Role of calcium channel in postvagal potentiation of contraction as evident from the effects of Mn2+, La3+, D-600, and deoxycholate on isolated guinea pig atria–vagus nerve preparation

1986 ◽  
Vol 64 (5) ◽  
pp. 575-580
Author(s):  
Onkar N. Tripathi ◽  
M. Mehrotra ◽  
B. N. Dhawan
Keyword(s):  
Guinea Pig ◽  
Calcium Channel ◽  
Vagal Stimulation ◽  
Channel Blockers ◽  
Triggered Release ◽  
High Concentrations ◽  
Spontaneous Contractions ◽  
Guinea Pig Atria ◽  
Large Contraction

The role of the calcium channel in the first large contraction (postvagal potentiation, PVP) of the atria at the end of the inhibitory phase of its response (IPR) to vagal stimulation has been investigated by studying the effects of agents acting on the calcium channel (e.g., Ca2+, Mn2+, La3+, and D-600) or sarcoplasmic reticulum (SR) (e.g., deoxycholate (DOC)). IPR was potentiated by high [Ca2+]o (3–16 mM) and also by the calcium channel blockers, Mn2+ (1 μM–0.5 mM), La3+ (0.1 μM–0.5 mM), D-600 (1.0–10 μM), and DOC (1 μM–0.5 mM). PVP was also potentiated by enhanced [Ca2+]o, but the PVP ratio, which employs a correction for the simultaneous changes in the force of spontaneous contraction was inhibited. This indicated greater potentiation of contractility during spontaneous activity by Ca2+ than during PVP. Mn2+, La3+, and D-600 and even DOC in the above concentrations inhibited PVP but increased the PVP ratio. High concentrations of DOC (>1 mM), which disrupt SR, strongly inhibited PVP. It is concluded that the calcium channel plays a more prominent role in spontaneous contractions than in PVP in guinea pig atria. PVP is suggested to be generated by excessive triggered release of Ca2+ from SR leading to a marked increase in [Ca2+]i. The calcium channel and the calcium trapped in the glycocalyx also play significant roles in PVP.

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.

Sources and implications of basal nitric oxide in spontaneous contractions of guinea pig taenia caeci

2003 ◽  
Vol 285 (4) ◽  
pp. G747-G753 ◽  
Author(s):  
Catalina Caballero-Alomar ◽  
Carmen Santos ◽  
Diego Lopez ◽  
M. Teresa Mitjavila ◽  
Pere Puig-Parellada
Keyword(s):  
Nitric Oxide ◽  
Guinea Pig ◽  
Inhibitory Effect ◽  
No Production ◽  
Paramagnetic Resonance ◽  
Synthase Inhibitor ◽  
Spontaneous Contractions ◽  
Electron Paramagnetic

We examined in vitro the source and role of basal nitric oxide (NO) in proximal segments of guinea pig taenia caeci in nonadrenergic, noncholinergic (NANC) conditions. Using electron paramagnetic resonance (EPR), we measured the effect of the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 10–4 M), the neuronal blocker tetrodotoxin (TTX, 10–6 M), or both on spontaneous contractions and on the production of basal NO. Both l-NAME and TTX, when tested alone, increased the amplitude and frequency of contractions. NO production was abolished by l-NAME and was inhibited by 38% by TTX. When tested together, l-NAME in the presence of TTX or TTX in the presence of l-NAME had no further effect on the amplitude or frequency of spontaneous contractions, and the NO production was inhibited. These findings suggest that basal NO consists of TTX-sensitive and TTX-resistant components. The TTX-sensitive NO has an inhibitory effect on spontaneous contractions; the role of TTX-resistant NO is unknown.

scholarly journals FP450THE ROLE OF T-TYPE CALCIUM CHANNEL BLOCKERS IN ANGIOGENESIS IN DIABETES

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii222-iii222
Author(s):  
Jenq-Shyong Chan ◽  
Tao-Cheng Wu ◽  
Jaw-Wen Chen
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Channel Blockers

Dual Therapy in Hypertensive Patients with Coronary Artery Disease: The Role of Calcium Channel Blockers and ??-Blockers

