Evidence for a contribution of store-operated Ca 2+ channels to NO-mediated endothelium-dependent relaxation of guinea-pig aorta in response to a Ca 2+ ionophore, A23187

1999 ◽  
Vol 360 (1) ◽  
pp. 69-79 ◽  
Author(s):  
H. Taniguchi ◽  
Y. Tanaka ◽  
H. Hirano ◽  
H. Tanaka ◽  
K. Shigenobu
Keyword(s):  
Guinea Pig ◽  
Ionophore A23187 ◽  
Endothelium Dependent Relaxation

Glutathione depletion inhibits amylase release in guinea pig pancreatic acini

1983 ◽  
Vol 244 (3) ◽  
pp. G273-G277
Author(s):  
W. F. Stenson ◽  
E. Lobos ◽  
H. J. Wedner
Keyword(s):  
Guinea Pig ◽  
Reduced Glutathione ◽  
Glutathione Depletion ◽  
Amylase Secretion ◽  
Ionophore A23187 ◽  
Amylase Release ◽  
Pancreatic Acini ◽  
Stimulus Secretion Coupling ◽  
Dose Dependent ◽  
Higher Doses

Isolated guinea pig pancreatic acini were specifically depleted of glutathione by treatment with 2-cyclohexene-1-one (2-CHX-1). Untreated acini contained 4.3 +/- 0.6 micrograms of glutathione per milligram protein. Incubation with 1 mM 2-CHX-1 for 5 min at 37 degrees C depleted glutathione to 17% of control values; 5 mM 2-CHX-1 depleted glutathione to less than 4% of control values. Incubation with 2-CHX-1 also impaired the ability of the isolated acini to secrete amylase in response to stimulation with carbachol and the ionophore A23187. The depletion of glutathione and the inhibition of amylase secretion by 2-CHX-1 were both dose dependent and time dependent. Incubation of acini with 2 mM 2-CHX-1 for 15 min at 37 degrees C reduced glutathione levels to 6.6% of control and reduced carbachol-stimulated amylase release to 63% of control. Higher doses of 2-CHX-1 or longer incubations resulted in greater depletion of glutathione and greater inhibition of carbachol-induced amylase release. These data indicate that specific depletion of glutathione impairs the ability of isolated acini to secrete amylase in response to physiological and pharmacologic stimuli and suggest that glutathione has a role in stimulus-secretion coupling in the exocrine pancreas.

Involvement of Ca2+/calmodulin-dependent protein kinase II in endothelial NO production and endothelium-dependent relaxation

2003 ◽  
Vol 284 (6) ◽  
pp. H2311-H2319 ◽  
Author(s):  
Jean-Christophe Schneider ◽  
Driss El Kebir ◽  
Christiane Chéreau ◽  
Sophie Lanone ◽  
Xiao-Lin Huang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase ◽  
No Production ◽  
Ionophore A23187 ◽  
Dependent Protein Kinase ◽  
Aortic Endothelial Cells ◽  
Protein Kinase Ii ◽  
Dependent Protein ◽  
Endothelium Dependent Relaxation ◽  
Aortic Endothelial

Nitric oxide (NO) is synthesized froml-arginine by the Ca2+/calmodulin-sensitive endothelial NO synthase (NOS) isoform (eNOS). The present study assesses the role of Ca2+/calmodulin-dependent protein kinase II (CaMK II) in endothelium-dependent relaxation and NO synthesis. The effects of three CaMK II inhibitors were investigated in endothelium-intact aortic rings of normotensive rats. NO synthesis was assessed by a NO sensor and chemiluminescence in culture medium of cultured porcine aortic endothelial cells stimulated with the Ca2+ ionophore A23187 and thapsigargin. Rat aortic endothelial NOS activity was measured by the conversion ofl-[3H]arginine tol-[3H]citrulline. Three CaMK II inhibitors, polypeptide 281–302, KN-93, and lavendustin C, attenuated the endothelium-dependent relaxation of endothelium-intact rat aortic rings in response to acetylcholine, A23187, and thapsigargin. None of the CaMK II inhibitors affected the relaxation induced by NO donors. In a porcine aortic endothelial cell line, KN-93 decreased NO synthesis and caused a rightward shift of the concentration-response curves to A23187 and thapsigargin. In rat aortic endothelial cells, KN-93 significantly decreased bradykinin-induced eNOS activity. These results suggest that CaMK II was involved in NO synthesis as a result of Ca2+-dependent activation of eNOS.

