Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

ACL myotoxin (ACLMT) is a Lys49 phospholipase A(2)-like protein isolated from the venom of the snake Agkistrodon contortrix laticinctus. The aim of this work was to study the effect of ACLMT on water transport in the toad bladder. Water flow through the membrane was measured gravimetrically in bag preparations of the bladder. ACLMT (20 nM) increased the baseline water flow and partially inhibited arginine-vasopressin (AVP), 8-chlorophenylthio-cAMP (8-CPT-cAMP) and forskolin-stimulated water flow. The effect of ACLMT on baseline or AVP-stimulated water flow was prevented by lanthanum (0.1 mM) indicating that the effect of ACLMT on water transport may be mediated through an increase in intracellular calcium. The effect of ACLMT on baseline water flow was also prevented by nifedipine (0.1 mM) indicating the participation of exogenous calcium in this effect. Carbachol (0.1 mM) has been shown to enhance baseline water flow while inhibiting AVP-stimulated water flow. The effects of ACLMT and carbachol on baseline water flow and AVP-stimulated water flow were not additive, suggesting that both agents alter water transport by a similar mechanism. Indomethacin (10 microM) reduced the effect of ACLMT on forskolin-stimulated water flow, suggesting an increase in prostaglandin biosynthesis. These results suggest that the effects of ACLMT on water transport may be mediated by increasing intracellular calcium and stimulation prostaglandin biosynthesis.
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PMID:Effects of ACL myotoxin, a Lys49 phospholipase A(2) from Agkistrodon contortrix laticinctus snake venom, on water transport in the isolated toad urinary bladder. 1503 32

Recently, we reported that intracerebroventricularly (i.c.v.) administered arginine-vasopressin evokes the release of noradrenaline and adrenaline from adrenal medulla by brain thromboxane A2-mediated mechanisms in rats. These results suggest the involvement of brain arachidonic acid in the vasopressin-induced activation of the central adrenomedullary outflow. Arachidonic acid is released mainly by two pathways: phospholipase A2 (PLA2)-dependent pathway; phospholipase C (PLC)- and diacylglycerol lipase-dependent pathway. In the present study, therefore, we attempted to identify which pathway is involved in the vasopressin-induced release of both catecholamines from adrenal medulla using urethane-anesthetized rats. Vasopressin (0.2 nmol/animal, i.c.v.)-induced elevation of plasma noradrenaline and adrenaline was dose-dependently reduced by neomycin [0.28 and 0.55 micromol (250 and 500 microg)/animal, i.c.v.] and 1-[6-[[(17beta)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U-73122) [5 and 10 nmol (2.3 and 4.6 microg)/animal, i.c.v.] (inhibitors of PLC), and also by 1,6-bis(cyclohexyloximinocarbonylamino)hexane (RHC-80267) [1.3 and 2.6 micromol (500 and 1000 microg)/animal, i.c.v.] (an inhibitor of diacylglycerol lipase). On the other hand, mepacrine [1.1 and 2.2 micromol (500 and 1000 microg)/animal, i.c.v.] (an inhibitor of PLA2) was largely ineffective on the vasopressin-induced elevation of plasma catecholamines. These results suggest that vasopressin evokes the release of noradrenaline and adrenaline from adrenal medulla by the brain PLC- and diacylglycerol lipase-dependent mechanisms in rats.
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PMID:Brain phospholipase C-diacylglycerol lipase pathway is involved in vasopressin-induced release of noradrenaline and adrenaline from adrenal medulla in rats. 1536 56