2007 ◽  
Vol 7 (Suppl 1) ◽  
pp. 25???29 ◽  
Author(s):  
George L Bakris ◽  
Rhonda M Cooper-DeHoff ◽  
Qian Zhou ◽  
Stuart Kupfer ◽  
Annette Champion ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Dual Therapy ◽  
Channel Blockers ◽  
Hypertensive Patients ◽  
Artery Disease

scholarly journals CRT-200.42 The Role of Calcium Channel Blockers in Radial Cocktail on Radial Artery Spasm, A Meta Analysis

2016 ◽  
Vol 9 (4) ◽  
pp. S15-S16
Author(s):  
Muhammad S. Azzouz ◽  
Saurabh Aggarwal ◽  
Abhilash Akinapelli ◽  
Toufik Mahfood Haddad ◽  
Manu Kaushik ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Radial Artery ◽  
Calcium Channel Blockers ◽  
Meta Analysis ◽  
Channel Blockers

scholarly journals Role of combination therapy with ACE inhibitors and calcium channel blockers in renal protection

2002 ◽  
Vol 62 ◽  
pp. S53-S60 ◽  
Author(s):  
Francesco Locatelli ◽  
Lucia Del Vecchio ◽  
Simeone Andrulli ◽  
Sara Colzani
Keyword(s):  
Combination Therapy ◽  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Ace Inhibitors ◽  
Channel Blockers ◽  
Renal Protection

scholarly journals Photoaffinity labelling of the cardiac calcium channel. (−)-[3H]azidopine labels a 165 kDa polypeptide, and evidence against a [3H]-1,4-dihydropyridine-isothiocyanate being a calcium-channel-specific affinity ligand

1987 ◽  
Vol 243 (1) ◽  
pp. 127-135 ◽  
Author(s):  
D R Ferry ◽  
A Goll ◽  
H Glossmann
Keyword(s):  
Guinea Pig ◽  
Calcium Channel ◽  
Polyacrylamide Gel Electrophoresis ◽  
Dimethyl Ester ◽  
High Capacity ◽  
Bay K 8644 ◽  
Channel Blockers ◽  
Guinea Pig Heart ◽  
Affinity Ligand ◽  
Heart Membranes

The arylazide 1,4-dihydropyridine (-)-[3H]azidopine binds to a saturable population of sites in guinea-pig heart membranes with a dissociation constant (KD) of 30 +/- 7 pM and a density (Bmax.) of 670 +/- 97 fmol/mg of protein. This high-affinity binding site is assumed to reside on voltage-operated calcium channels because reversible binding is blocked stereoselectively by 1,4-dihydropyridine channel blockers and by the enantiomers of Bay K 8644. A low-affinity (KD 25 +/- 7 nM) high-capacity (Bmax. 21.6 +/- 9 pmol/mg of protein) site does not bind (-)- or (+)-Bay K 8644, but is blocked by high concentrations (greater than 500 nM) of dihydro-2,6-dimethyl-4-(2-isothiocyanatophenyl)-3,5-pyridinedicarboxy lic acid dimethyl ester (1,4-DHP-isothiocyanate) or, e.g., (+/-)-nicardipine. (-)-[3H]Azidopine was photoincorporated covalently into bands of 165 +/- 8, 39 +/- 2 and 35 +/- 3 kDa, as determined by SDS/polyacrylamide-gel electrophoresis. Labelling of the 165 kDa band is protected stereoselectively by 1,4-dihydropyridine enantiomers at low (nM) concentrations and by (-)- and (+)-Bay K 8644, whereas the lower-Mr bands are not. Thus, only the 165 kDa band is the calcium-channel-linked 1,4-dihydropyridine receptor. Photolabelling of the 39 or 35 kDa bands was only blocked by 10 microM-1,4-DHP-isothiocyanate or 50 microM-(+/-)-nicardipine but not by 10 microM-(-)-Bay K 8644. [3H]-1,4-DHP-isothiocyanate binds to guinea-pig heart membranes with a KD of 0.35 nM and dissociates with a k-1 of 0.2 min-1 at 30 degrees C. [3H]-1,4 DHP-isothiocyanate irreversibly labels bands of 39 and 35 kDa which are protected by greater than 10 microM-(+/-)-nicardipine or unlabelled ligand but not by 10 microM-(-)-Bay K 8644. Thus, [3H]-1,4-DHP-isothiocyanate is not an affinity probe for the calcium channel.

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