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

C. A. Witczak, M. Sturek

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

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 Ca 2+ influx is decreased and SR Ca2+ uptake is increased. Exercise prevents diabetic dyslipidemia-induced increases in basal Ca 2+ 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 Ca 2+ 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 plasmalemrnal Ca2+ extrusion. On the basis of these results, we conclude exercise attenuates the diabetic dyslipidemia-induced impairment in intracellular Ca 2+ regulation.

Original languageEnglish (US)
Pages (from-to)1069-1079
Number of pages11
JournalJournal of Applied Physiology
Volume96
Issue number3
DOIs
StatePublished - Mar 1 2004

Fingerprint

Sarcoplasmic Reticulum
Smooth Muscle
Dyslipidemias
Buffers
Swine
Calcium-Transporting ATPases
Iodides
Caffeine
Smooth Muscle Myocytes
Coloring Agents
Control Groups
Membranes

Keywords

  • Plasma membrane calcium-adenosine-triphosphatase
  • Sarco(endo)plasmic reticulum calcium-transporting adenosinetriphosphatase
  • Sodium-calcium exchanger

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Exercise prevents diabetes-induced impairment in superficial buffer barrier in porcine coronary smooth muscle. / Witczak, C. A.; Sturek, M.

In: Journal of Applied Physiology, Vol. 96, No. 3, 01.03.2004, p. 1069-1079.

Research output: Contribution to journalArticle

@article{8359d9dd9d5a4471851eab8b598998af,
title = "Exercise prevents diabetes-induced impairment in superficial buffer barrier in porcine coronary smooth muscle",
abstract = "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 Ca 2+ influx is decreased and SR Ca2+ uptake is increased. Exercise prevents diabetic dyslipidemia-induced increases in basal Ca 2+ 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 Ca 2+ 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 plasmalemrnal Ca2+ extrusion. On the basis of these results, we conclude exercise attenuates the diabetic dyslipidemia-induced impairment in intracellular Ca 2+ regulation.",
keywords = "Plasma membrane calcium-adenosine-triphosphatase, Sarco(endo)plasmic reticulum calcium-transporting adenosinetriphosphatase, Sodium-calcium exchanger",
author = "Witczak, {C. A.} and M. Sturek",
year = "2004",
month = "3",
day = "1",
doi = "10.1152/japplphysiol.00460.2003",
language = "English (US)",
volume = "96",
pages = "1069--1079",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "3",

}

TY - JOUR

T1 - Exercise prevents diabetes-induced impairment in superficial buffer barrier in porcine coronary smooth muscle

AU - Witczak, C. A.

AU - Sturek, M.

PY - 2004/3/1

Y1 - 2004/3/1

N2 - 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 Ca 2+ influx is decreased and SR Ca2+ uptake is increased. Exercise prevents diabetic dyslipidemia-induced increases in basal Ca 2+ 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 Ca 2+ 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 plasmalemrnal Ca2+ extrusion. On the basis of these results, we conclude exercise attenuates the diabetic dyslipidemia-induced impairment in intracellular Ca 2+ regulation.

AB - 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 Ca 2+ influx is decreased and SR Ca2+ uptake is increased. Exercise prevents diabetic dyslipidemia-induced increases in basal Ca 2+ 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 Ca 2+ 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 plasmalemrnal Ca2+ extrusion. On the basis of these results, we conclude exercise attenuates the diabetic dyslipidemia-induced impairment in intracellular Ca 2+ regulation.

KW - Plasma membrane calcium-adenosine-triphosphatase

KW - Sarco(endo)plasmic reticulum calcium-transporting adenosinetriphosphatase

KW - Sodium-calcium exchanger

UR - http://www.scopus.com/inward/record.url?scp=1342346636&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1342346636&partnerID=8YFLogxK

U2 - 10.1152/japplphysiol.00460.2003

DO - 10.1152/japplphysiol.00460.2003

M3 - Article

C2 - 14634027

AN - SCOPUS:1342346636

VL - 96

SP - 1069

EP - 1079

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 3

ER -