ACLMT is a myotoxic Lys49 phospholipase A(2) isolated from the venom of the snake Agkistrodon contortrix laticinctus. We have previously shown that ACLMT increases baseline water transport and partially inhibits vasopressin-stimulated water transport across toad bladders due to an increase in cytosolic calcium. However, these evidences provide insufficient insight into the mechanisms involved in the effects of ACLMT on membrane permeability. In an attempt to better understand such mechanisms, the current study aimed to investigate whether the Na(+)/K(+)-ATPase activity of isolated toad bladders can be affected by the ACLMT and the synthetic peptide from its C-terminal region. The toxin significantly decreased the Na(+)/K(+)-ATPase, while the peptide did not alter it. These findings suggest that the effects of ACLMT on membrane permeability may be due to the inhibition of the Na(+)/K(+)-ATPase activity, and that the C-terminal region may not play a relevant role in this effect. This study contributes toward a better understanding of the mechanisms involved in the toxicity of the snake venom Lys49 PLA(2) myotoxins on biological tissues.
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PMID:The effect of the myotoxic Lys49 phospholipase A(2) from Agkistrodon contortrix laticinctus snake venom on Na+/K+ -ATPase activity of toad bladders. 1679 14

ACLMT is a myotoxic Lys49 phospholipase A2 isolated from the venom of the snake Agkistrodon contortrix laticinctus. We have previously demonstrated that ACLMT affects the water transport in toad bladders through a mechanism partially mediated by an increase in the cytosolic calcium. This study aims to further investigate the sites and mechanisms involved in the effects of ACLMT on water transport in toad bladders by examining the role of microtubules and calmodulin. Water flow across the membrane was gravimetrically measured in bladder sac preparations. ACLMT increased basal water transport and inhibited water transport stimulated by vasopressin. Colchicine and trifluoperazine reduced the effect of the toxin on basal water transport and enhanced it on vasopressin-stimulated water transport. The results suggest that both microtubules and calmodulin may be involved in the effect of ACLMT on basal water transport. On the other hand, the effect of the toxin on vasopressin-stimulated water transport appears to be neither dependent on the microtubules integrity nor directly mediated by calmodulin. This study provides a deeper understanding of the effects of the Lys49 PLA2 myotoxins on membrane permeability, thus contributing to elucidate the toxicity mechanism of these myotoxins on biological tissues.
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PMID:Effects of the myotoxic Lys49 phospholipase A2 from Agkistrodon contortrix laticinctus snake venom on water transport in the toad bladder epithelium: evidence for a role of microtubules and calmodulin. 1730 30

We have previously shown that centrally injected melittin, a phospholipase A(2) (PLA(2)) activator, increases blood pressure and decreases heart rate in the normotensive conscious rats. In the current study we aimed to determine the cardiovascular effects of melittin in hemorrhaged hypotensive rats and to investigate the mediation of peripheral adrenergic, vasopressinergic and renin angiotensin system in the pressor effect of centrally administrated melittin in both normotensive and hypotensive conditions. Acute hypotensive hemorrhage was performed by withdrawing a total volume of 2.2ml of blood/100g body weight over a period of 10min. Melittin was injected intracerebroventricularly (i.c.v.) at the doses of 1.5microg, 3.0microg or 6.0microg after the stabilization period of hemorrhage procedure. We also repeated previous experiments by injecting melittin (1.5microg, 3.0microg or 6.0microg; i.c.v.) to the normotensive animals. Melittin caused dose- and time-dependent increases in mean arterial pressure (MAP) in normal and hypotensive conditions and decreases in heart rate (HR) in normotensive conscious animals. In hypotensive rats, melittin injected at the dose of 6.0microg completely restored the decrease in blood pressure. Plasma adrenaline, noradrenaline, vasopressin levels and renin activity increased after melittin (3.0microg; i.c.v) administration in normal conditions. Hemorrhage, itself, produced an increase in these plasma hormone levels and melittin (3.0microg; i.c.v.) caused additional increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity in hypotensive conditions. Intravenous pretreatments of rats with prazosin (0.5mg/kg), an alpha(1) adrenoceptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1), O-Me-Tyr(2)-Arg(8)]-vasopressin (10microg/kg), a vasopressin V(1) receptor antagonist, or saralasin (250microg/kg), an angiotensin II receptor antagonist, partially blocked the pressor response to melittin (3.0microg; i.c.v.) in both normotensive and hypotensive conditions. Besides, the combined administration of these three antagonists before melittin completely abolished the pressor responses to drug in both conditions. Results show that centrally administered melittin, a PLA(2) activator, increases blood pressure and reverses hypotension in hemorrhagic shock. The increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity mediate the pressor responses to melittin in normal and hypotensive conditions.
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PMID:Cardiovascular effects of centrally injected melittin in hemorrhaged hypotensive rats: the investigation of peripheral mechanisms. 1789 13

