Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ciguatoxin (CTX; 10(-7) X 10(-7) g/ml), the most potent marine toxin isolated from a number of tropical and subtropical fishes, shifted the dose-contractile response curves for norepinephrine (NE) and K+ to the left in a parallel manner in the guinea-pig isolated vas deferens, indicating that CTX caused supersensitivity. The CTX-induced potentiation was inhibited or abolished in the presence of tetrodotoxin (5 X 10(-7) M) or saxitoxin (5 X 10(-7) M) and in Na+-deficient medium, but was not affected by phentolamine (10(-6) M) and verapamil (10(-6) M). Treatment with reserpine (2 mg/kg/day, twice) almost completely prevented the release of NE by CTS, such pretreatment had no affect on the ability of CTX to potentiate responses to NE and K+. Furthermore, after cold storage (4 degrees C for 7 days) of tissues, the contractile response to NE (3 X 10(-6) M) and K+ (20 mM) was still profoundly potentiated after treatment with CTX (5 X 10(-7) g/ml). CTX (10(-7)-10(-5) g/ml) by itself had no apparent effect on either Na+, K+-adenosine triphosphatase activity or Na+ content of the vas deferens. However, in the presence of ouabain, CTX elevated the Na content of the vas deferens treated with ouabain alone by 27%. This effect of CTX was abolished by tetrodotoxin. These data suggest that CTX causes an increasing Na+ permeability across the TTX sensitive Na+ channels of smooth muscle cell, and this may play an important role in its mechanism of potentiation.
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PMID:Mode of the ciguatoxin-induced supersensitivity in the guinea-pig vas deferens. 628 61

In primary sensory afferent neurons, Ca2+ plays a vital role in the regulation of cellular processes including receptor and synaptic plasticity, neurotransmitter and trophic factor release and gene regulation. Current understanding of the mechanisms underlying Ca2+ homeostasis of primary sensory afferent neurons is mostly derived from studies on dorsal root ganglia and nodose ganglia neuron cell bodies. Little is known about Ca2+ homeostasis in trigeminal ganglion neurons (TGNs). To determine what cellular processes contribute to electrically-evoked Ca2+ transients in TGNs, we probed Ca2+ regulatory mechanisms in TGN cell bodies from the ophthalmic division with a panel of pharmacological reagents. Ca2+ transients were evoked in fura-2 loaded TGNs by depolarizing the plasma membrane with brief (500 ms) puffs of 50 mM KCl. Cyclopiazonic acid (CPA; 5 microM), an inhibitor of the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA), significantly decreased the peak amplitude, and slowed the decay, of the KCl-evoked Ca2+ transients in TGNs. The mitochondrial protonophore, carbonyl cyanide 3-chloro-phenylhydrazone (CCCP; 5 microM) significantly increased the peak amplitude of KCl-evoked Ca2+ transients. These data demonstrate that Ca2+ stores do play a major role in Ca2+ homeostasis in TGN cell bodies. To determine the role of the sodium-calcium exchanger (NCX) in KCl-evoked Ca2+ transients in TGNs, we inhibited the exchanger with KB-R7943 (10 microM), or by replacing Na+ with Li+. NCX inhibition did not affect either the peak amplitude or the decay kinetics of the KCl-evoked Ca2+ transients. Therefore, the NCX does not play a significant role in removing cytosolic Ca2+ from TGNs. To test whether the plasma membrane calcium-ATPase (PMCA) contributes to Ca2+ extrusion, we inhibited its activity by a shift to alkaline pH (9.0). At pH 9.0, both the peak amplitude and decay time of the KCl-evoked Ca2+ transient were increased significantly. These data suggest that, in TGNs, the PMCA is the major mechanism for removing cytosolic Ca2+ following electrical activity.
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PMID:Calcium homeostasis in trigeminal ganglion cell bodies. 1704 58