Erratum: Evidence for mobilization of intracellular calcium during the contractile response of the rat aorta to U44069

1982 ◽  
Vol 60 (12) ◽  
pp. 1737-1737
Author(s):  
Richard J. Heaslip ◽  
Ralf G. Rahwan
Keyword(s):  
Intracellular Calcium ◽  
Contractile Response ◽  
Rat Aorta ◽  
Extracellular Calcium

On page 745, left column, the first complete sentence should read "Contractions induced by U44069 in the absence of extracellular calcium (and in the absence or the presence of nifedipine, bu-MDI, or Q-bu-MDI) were expressed as a percentage of the maximum contraction induced by U44069 alone in the presence of 2.5 mM bath calcium."On page 745, the second sentence of the Results section should read "Although tissues which had been washed in calcium-free buffer containing no EGTA contracted tonically upon exposure to 100 mM KCl to 14% of the maximum attainable contraction in the presence of extracellular calcium, tissues which had been washed in calcium-free EGTA buffers were refractory."

Evidence for mobilization of intracellular calcium during the contractile response of the rat aorta to U44069

1982 ◽  
Vol 60 (5) ◽  
pp. 743-746 ◽  
Author(s):  
Richard J. Heaslip ◽  
Ralf G. Rahwan
Keyword(s):  
Calcium Antagonist ◽  
Intracellular Calcium ◽  
Channel Blocker ◽  
Contractile Response ◽  
Rat Aorta ◽  
Extracellular Calcium ◽  
Pharmacological Mechanism ◽  
Persistent Effect ◽  
Contractile Effect ◽  
Intracellular Calcium Antagonist

The aim of the present investigation was to elucidate the pharmacological mechanism by which U44069, a stable PGH2 analogue, contracts the rat aorta. The results obtained demonstrate that while the contractile effect of potassium chloride is obliterated by removal of extracellular calcium, a substantial proportion of the contractile effect of U44069 persists under these conditions. The persistent effect of U44069 under calcium-free conditions was not diminished by nifedipine (a slow calcium channel blocker) but was blocked by 2-n-butyl-3-dimethylamino-5,6-methylenedioxyindene (an intracellular calcium antagonist). These results provide experimental evidence for the proposal that U44069 contracts the aorta in the absence of extracellular calcium by mobilizing intracellular calcium.

scholarly journals alpha-Adrenergic activation of phosphorylase in liver cells involves mobilization of intracellular calcium without influx of extracellular calcium.

1982 ◽  
Vol 257 (1) ◽  
pp. 190-197 ◽  
Author(s):  
P.F. Blackmore ◽  
B.P. Hughes ◽  
E.A. Shuman ◽  
J.H. Exton
Keyword(s):  
Intracellular Calcium ◽  
Liver Cells ◽  
Extracellular Calcium ◽  
Adrenergic Activation

The effect of 2-n-propyl-3-dimethylamino-5,6-methylenedioxyindene on caffeine-induced contractures of skeletal muscle

1981 ◽  
Vol 59 (6) ◽  
pp. 617-620 ◽  
Author(s):  
Ralf G. Rahwan ◽  
Michael C. Gerald
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Calcium ◽  
Extracellular Calcium ◽  
Site Of Action ◽  
Isolated Rat

It has been previously postulated that 2-n-propyl-3-dimethylamino-5,6-methylenedioxyindene (pr-MDI) exhibits calcium antagonistic properties with an intracellular site of action. The present investigation further substantiates this hypothesis by providing evidence that pr-MDI inhibits caffeine-induced contractures (which are mediated by intracellular calcium) of the isolated rat hemidiaphragm skeletal muscle both in the presence and in the absence of extracellular calcium.

Action potential propagation through embryonic dorsal root ganglion cells in culture. II. Decrease of conduction reliability during repetitive stimulation

1994 ◽  
Vol 72 (2) ◽  
pp. 634-643 ◽  
Author(s):  
C. Luscher ◽  
J. Streit ◽  
P. Lipp ◽  
H. R. Luscher
Keyword(s):  
Dorsal Root Ganglion ◽  
Action Potential ◽  
Intracellular Calcium ◽  
Dorsal Root ◽  
Channel Blocker ◽  
Extracellular Calcium ◽  
Repetitive Stimulation ◽  
Calcium Currents ◽  
Double Pulse ◽  
Extracellular Potassium