The induction of the acrosome reaction in guinea-pig sperm by the divalent metal cation ionophore A23187

1978 ◽  
Vol 32 (1) ◽  
pp. 137-151
Author(s):  
D.P. Green
Keyword(s):  
Guinea Pig ◽  
Metal Cation ◽  
Acrosome Reaction ◽  
Divalent Metal ◽  
Secretory Cells ◽  
Free Calcium ◽  
Ionophore A23187 ◽  
Divalent Metal Cation ◽  
Free Calcium Concentration ◽  
External Calcium

The divalent metal cation ionophore A23187 induces an acrosome reaction in guinea-pig sperm which is dependent on external calcium. Examination of this acrosome reaction by electron microscopy shows that it is morphologically normal. The known properties of A23187 and the morphological similarity between the acrosome reaction and the secretory discharges of other secretory cells suggests that the immediate cause of the acrosome reaction is an increase in the cytoplasmic free calcium concentration.

The activation of proteolysis in the acrosome reaction of guinea-pig sperm

1978 ◽  
Vol 32 (1) ◽  
pp. 153-164
Author(s):  
D.P. Green
Keyword(s):  
Guinea Pig ◽  
Acrosome Reaction ◽  
Morphological Changes ◽  
Divalent Metal ◽  
Free Calcium ◽  
Ionophore A23187 ◽  
Reaction Proceeds ◽  
Insoluble Form ◽  
Acrosin Activity ◽  
Sperm Population

The divalent metal cation ionophore A23187 rapidly induces a normal acrosome reaction in a population of guinea-pig sperm suspended in calcium medium. In the course of the acrosome reaction, proacrosin, the zymogen precursor of the protease acrosin, is activated. Although the acrosome reaction causes exocytosis of the acrosomal contents, ‘soluble’ acrosin is not released in significant amounts until well after the sperm population as a whole has undergone an acrosome reaction. This suggests that proacrosin is stored within the acrosome in an insoluble form and that exocytosis of the acrosomal contents in the acrosome reaction is insufficient, by itself, to cause its immediate dissolution. Electron micrographs of sperm undergoing an A23187-induced acrosome reaction in the presence of the acrosin inhibitors benzamidine, p-amino-benzamidine and phenylmethylsulphonyl fluoride show that the acrosome reaction proceeds normally but that dispersal of the acrosomal contents is inhibited. These morphological changes are, for the most part, below the limit of resolution of the light microscope and using light microscopy to assess whether an acrosome reaction has taken place, it can be mistakenly inferred that the reaction itself is inhibited by the acrosin inhibitors. The inhibition of the dispersal of the acrosomal contents by acrosin inhibitors suggests that acrosin activity is important in solubilizing acrosin. These experimental observations, taken with the evidence that the acrosome reaction is a response to an increase in intracellular free calcium, have been taken as the basis of a proposal for the mechanism of proacrosin activation in the acrosome reaction.