TRPC6 is a non-voltage-gated Ca(2+) entry/depolarization channel associated with vascular tone regulation and remodeling. Expressed TRPC6 channel responds to both neurohormonal and mechanical stimuli, the mechanism for which remains controversial. In this study, we examined the possible interactions of receptor and mechanical stimulations in activating this channel using the patch clamp technique. In HEK293 cells expressing TRPC6, application of mechanical stimuli (hypotonicity, shear, 2,4,6-trinitrophenol) caused, albeit not effective by themselves, a prominent potentiation of cationic currents (I(TRPC6)) induced by a muscarinic receptor agonist carbachol. This effect was insensitive to a tarantula toxin GsMTx-4 (5 mumol/L). A similar extent of mechanical potentiation was observed after activation of I(TRPC6) by GTPgammaS or a diacylglycerol analog 1-oleoyl-2-acetyl-sn-glycerol (OAG). Single TRPC6 channel activity evoked by carbachol was also enhanced by a negative pressure added in the patch pipette. Mechanical potentiation of carbachol- or OAG-induced I(TRPC6) was abolished by small interfering RNA knockdown of cytosolic phospholipase A(2) or pharmacological inhibition of omega-hydroxylation of arachidonic acid into 20-HETE (20-hydroxyeicosatetraenoic acid). Conversely, direct application of 20-HETE enhanced both OAG-induced macroscopic and single channel TRPC6 currents. Essentially the same results were obtained for TRPC6-like cation channel in A7r5 myocytes, where its activation by noradrenaline or Arg8 vasopressin was greatly enhanced by mechanical stimuli via 20-HETE production. Furthermore, myogenic response of pressurized mesenteric artery was significantly enhanced by weak receptor stimulation dependently on 20-HETE production. These results collectively suggest that simultaneous operation of receptor and mechanical stimulations may synergistically amplify transmembrane Ca(2+) mobilization through TRPC6 activation, thereby enhancing the vascular tone via phospholipase C/diacylglycerol and phospholipase A(2)/omega-hydroxylase/20-HETE pathways.
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PMID:Synergistic activation of vascular TRPC6 channel by receptor and mechanical stimulation via phospholipase C/diacylglycerol and phospholipase A2/omega-hydroxylase/20-HETE pathways. 1944 36

Cell swelling induces peptide exocytosis using unique signaling pathway. Hyposmotic-induced secretion in normal cells is not mediated by specific receptors, is independent from extra and intracellular Ca(2+), sodium and potassium channels activity, prostaglandins, leukotriens, does not involve cytoskeleton, cAMP generation, phospholipase A(2), G proteins, protein kinase C. It is promoted by swelling of the secretory vesicles. Resistance to endogenous inhibitors is frequent attribute of this type of secretion. Swelling-induced secretion involves also secretory vesicles not involved in conventional stimulation. Hyposmosis-induced insulin secretion is more sensitive to high cellular cholesterol than conventional one suggesting substantial difference between mechanisms. Participation of sequential exocytosis as dominating mechanism in swelling-induced exocytosis is hypothesized. Signaling and response in tumor cells often differs from native cells and varies markedly between cell lines. Pathogenetic implications: cell swelling could be involved in alcohol induced hypoglycemia in diabetic patients and release of peptides from pituitary and neurons. Swelling-induced products could be mediators of ischemic preconditioning involved also in protection of diabetic heart. Swelling-induced exocytosis is an ancient mechanism generally present in cells; in cells engaged in water and salt regulation is covered by specific response mediated by specific signaling. Disturbance of specific response leads to swelling-induced - inappropriate secretion of antidiuretic hormone - SIADH.
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PMID:Cell swelling-induced peptide hormone secretion. 2217 4


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