scholarly journals The relationship between intracellular calcium and contraction in calcium-overloaded ferret papillary muscles.

1985 ◽  
Vol 364 (1) ◽  
pp. 169-182 ◽  
Author(s):  
D G Allen ◽  
D A Eisner ◽  
J S Pirolo ◽  
G L Smith
1981 ◽  
Vol 61 (s7) ◽  
pp. 11s-12s ◽  
Author(s):  
N. Adragna ◽  
M. Canessa ◽  
I. Bize ◽  
H. Solomon ◽  
D. C. Tosteson

1. We describe in this paper a new ouabain-insensitive pathway for Na+ and K+ in human erythrocytes. K+ efflux was measured in cells loaded by the p-chloromercuribenzene-sulphonate (PCMBS) procedure to contain approximately equal amounts of Na+ and K+. K+ efflux was stimulated by external Na+ in the presence of ouabain and frusemide. Na+-stimulated K+ efflux was 0.35 ± 0.12 (mmol h−1 l−1 of cells) in eight normal subjects and 0.64 ± 0.13 in 13 patients with essential hypertension. 2. The Na+-stimulated K+ efflux was not observed in cells loaded in the presence of EGTA. This inhibition by EGTA suggests that K+ efflux is dependent on intracellular calcium. The Ki+-Nao+ countertransport of hypertensive patients was also inhibited by EGTA. The elevated K+—Na+ countertransport of hypertensive patients could be due to a higher intracellular Ca2+ content (Cai2+) or to an increased affinity for Cai2+. The relationship of this pathway to the Gardos effect is not clear since Na+-stimulated K+ efflux occurs without metabolic depletion or inhibition of the Ca2+ pump. As a tentative hypothesis, we relate the Ca2+-dependent downhill movement of K+ and Na+ to the Ca2+-dependent channels described in muscle and nerve, but other hypotheses cannot be excluded at this stage of our research.


2008 ◽  
Vol 41 (6) ◽  
pp. 487-490 ◽  
Author(s):  
Nina Hakacova ◽  
Anna M.C. Robinson ◽  
Charles W. Olson ◽  
Ronald H. Selvester ◽  
Galen S. Wagner

2013 ◽  
Vol 89 (5) ◽  
Author(s):  
Shavahn C. Loux ◽  
Kristin R. Crawford ◽  
Nancy H. Ing ◽  
Lauro González-Fernández ◽  
Beatriz Macías-García ◽  
...  

2004 ◽  
Vol 101 (3) ◽  
pp. 675-686 ◽  
Author(s):  
James D. Hannon ◽  
Mark J. Cody ◽  
David X. Sun ◽  
Philippe R. Housmans

Background Depression of myocardial contractility as a result of isoflurane appears to be greater in myocardial hypertrophy, and the cellular basis for this difference in susceptibility is not clear. In this study we examined the effects of isoflurane and sevoflurane on contractility and intracellular calcium in an animal model of pressure-overload hypertrophy. Methods Pressure-overload hypertrophy was established in young male ferrets by banding the main pulmonary artery for 1 month and the effects of isoflurane and sevoflurane on contractility and intracellular calcium ([Ca]i) were examined in isolated right ventricular papillary muscles, trabeculae, and myocytes. Intracellular calcium was measured with the bioluminescent photoprotein aequorin in isolated papillary muscles, and also with the fluorescent indicator fluo-3 in isolated ventricular myocytes. In addition, Ca sensitivity was assessed in isolated trabeculae after disruption of the surface membrane with a nonionic detergent (skinned fibers). Results In the presence of isoflurane and sevoflurane, papillary muscles from banded animals exhibited a greater depression of contractility and isolated ventricular myocytes showed a greater decrease in peak [Ca]i. Furthermore, baseline calcium sensitivity was decreased and the slope of the relationship between [Ca] and force was increased in skinned trabeculae from banded animals. Isoflurane decreased calcium sensitivity in trabeculae from both normal and banded animals. Conclusions These results suggest that changes in [Ca]i and altered calcium sensitivity are both responsible for the exaggerated effects of some volatile anesthetics on contractility in pressure-overload hypertrophy.


2015 ◽  
Vol 22 (1) ◽  
pp. 37-46
Author(s):  
Vygantas Barsys ◽  
Vida Garalienė ◽  
Gediminas Urbonas

Background. Identification of activity properties of new synthesized compounds is important to help choose the adequate research methodology. The goal of this experimental research was to determine the relationship between the chemical structure of 25 compounds of 1,4-dihydropyridine derivatives and their effects on the contraction force of guinea pig papillary muscles and the action potential (AP) duration. Methods. AP recordings were obtained with standard microelectrodes that were made from borosilicate glass capillaries, filled with 2.5 M KCl and connected to the high-input impedance amplification system. 1.0 Hz stimulation frequency was used. The contraction of papillary muscles was recorded by using a force transducer. Both signals (inotropic response and AP) were digitised by an A/D converter and registered by a computer specialised program. Results. The results have shown that most of 1,4-dihydropyridine derivatives possessed the negative inotropic action and had the negligible impact on the AP duration. It was identified that 1,4-dihydropyridine compound OSI 9719 (2-propoxyethyl-4-difloemethoxyphenyl-2-methyl-5-nitro-1,4-dihydro­pyridine-3carbo­xylate) had a prolonged duration of AP and simultaneously increased the force of contraction (p 


2000 ◽  
Vol 170 (4) ◽  
pp. 295-306 ◽  
Author(s):  
C. S. Kim ◽  
A. J. Davidoff ◽  
T. M. Maki ◽  
A. A. Doye ◽  
J. K. Gwathmey

1990 ◽  
Vol 258 (4) ◽  
pp. H1144-H1150 ◽  
Author(s):  
F. Mast ◽  
G. Elzinga

Contraction-related O2 consumption of rabbit papillary muscles was determined at 20 degrees C by measuring change in saline PO2 during and after trains of 120 twitches at 0.125-1 Hz in a microrespirometer. Although anoxic cores occurred at twitch frequencies greater than 0.2 Hz, no lactate was found in saline after twitch train. To measure lactate accumulation in muscle, fully oxygenated muscles were frozen at rest and during steady-state twitches at 0.2 Hz. We also measured nucleotides and creatine (Cr) compounds. There were no differences in lactate, ATP, and phosphocreatine (PCr) content between the resting and active muscles. When a P-to-O2 ratio of 6.3 is assumed, aerobic ATP formation was compared with glycolytic ATP formation during anoxia at a stimulus frequency of 0.2 Hz. The latter value was obtained by freezing muscles between 6 and 25 min after changing from O2- to N2-saturated saline. Withdrawal of O2 caused the ratio of PCr to total Cr to fall in less than 6 min from 0.77 to 0.23, while ATP remained at approximately 15 mumol/g dry wt. Force fell initially within 4 min to approximately 70% of control value, decreasing thereafter more slowly to approximately 40% at 20 min. From the relationship between amount of lactate formed and duration of anoxia, rate of anaerobic ATP formation was calculated assuming a P-to-lactate ratio of 1. We found that despite continuing contractile activity, anaerobic ATP formation was less than that required by a fully oxygenated resting muscle and was about the same magnitude as the estimated ATP hydrolysis for the contractions in N2. We conclude that in fully oxygenated rabbit papillary muscles no net lactate is produced during stimulation and that in anoxia anaerobic glycolytic capacity may not provide sufficient ATP for processes other than the uptake of Ca by the sarcoplasmic reticulum and cross-bridge cycling.


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