Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of central and peripheral stimuli on gastric acid secretion is mediated via activation of histaminergic, gastrinergic, and cholinergic pathways coupled to intracellular second-messenger systems that determine the trafficking and activity of H+ K+-ATPase, the proton pump of the parietal cell. Histamine, released from enterochromaffin-like cells stimulates the parietal cell directly via H-2 receptors coupled to generation of cAMP. Gastrin, acting via cholecystokinin-2 receptors on enterochromaffin-like cells coupled to an increase in intracellular calcium, stimulates the parietal cell indirectly by activating histidine decarboxylase, releasing histamine, and inducing enterochromaffin-like cell hypertrophy and hyperplasia. Acetylcholine, released from gastric postganglionic intramural neurons, stimulates the parietal cell directly via M-3 receptors coupled to intracellular calcium release and calcium entry. The second-messenger systems activated in the parietal cell converge on H+ K+-ATPase that catalyzes the exchange of luminal K+ for cytoplasmic H+ and is responsible for gastric luminal acidification. The main inhibitor of acid secretion is somatostatin which, acting via sst2 receptors, exerts a tonic inhibitory influence on parietal, enterochromaffin-like, and gastrin cells. Acute infection with Helicobacter pylori results in hypochlorhydria, whereas chronic infection may be associated with either hypo- or hyperchlorhydria. Although prostaglandins are thought to play a physiologic role in the regulation of acid secretion and maintenance of gastric mucosal integrity, the precise roles of cyclooxygenase-1 and cyclooxygenase-2 in these processes still eludes us.
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PMID:Gastric secretion. 1703 Dec 7

Activation of muscarinic acetylcholine receptors (mAChR) is one of the most important signal transduction pathways in the human body. In this study, we investigated the role of mAChR activation in relation to its subtypes in human retinoblastoma cell-lines (WERI-Rb-1) using Ca(2+) measurement, real-time PCR, and Western Blot techniques. Acetylcholine (ACh) produced prominent [Ca(2+)](i) transients in a repeated manner in WERI-Rb-1 cells. The maximal amplitude of the [Ca(2+)](i) transient was almost completely suppressed by 97.3 +/- 0.8% after atropine (1 microM) pretreatment. Similar suppressions were noted after pretreatments with thapsigargin (1 microM), an ER Ca(2+)-ATPase (SERCA) inhibitor, whereas the ACh-induced [Ca(2+)](i) transient was not affected even in the absence of extracellular calcium. U-73122 (1 microM), a PLC inhibitor, and xestospongin C (2 microM), an IP(3)-receptor antagonist, elicited 11.5 +/- 2.9% and 17.8 +/- 1.9% suppressions, respectively. The 50% inhibitory concentration of (IC(50)) values for blockade of a 100 microM ACh response by pirenzepine and 4-DAMP were 315.8 and 9.1 nM, respectively. Moreover, both M(3) and M(5) mAChRs were prominent in quantitative real-time-PCR. Taken together, the M(3)/M(5) subtypes appear to be the major contributor, leading to intracellular calcium mobilization from the internal store via an IP(3)-dependent pathway in the undifferentiated retinoblastoma cells.
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PMID:Calcium mobilization by activation of M(3)/M(5) muscarinic receptors in the human retinoblastoma. 1795 79

In order to study the anti-viral mechanism of extracted ZG from Gardenia, the effect of extracted ZG on Hep-2 cell membrane potential, Na -K+-ATPase activity and membrane fluidity post infected with parainfluenza virus type 1 (PIV-1) was observed. Acetylcholine which was fluorescent labeled with DiBAC4 (3) was taken as positive control to observe the changes of membrane potential and was measured by flow cytometer. The phosphorus determination method and spectrophotometer were used to measure the Na+-K+-ATPase activity of Hep-2 cell membrane post PIV-1 infection. Hep-2 cell membrane phospholipids was labeled with fluorescent NBD-C6-HPC and membrane fluidity was measured by confocal laser scanning microscope. The results demonstated that after PIV-1 infection the Hep-2 cell membrane potential decreased significantly and the membrane was in the state of hyperpolarization, Na+-K+-ATPase activity increased and membrane fluidity decreased significantly. There was no apparent interferring effect of extracted ZG on the changes of membrane potential and Na+-K+-ATPase activity post PIV-1 infection, while membrane fluidity was improved significantly. Acetylcholine improved the state of hyperpolarization. The changes of membrane potential, Na -K+-ATPase activity and membrane fluidity might be the biomechanism of PIV-1 infectoin. The extracted ZG improved membrane fluidity to prevent from PIV-1 infection by protecting the cell membrane, which was probably the mechanism of anti-PIV-1 activity of the extracted ZG, but ZG probably had nothing to do with membrane potential and Na+-K+-ATPase activity.
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PMID:[Effect of extracted ZG from gardenia on Hep-2 cell membrane post infected with parainfluenza virus type 1 (PIV-1)]. 1796 56

