Short-term Exercise Training Prevents Micro-and Macrovascular Disease Following Coronary Stenting
aortic smooth-muscle; artery-disease; cholesterol-lowering therapy; diabetic dyslipidemic swine; dysfunction; endothelial; exercise; flow-velocity reserve; hyperlipidemia; low-fat diet; microvessel; myocardial-perfusion; ossabaw miniature swine; physical-exercise; Physiology; regular; restenosis; Sport Sciences; Yucatan swine
Long X; Bratz I N; Alloosh M; Edwards J M; Sturek M
Journal of Applied Physiology
2010
2010-06
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1152/japplphysiol.01014.2009" target="_blank" rel="noreferrer noopener">10.1152/japplphysiol.01014.2009</a>
Exercise Training Decreases Store-operated Ca2+ Entry Associated With Metabolic Syndrome And Coronary Atherosclerosis
artery-disease; calcium; calcium channel; Cardiovascular System & Cardiology; cardiovascular-disease; channels; Coronary smooth muscle; diabetic dyslipidemia; endothelial-cells; hyperplasia; Intravascular ultrasound; neointimal; Orai1; ossabaw miniature swine; ossabaw miniature swine; porcine model; smooth-muscle; STIM1; Store-operated; Transient receptor potential 1 channel
Edwards J M; Neeb Z P; Alloosh M; Long X; Bratz I N; Peller C R; Byrd J P; Kumar S; Obukhov A G; Sturek M
Cardiovascular Research
2010
2010-02
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1093/cvr/cvp308" target="_blank" rel="noreferrer noopener">10.1093/cvr/cvp308</a>
Contribution of BKCa channels to local metabolic coronary vasodilation: effects of metabolic syndrome
exercise; Physiology; Cardiovascular System & Cardiology; nitric-oxide; blood flow; coronary blood flow; smooth-muscle-cells; insulin-resistance; cardiovascular-disease; pigs; ca2+-activated k+ channels; induced relaxation; Ossabaw miniature swine; A; diabetic dyslipidemic; exercising dogs; myocardial oxygen consumption; myocardial-metabolism; penitrem
Borbouse L, Dick GM, Payne GA, Payne BD, Svendsen MC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Contribution of BKCa channels to local metabolic coronary vasodilation: effects of metabolic syndrome. Am J Physiol Heart Circ Physiol 298: H966-H973, 2010. First published December 31, 2009; doi:10.1152/ajpheart.00876.2009.-This investigation was designed to examine the hypothesis that impaired function of coronary microvascular large-conductance Ca2+-activated K+ (BKCa) channels in metabolic syndrome (MetS) significantly attenuates the balance between myocardial oxygen delivery and metabolism at rest and during exercise-induced increases in myocardial oxygen consumption (M(V) over dotO(2)). Studies were conducted in conscious, chronically instrumented Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) that induces many common features of MetS. Data were collected under baseline/resting conditions and during graded treadmill exercise before and after selective blockade of BKCa channels with penitrem A (10 mu g/kg iv). We found that the exercise-induced increases in blood pressure were significantly elevated in MetS swine. No differences in baseline cardiac function or heart rate were noted. Induction of MetS produced a parallel downward shift in the relationship between coronary venous PO2 and M(V) over dotO(2) (P < 0.001) that was accompanied by a marked release of lactate (negative lactate uptake) as M(V) over dotO(2) was increased with exercise (P < 0.005). Inhibition of BKCa channels with penitrem A did not significantly affect blood pressure, heart rate, or the relationship between coronary venous PO2 and M(V) over dotO(2) in lean or MetS swine. These data indicate that BKCa channels are not required for local metabolic control of coronary blood flow under physiological (lean) or pathophysiological (MetS) conditions. Therefore, diminished function of BKCa channels does not contribute to the impairment of myocardial oxygen-supply demand balance in MetS.
Borbouse L; Dick G M; Payne G A; Payne B D; Svendsen M C; Neeb Z P; Alloosh M; Bratz I N; Sturek M; Tune J D
American Journal of Physiology-Heart and Circulatory Physiology
2010
2010-03
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1152/ajpheart.00876.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00876.2009</a>
Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation
potassium channels; exercise; Physiology; Cardiovascular System & Cardiology; blood flow; activation; smooth-muscle-cells; heart; adenosine; adenosine triphosphate-dependent; arterioles; calcium-activated potassium channels; cardiovascular-disease mortality; coronary reactive hyperemia; myocardial reactive hyperemia; Ossabaw miniature swine; sensitive potassium channels; type 2 diabetes; voltage-activated potassium channels
Borbouse L, Dick GM, Payne GA, Berwick ZC, Neeb ZP, Alloosh M, Bratz IN, Sturek M, Tune JD. Metabolic syndrome reduces the contribution of K+ channels to ischemic coronary vasodilation. Am J Physiol Heart Circ Physiol 298: H1182-H1189, 2010. First published January 29, 2010; doi: 10.1152/ajpheart.00888.2009.-This investigation tested the hypothesis that metabolic syndrome decreases the relative contribution of specific K+ channels to coronary reactive hyperemia. Ca2+-activated (BKCa), voltage-activated (K-V), and ATP-dependent (K-ATP) K+ channels were investigated. Studies were conducted in anesthetized miniature Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) for 20 wk. The latter diet induces metabolic syndrome, increasing body weight, fasting glucose, total cholesterol, and triglyceride levels. Ischemic vasodilation was determined by the coronary flow response to a 15-s occlusion before and after cumulative administration of antagonists for BKCa (penitrem A; 10 mu g/kg iv), K-V (4-aminopyridine; 0.3 mg/kg iv) and K-ATP (glibenclamide; 1 mg/kg iv) channels. Coronary reactive hyperemia was diminished by metabolic syndrome as the repayment of flow debt was reduced similar to 30% compared with lean swine. Inhibition of BKCa channels had no effect on reactive hyperemia in either lean or metabolic syndrome swine. Subsequent inhibition of KV channels significantly reduced the repayment of flow debt (similar to 25%) in both lean and metabolic syndrome swine. Additional blockade of K-ATP channels further diminished (similar to 45%) the repayment of flow debt in lean but not metabolic syndrome swine. These data indicate that the metabolic syndrome impairs coronary vasodilation in response to cardiac ischemia via reductions in the contribution of K+ channels to reactive hyperemia.
Borbouse L; Dick G M; Payne G A; Berwick Z C; Neeb Z P; Alloosh M; Bratz I N; Sturek M; Tune J D
American Journal of Physiology-Heart and Circulatory Physiology
2010
2010-04
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1152/ajpheart.00888.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00888.2009</a>
Store-operated Ca2+influx predicts coronary artery disease and is induced by dyslipidemia in metabolic syndrome and type 2 diabetes
Biochemistry & Molecular Biology; Cell Biology; Life Sciences & Biomedicine - Other; Topics
Neeb Z P; Alloosh M; Edwards J; Bratz I N; Sturek M
Faseb Journal
2010
2010-04
Journal Article
n/a