Cholinergic regulation of guinea pig duodenal bicarbonate secretion

1993 ◽  
Vol 265 (2) ◽  
pp. G270-G276 ◽  
Author(s):  
H. S. Odes ◽  
R. Muallem ◽  
R. Reimer ◽  
W. Beil ◽  
M. Schwenk ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Vagal Stimulation ◽  
Ionophore A23187 ◽  
Loop Model ◽  
Cholinergic Regulation ◽  
Intracellular Signals ◽  
Duodenal Bicarbonate Secretion ◽  
Series Of Experiments

Although it is well known that vagal stimulation induces duodenal HCO3- secretion, there is presently no information about the nature of the cholinoceptor and the intracellular signals involved. In a series of experiments performed in a guinea pig duodenal loop model in situ, intravenous carbachol, atropine, pirenzepine, and hexamethonium were used to determine the extent of cholinergic stimulation and the types of cholinoceptors. Carbachol (2 micrograms.kg-1.5 min-1) stimulated HCO3- secretion threefold, and atropine (0.1 mg.kg-1.5 min-1) and pirenzepine (1 mg.kg-1.5 min-1) both abolished this effect. In addition, hexamethonium (0.3 mg.kg-1.5 min-1) inhibited carbachol-stimulated duodenal HCO3- secretion. Vasoactive intestinal peptide (VIP, 5 micrograms.kg-1.5 min-1) stimulated duodenal HCO3- secretion, and this action was partly inhibited by atropine (0.1 mg.kg-1.5 min-1) but not by pirenzepine (1 mg.kg-1.5 min-1). [4Cl-D-Phe6,Leu17]VIP (3.3 mg/kg), an antagonist to VIP, reduced basal, VIP-stimulated, and carbachol-stimulated HCO3- secretion. To examine the role of Ca2+ in this process, Ca2+ ionophore A23187, verapamil, and nifedipine were employed. A23187 (5, 50, 500 micrograms.kg-1.5 min-1) stimulated duodenal HCO3- secretion, an effect blocked by the VIP antagonist, and modestly augmented the effect of carbachol. Verapamil (0.2 mg.kg-1.5 min-1) and nifedipine (1.7 mg.kg-1.5 min-1) stopped the effect of carbachol on duodenal HCO3- secretion. These results suggest, that in cholinergic regulation of duodenal HCO3- secretion, the M-cholinoceptor pathway, Ca2+, and VIP are involved.

Endothelial modulation of porcine coronary microcirculation perfused via immature collaterals

1992 ◽  
Vol 262 (6) ◽  
pp. H1669-H1675 ◽  
Author(s):  
F. W. Sellke ◽  
Y. Kagaya ◽  
R. G. Johnson ◽  
T. Shafique ◽  
F. J. Schoen ◽  
...  
Keyword(s):  
Sodium Nitroprusside ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Flow State ◽  
Vascular Studies ◽  
Collateral Vessels ◽  
Endothelium Dependent Relaxation ◽  
Minimal Evidence ◽  
Dependent Agents

Porcine hearts have relatively few native collateral vessels and lack the propensity to develop normal perfusion to the collateral-dependent myocardium. To examine microvascular responses in the collateral-dependent region, collateral vessels were stimulated in pigs by the Ameroid constrictor technique. After 4–7 wk, isolated microarterial vessels (90–170 microns ID) were studied in a pressurized (40 mmHg), no-flow state. Microvessels from noninstrumented pigs were used as controls for vascular studies. Although myocardium in the collateral-dependent region showed minimal evidence of infarction, percent systolic shortening was reduced at rest and after pacing compared with myocardium in the normally perfused region. Relaxations to the receptor-mediated endothelium-dependent agents ADP and bradykinin were impaired in collateral-dependent coronary microvessels. Relaxations to the calcium ionophore A23187, which acts through a non-receptor-mediated mechanism, were similar in control and Ameroid microvessels. Relaxations to the endothelium-independent agent sodium nitroprusside were markedly enhanced in microvessels from the collateral-dependent region compared with microvessels from control hearts. In conclusion, receptor-mediated endothelium-dependent relaxation is impaired and endothelium-independent relaxation to sodium nitroprusside is enhanced in microvessels from myocardium perfused by immature collateral vessels.

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