acidification-induced [Ca
2+
]
i
elevation in cultured rat ventricular cardiomyocytes. 2833 58