1. The reliability of the propagation of action potentials (AP) through dorsal root ganglion (DRG) cells in embryonic slice cultures was investigated during repetitive stimulation at 1–20 Hz. Membrane potentials of DRG cells were recorded intracellularly while the axons were stimulated by an extracellular electrode. 2. In analogy to the double-pulse experiments reported previously, either one or two types of propagation failures were recorded during repetitive stimulation, depending on the cell morphology. In contrast to the double-pulse experiments, the failures appeared at longer interpulse intervals and usually only after several tens of stimuli with reliable propagation. 3. In the period with reliable propagation before the failures, a decrease in the conduction velocity and in the amplitude of the afterhyperpolarization (AHP), an increase in the total membrane conductance, and the disappearance of the action potential “shoulder” were observed. 4. The reliability of conduction during repetitive stimulation was improved by lowering the extracellular calcium concentration or by replacing the extracellular calcium by strontium. The reliability of conduction decreased by the application of cadmium, a calcium channel blocker, 4-amino pyridine, a fast potassium channel blocker, or apamin or muscarine, the blockers of calcium-dependent potassium channels. The reliability of conduction was not effected by blocking the sodium potassium pump with ouabain or by replacing extracellular sodium with lithium. 5. In the period with reliable propagation cadmium, apamin, and muscarine reduced the amplitude of the AHP. The shoulder of the action potential was more pronounced and not sensitive to repetitive stimulation when extracellular calcium was replaced by strontium. It disappeared when cadmium was applied. 6. In DRG somata changes of the intracellular Ca2+ concentration were monitored by measuring the fluorescence of the Ca2+ indicator Fluo-3 with a laser-scanning confocal microscope. During repetitive stimulation, an accumulation of intracellular calcium occurred that recovered very slowly (tens of seconds) after the AP trains. 7. Computer model simulations performed in analogy to the experimental protocols produced conduction failures during repetitive stimulation only when the calcium currents during the APs were reduced. 8. From these findings it is concluded that conduction failures during repetitive stimulation are dependent on an accumulation of intracellular calcium leading to an inactivation of calcium currents, combined with small contributions of an accumulation of extracellular potassium and a summation of slow potassium conductances.

scholarly journals Intracellular calcium mobilization and activation of the Na+/H+ exchanger in platelets

1993 ◽  
Vol 290 (2) ◽  
pp. 617-622 ◽  
Author(s):  
E Poch ◽  
A Botey ◽  
J Gaya ◽  
A Cases ◽  
F Rivera ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Fluorescent Dyes ◽  
Extracellular Calcium ◽  
Free Calcium ◽  
Regulatory Relationship ◽  
Cytosolic Ph ◽  
Intracellular Calcium Mobilization ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration ◽  
Intracellular Alkalinization

The aim of the present study was to evaluate the regulatory relationship between the cytosolic free calcium concentration ([Ca2+]i and cytosolic pH (pHi). [Ca2+]i and pHi were measured using the fluorescent dyes fura-2 and BCECF [2′,7′-bis-(carboxyethyl)-5,6-carboxyfluorescein] respectively. In a medium with 1 mmol/l extracellular calcium, thrombin (2.5 units/ml) induced an increment in [Ca2+]i of 638 +/- 31 nmol/l (n = 5) and an intracellular alkalinization of 0.14 +/- 0.01 pH units (n = 8). Both responses were dependent on the concentration of thrombin, displaying a sigmoidal dose-response pattern. The intracellular alkalinization was dependent upon extracellular Na+ and was amiloride-sensitive, indicating that it was mediated by activation of the Na+/H+ exchanger. When extracellular calcium was chelated with EGTA prior to the addition of thrombin, the intracellular alkalinization was not affected (0.15 +/- 0.02 at 2.5 units/ml thrombin, n = 8). Under these circumstances, the [Ca2+]i increment represents mobilization from internal stores, reaching 157 +/- 42 nmol/l at 2.5 units/ml thrombin. When platelets were preloaded with the intracellular calcium chelator MAPTAM (1,2-bis-5-methylaminophenoxylethane-NNN'-tetraacetoxymethyl acetate) to block the increase in [Ca2+]i induced by thrombin, no increment in pHi was observed. Moreover, MAPTAM-loaded calcium-depleted platelets had a basal pHi that was more acidic than in the presence of 1 mmol/l extracellular calcium (6.93 +/- 0.09 versus 7.14 +/- 0.01, n = 26, P < 0.001). Ionomycin induced an elevation of [Ca2+]i that was accompanied by a concomitant increase in pHi, which was Na(+)-dependent and amiloride-sensitive. [Ca2+]i and pHi increases induced by ionomycin were both dependent on the concentration of ionomycin. In conclusion, an increase in [Ca2+]i is necessary for the agonist-induced activation of the Na+/H+ exchanger in platelets. Non-agonist-induced increases in [Ca2+]i seems to prompt activation of the exchanger. In addition, Ca(2+)-depleted platelets have a more acidic basal pHi, indicating that the basal level of [Ca2+]i is also important for maintaining the basal pHi.

Effect of Divalent Cations on the Contractile Response of Rat Aorta to Depolarization before and after Nifedipine Treatment

Pharmacology ◽  
1996 ◽  
Vol 53 (2) ◽  
pp. 98-108 ◽  
Author(s):  
M.A. Noguera ◽  
S. Chulia ◽  
M. Elorriaga ◽  
M.D. Ivorra ◽  
P. D&rsquo;Ocon
Keyword(s):  
Contractile Response ◽  
Divalent Cations ◽  
Rat Aorta ◽  
Before And After

scholarly journals Effect of lysophosphatidylcholine on intracellular calcium levels and contraction in rat aorta

1998 ◽  
Vol 76 ◽  
pp. 216
Author(s):  
Hiroshi Suenaga ◽  
Katsuo Kamata
Keyword(s):  
Intracellular Calcium ◽  
Rat Aorta
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