scholarly journals Role of Calcium Binding by Sarcoplasmic Reticulum in the Contraction and Relaxation of Uterine Smooth Muscle

1969 ◽  
Vol 53 (4) ◽  
pp. 414-426 ◽  
Author(s):  
Mary E. Carsten

The binding of calcium by isolated sarcoplasmic reticulum from cow uterus was studied. Sarcoplasmic reticulum was prepared by differential centrifugation. Three fractions were obtained: I, sedimented between 2,500–15,000 x g; II at 40,000 x g; and III, at 150,000 x g. Fraction II was further purified on a sucrose density gradient. All three fractions contained considerable amounts of intrinsic calcium, mostly in fraction I. Calcium binding in the presence of ATP1 and Mg also was greatest in fraction I, followed by fraction II, with less in fraction III. Without ATP no calcium was taken up. 5 and 10 mM sodium azide partially inhibited calcium binding in fraction I, but not in fraction II, suggesting the presence of some mitochondria or mitochondrial fragments in fraction I. Calcium binding in fraction II was completely inhibited by 3 mM salyrgan; this fraction thus appears to be sarcoplasmic reticulum. ATPase activity was found in all three fractions, highest in fraction II. It is computed that calcium binding in fractions I and II, on the basis of a 50% yield of protein, is sufficient to elicit contraction by supplying calcium to the contractile proteins of the smooth muscle cell and to regulate relaxation and contraction.

1996 ◽  
Vol 63 (3) ◽  
pp. 145-147 ◽  
Author(s):  
E. Resnik ◽  
S. K. Chambers ◽  
M. L. Carcangiu ◽  
E. I. Kohorn ◽  
P. E. Schwartz ◽  
...  

2014 ◽  
Vol 90 (2) ◽  
pp. 102-110 ◽  
Author(s):  
Et Uluer ◽  
S Inan ◽  
K Ozbilgin ◽  
F Karaca ◽  
N Dicle ◽  
...  

Neurosignals ◽  
1992 ◽  
Vol 1 (4) ◽  
pp. 182-193 ◽  
Author(s):  
Hiroyuki Shimamoto ◽  
Ingrid L.A. Majarais ◽  
Yoriko Shimamoto ◽  
Chiu-Yin Kwan ◽  
Edwin E. Daniel

2004 ◽  
Vol 96 (3) ◽  
pp. 1069-1079 ◽  
Author(s):  
C. A. Witczak ◽  
M. Sturek

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.


Author(s):  
Eric W. Peterson ◽  
Richard Leblanc

SUMMARY:It is proposed that the basic mechanism of vasospasm which sometimes follows subarachnoid hemorrhage is dependent on increased free intracellular calcium ion produced by spasmogens from closely applied extravasated blood. Relaxation of this spasm occurs when the intracellular cyclic AMP levels are raised, resulting in sequestration of calcium ion by the vascular smooth muscle cell sarcoplasmic reticulum.


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