Regulation of intracellular Ca(2+) concentration ([Ca(2+)](i)) in airway smooth muscle (ASM) during agonist stimulation involves sarcoplasmic reticulum (SR) Ca(2+) release and reuptake. The sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) is key to replenishment of SR Ca(2+) stores. We examined regulation of SERCA in porcine ASM: our hypothesis was that the regulatory protein phospholamban (PLN) and the calmodulin (CaM)-CaM kinase (CaMKII) pathway (both of which are known to regulate SERCA in cardiac muscle) play a role. In porcine ASM microsomes, we examined the expression and extent of PLN phosphorylation after pharmacological inhibition of CaM (with W-7) vs. CaMKII (with KN-62/KN-93) and found that PLN is phosphorylated by CaMKII. In parallel experiments using enzymatically dissociated single ASM cells loaded with the Ca(2+) indicator fluo 3 and imaged using fluorescence microscopy, we measured the effects of PLN small interfering RNA, W-7, and KN-62 on [Ca(2+)](i) responses to ACh and direct SR stimulation. PLN small interfering RNA slowed the rate of fall of [Ca(2+)](i) transients to 1 microM ACh, as did W-7 and KN-62. The two inhibitors additionally slowed reuptake in the absence of PLN. In other cells, preexposure to W-7 or KN-62 did not prevent initiation of ACh-induced [Ca(2+)](i) oscillations (which were previously shown to result from repetitive SR Ca(2+) release/reuptake). However, when ACh-induced [Ca(2+)](i) oscillations reached steady state, subsequent exposure to W7 or KN-62 decreased oscillation frequency and amplitude and slowed the fall time of [Ca(2+)](i) transients, suggesting SERCA inhibition. Exposure to W-7 completely abolished ongoing ACh-induced [Ca(2+)](i) oscillations in some cells. Preexposure to W-7 or KN-62 did not affect caffeine-induced SR Ca(2+) release, indicating that ryanodine receptor channels were not directly inhibited. These data indicate that, in porcine ASM, the CaM-CaMKII pathway regulates SR Ca(2+) reuptake, potentially through altered PLN phosphorylation.
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PMID:Regulation of sarcoplasmic reticulum Ca2+ reuptake in porcine airway smooth muscle. 1824 64

Descending vasa recta (DVR) are 15-microm vessels that perfuse the renal medulla. Ouabain has been shown to augment DVR endothelial cytoplasmic Ca(2+) ([Ca(2+)](CYT)) signaling. In this study, we examined the expression of the ouabain-sensitive Na-K-ATPase alpha2 subunit in the rat renal vasculature and tested effects of acute ouabain exposure and chronic ouabain treatment on DVR. Immunostaining with antibodies directed against the alpha2 subunit verified its expression in both DVR pericytes and endothelium. Acute application of ouabain (100 or 500 nM) augmented the DVR nitric oxide generation stimulated by acetylcholine (ACh; 10 microM). At a concentration of 1 mM, ouabain constricted microperfused DVR, whereas at 100 nM, it was without effect. Acute ouabain (100 nM) did not augment constriction by angiotensin II (0.5 or 10 nM), whereas l-nitroarginine methyl ester-induced contraction of DVR was slightly enhanced. Ouabain-hypertensive (OH) rats were generated by chronic ouabain treatment (30 microg.kg(-1).day(-1), 5 wk). The acute endothelial [Ca(2+)](CYT) elevation by ouabain (100 nM) was absent in DVR endothelia of OH rats. The [Ca(2+)](CYT) response to 10 nM ACh was also eliminated, whereas the response to 10 microM ACh was not. The endothelial [Ca(2+)](CYT) response to bradykinin (100 nM) was significantly attenuated. We conclude that endothelial responses may offset the ability of acute ouabain exposure to enhance DVR vasoconstriction. Chronic exposure to ouabain, in vivo, leads to hypertension and DVR endothelial dysfunction, manifested as reduced [Ca(2+)](CYT) responses to both ouabain- and endothelium-dependent vasodilators.
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PMID:Chronic ouabain treatment induces vasa recta endothelial dysfunction in the rat. 1894 26

