Functional Nucleotide Receptor Expression and Sarcoplasmic Reticulum Morphology in Dedifferentiated Porcine Coronary Smooth Muscle Cells

2001 ◽  
Vol 38 (5) ◽  
pp. 432-443 ◽  
Author(s):  
Brent J.F. Hill ◽  
Brian R. Wamhoff ◽  
Michael Sturek
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Receptor Expression ◽  
Nucleotide Receptor ◽  
Coronary Smooth Muscle

Exercise prevents diabetes-induced impairment in superficial buffer barrier in porcine coronary smooth muscle

2004 ◽  
Vol 96 (3) ◽  
pp. 1069-1079 ◽  
Author(s):  
C. A. Witczak ◽  
M. Sturek
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Diabetic Dyslipidemia ◽  
Coronary Smooth Muscle ◽  
Treatment Groups ◽  
Analysis Techniques ◽  
Intracellular Ca

In healthy coronary smooth muscle cells, the superficial sarcoplasmic reticulum (SR) buffers rise in intracellular Ca2+ levels. In diabetic dyslipidemia, basal Ca2+ levels are increased, yet Ca2+ influx is decreased and SR Ca2+ uptake is increased. Exercise prevents diabetic dyslipidemia-induced increases in basal Ca2+ levels and decreases in Ca2+ influx. We tested the hypothesis that diabetic dyslipidemia impairs Ca2+ extrusion via a decrease in superficial SR and that exercise will prevent these losses. Male Yucatan swine were maintained in four treatment groups: control, hyperlipidemic, diabetic dyslipidemic, and diabetic dyslipidemic plus aerobically exercise trained. Intracellular Ca2+ levels were measured during depolarization-induced Ca2+ influx and caffeine-induced SR Ca2+ release. Na+/Ca2+ exchanger and plasmalemmal Ca2+-ATPase activity were assessed by inhibition with low extracellular Na+ and 5,6-carboxyeosin, respectively. Superficial SR was quantified using the internal membrane dye 3,3′-dihexyloxacarbocyanine iodide (DiOC6) and novel analysis techniques. We found that, in diabetic dyslipidemia, Ca2+ extrusion was impaired and superficial SR was decreased. Exercise prevented the diabetic dyslipidemia-induced decrease in superficial SR and restored plasmalemmal Ca2+ extrusion. On the basis of these results, we conclude exercise attenuates the diabetic dyslipidemia-induced impairment in intracellular Ca2+ regulation.

Exercise training depletes sarcoplasmic reticulum calcium in coronary smooth muscle

1991 ◽  
Vol 71 (5) ◽  
pp. 1764-1773 ◽  
Author(s):  
L. Stehno-Bittel ◽  
M. H. Laughlin ◽  
M. Sturek
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Exercise Training ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Single Coronary Artery ◽  
Coronary Smooth Muscle ◽  
Low Concentrations ◽  
K Current ◽  
In Cells

We examined the effects of chronic exercise training on sarcoplasmic reticulum (SR) Ca uptake, spontaneous SR Ca release, and whole-cell currents in coronary smooth muscle cells. Single coronary artery smooth muscle cells demonstrated increases in intracellular free Ca (Cai) during depolarization (measured with fura-2) that were abolished by diltiazem (10(-4) M). Diltiazem significantly inhibited (80%) refilling of the SR Ca store. The SR Ca store of exercise-trained pigs was 64% less after 11 min vs. 2 min of recovery, whereas cells from sedentary pigs showed no depletion. Exercise-training-induced depletion of the SR Ca store was abolished when ryanodine (10(-5) M) was applied during the recovery, but depletion was enhanced by low concentrations of ryanodine (10(-8) M). In smooth muscle from sedentary pigs, 10(-8) M ryanodine mimicked the effects of exercise training by depleting the SR Ca store during 11 min of recovery (54% depletion). When allowed a longer recovery without ryanodine (14 min or without prior depolarization), the SR Ca store in cells from exercise-trained pigs returned toward peak levels. The outward K current vs. voltage relationship did not differ in cells from exercise-trained or sedentary pigs. Exercise training reduced the number of spontaneous transient outward currents normally found in cells from sedentary pigs. We introduce a model that provides a rational basis to explain the results obtained in this study.

Regulation of Scavenger Receptor Expression in Smooth Muscle Cells by Protein Kinase C

1997 ◽  
Vol 17 (5) ◽  
pp. 969-978 ◽  
Author(s):  
Michele Mietus-Snyder ◽  
Annabelle Friera ◽  
Christopher K. Glass ◽  
Robert E. Pitas
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Scavenger Receptor ◽  
Muscle Cells ◽  
Receptor Expression ◽  
Kinase C

Ethanol Modulates Cyclic GMP Metabolism in Cultured Coronary Smooth Muscle Cells

Angiology ◽  
1993 ◽  
Vol 44 (1) ◽  
pp. 62-68 ◽  
Author(s):  
Yukio Kishi ◽  
Toshiyuki Oniki ◽  
Takashi Ashikaga ◽  
Fujio Numano
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cyclic Gmp ◽  
Muscle Cells ◽  
Coronary Smooth Muscle
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