Airway inflammation leads to increased intracellular Ca(2+) ([Ca(2+)](i)) levels in airway smooth muscle (ASM) cells. Sarcoplasmic reticulum Ca(2+) release and reuptake are key components of ASM [Ca(2+)](i) regulation. Ca(2+) reuptake occurs via sarcoendoplasmic reticulum Ca(2+) ATPase (SERCA) and is regulated by the inhibitory protein phospholamban (PLB) in many cell types. In human ASM, we tested the hypothesis that inflammation increases PLB, thus inhibiting SERCA function, and leading to maintained [Ca(2+)](i) levels. Surprisingly, we found that human ASM does not express PLB protein (although mRNA is detectable). Overnight exposure to the proinflammatory cytokines TNFalpha and IL-13 did not induce PLB expression, raising the issue of how SERCA is regulated. We then found that direct SERCA phosphorylation (via CaMKII) occurs in human ASM. In fura-2-loaded human ASM cells, we found that the CaMKII antagonist KN-93 significantly slowed the rate of fall of [Ca(2+)](i) transients induced by ACh or bradykinin (in zero extracellular Ca(2+)), suggesting a role for CaMKII-mediated SERCA regulation. SERCA expression was decreased by cytokine exposure, and the rate of fall of [Ca(2+)](i) transients was slowed in cells exposed to TNFalpha and IL-13. Cytokine effects on Ca(2+) reuptake were unaffected by additional exposure to KN-93. These data indicate that in human ASM, SERCA is regulated by mechanisms such as CaMKII and that airway inflammation maintains [Ca(2+)](i) levels by decreasing SERCA expression and slowing Ca(2+) reuptake.
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PMID:Effect of proinflammatory cytokines on regulation of sarcoplasmic reticulum Ca2+ reuptake in human airway smooth muscle. 1978 41

The present experiment was conducted to establish the relationship between selected physiological parameters and histological responses of Channa punctatus brain tissue to endosulfan exposure. The fish (35.6 +/- 0.7 g) was exposed to sublethal endosulfan concentration (8.1 microg l(-1)) for a period of 12, 24, 36, 48, 72, and 96 h. Results showed that brain glucose level increased significantly after exposure, indicating a hyperglycemic state of the fish. Brain vitamin C level decreased with an increase in the exposure time. Acetylcholine esterase and adenosine triphosphatase enzyme activities also showed a significant reduction upon endosulfan exposure. Brain histopathology after 96 h endosulfan exposure showed that the apical lobe of the cerebrum (the only portion examined) had mild necrosis. Focal area of gliosis could be seen in the cerebrum, which were absent in the control fish. The results indicate that exposure of sublethal concentration of endosulfan to C. punctatus may have a direct effect on the histology of the fish's brain tissue, thereby affecting its metabolism.
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PMID:Biochemical and histological changes in the brain tissue of spotted murrel, Channa punctatus (Bloch), exposed to endosulfan. 1952 21

The aim of this study was to determine whether losartan, an angiotensin II (Ang II) type 1 (AT(1)) receptor could influence the CA release from the isolated perfused model of the rat adrenal medulla. Losartan (5~50 microM) perfused into an adrenal vein for 90 min produced dose- and time-dependent inhibition of the CA secretory responses evoked by ACh (5.32 mM), high K(+) (56 mM, a direct membrane depolarizer), DMPP (100 microM) and McN-A-343 (100 microM). Losartan failed to affect basal CA output. Furthermore, in adrenal glands loaded with losartan (15 microM) for 90 min, the CA secretory responses evoked by Bay-K-8644 (10 microM, an activator of L-type Ca(2+) channels), cyclopiazonic acid (10 microM, an inhibitor of cytoplasmic Ca(2+)-ATPase), veratridine (100 microM, an activator of Na(+) channels), and Ang II (100 nM) were markedly inhibited. However, at high concentrations (150~300 microM), losartan rather enhanced the CA secretion evoked by ACh. Collectively, these experimental results suggest that losartan at low concentrations inhibits the CA secretion evoked by cholinergic stimulation (both nicotininc and muscarinic receptors) as well as by membrane depolarization from the rat adrenal medulla, but at high concentration it rather inhibits ACh-evoked CA secretion. It seems that losartan has a dual action, acting as both agonist and antagonist to nicotinic receptors of the rat adrenal medulla, which might be dependent on the concentration. It is also thought that this inhibitory effect of losartan may be mediated by blocking the influx of both Na(+) and Ca(2+) into the rat adrenomedullary chromaffin cells as well as by inhibiting the Ca(2+) release from the cytoplasmic calcium store, which is thought to be relevant to the AT(1) receptor blockade, in addition to its enhancement of the CA release.
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PMID:Effects of losartan on catecholamine release in the isolated rat adrenal gland. 1988 18

The aim of the present study was to examine the effect of provinol, which is a mixture of polyphenolic compounds from red wine, on the secretion of catecholamines (CA) from isolated perfused rat adrenal medulla, and to elucidate its mechanism of action. Provinol (0.3~3 microg/ml) perfused into an adrenal vein for 90 min dose- and time-dependently inhibited the CA secretory responses evoked by ACh (5.32 mM), high K(+) (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic N(N) receptor agonist, 100 microM) and McN-A-343 (a selective muscarinic M(1) receptor agonist, 100 microM). Provinol itself did not affect basal CA secretion. Also, in the presence of provinol (1 microg/ml), the secretory responses of CA evoked by Bay-K-8644 (a voltage-dependent L-type dihydropyridine Ca(2+) channel activator, 10 microM), cyclopiazonic acid (a cytoplasmic Ca(2+)-ATPase inhibitor, 10 microM) and veratridine (an activator of voltage-dependent Na(+) channels, 10 microM) were significantly reduced. Interestingly, in the simultaneous presence of provinol (1 microg/ml) plus L-NAME (a selective inhibitor of NO synthase, 30 microM), the CA secretory responses evoked by ACh, high K(+), DMPP, McN-A-343, Bay-K-8644 and cyclpiazonic acid recovered to the considerable extent of the corresponding control secretion in comparison with the inhibition of provinol-treatment alone. Under the same condition, the level of NO released from adrenal medulla after the treatment of provinol (3 microg/ml) was greatly elevated in comparison to its basal release. Taken together, these data demonstrate that provinol inhibits the CA secretory responses evoked by stimulation of cholinergic (both muscarinic and nicotinic) receptors as well as by direct membrane-depolarization from the perfused rat adrenal medulla. This inhibitory effect of provinol seems to be exerted by inhibiting the influx of both calcium and sodium into the rat adrenal medullary cells along with the blockade of Ca(2+) release from the cytoplasmic calcium store at least partly through the increased NO production due to the activation of nitric oxide synthase.
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PMID:Provinol inhibits catecholamine secretion from the rat adrenal medulla. 1988 42

Resveratrol has been known to possess various potent cardiovascular effects in animal, but there is little information on its functional effect on the secretion of catecholamines (CA) from the perfused model of the adrenal medulla. Therefore, the aim of the present study was to determine the effect of resveratrol on the CA secretion from the isolated perfused model of the normotensive rat adrenal gland, and to elucidate its mechanism of action. Resveratrol (10~100microM) during perfusion into an adrenal vein for 90 min inhibited the CA secretory responses evoked by ACh (5.32 mM), high K(+) (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic N(n) receptor agonist, 100microM) and McN-A-343 (a selective muscarinic M(1) receptor agonist, 100microM) in both a time- and dose-dependent fashion. Also, in the presence of resveratrol (30microM), the secretory responses of CA evoked by veratridine 8644 (an activator of voltage-dependent Na(+) channels, 100microM), Bay-K-8644 (a L-type dihydropyridine Ca(2+) channel activator, 10microM), and cyclopiazonic acid (a cytoplasmic Ca(2+)-ATPase inhibitor, 10microM) were significantly reduced. In the simultaneous presence of resveratrol (30microM) and L-NAME (an inhibitor of NO synthase, 30microM), the CA secretory evoked by ACh, high K(+) , DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were recovered to a considerable extent of the corresponding control secretion compared with the inhibitory effect of resveratrol alone. Interestingly, the amount of nitric oxide (NO) released from the adrenal medulla was greatly increased in comparison to its basal release. Taken together, these experimental results demonstrate that resveratrol can inhibit the CA secretory responses evoked by stimulation of cholinergic nicotinic receptors, as well as by direct membrane-depolarization in the isolated perfused model of the rat adrenal gland. It seems that this inhibitory effect of resveratrol is exerted by inhibiting an influx of both ions through Na(+) and Ca(2+) channels into the adrenomedullary cells as well as by blocking the release of Ca(2+) from the cytoplasmic calcium store, which are mediated at least partly by the increased NO production due to the activation of NO synthase.
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PMID:Resveratrol inhibits nicotinic stimulation-evoked catecholamine release from the adrenal medulla. 1996 50


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