scholarly journals Exercise training increases basal tone in arterioles distal to chronic coronary occlusion

2006 ◽  
Vol 290 (3) ◽  
pp. H1128-H1135 ◽  
Author(s):  
Cristine L. Heaps ◽  
Mildred L. Mattox ◽  
Katherine A. Kelly ◽  
Cynthia J. Meininger ◽  
Janet L. Parker
Keyword(s):  
Nitric Oxide ◽  
Exercise Training ◽  
Coronary Occlusion ◽  
External Solution ◽  
Nitric Oxide Production ◽  
Miniature Swine ◽  
Oxide Production ◽  
Chronic Coronary Occlusion ◽  
Basal Tone ◽  
Coronary Arterioles

Endurance exercise training increases basal active tone in coronary arteries and enhances myogenic tone in coronary arterioles of control animals. Paradoxically, exercise training has also been shown to augment nitric oxide production and nitric oxide-mediated relaxation in coronary arterioles. The purpose of the present study was to examine the effect of exercise training on basal active tone of arterioles (∼150 μm ID) isolated from the collateral-dependent region of hearts exposed to chronic coronary occlusion. Ameroid occluders were surgically placed around the proximal left circumflex coronary artery of miniature swine. Arterioles were isolated from both the collateral-dependent and nonoccluded myocardial regions of sedentary (pen confined) and exercise-trained (treadmill run; 14 wk) pigs. Coronary tone was studied in isolated arterioles using microvessel myographs and standard isometric techniques. Exposure to nominally Ca2+-free external solution reduced resting tension in all arterioles; decreases were most profound ( P < 0.05) in arterioles from the collateral-dependent region of exercise-trained animals. Furthermore, nitric oxide synthase (NOS) inhibition ( Nω-nitro-l-arginine methyl ester; 100 μM) unmasked markedly increased nitric oxide-sensitive tone in arterioles from the collateral-dependent region of exercise-trained swine. Blockade of K+ channels revealed significantly enhanced K+ channel contribution to basal tone in collateral-dependent arterioles of exercise-trained pigs. Protein content of endothelial NOS (eNOS) and phosphorylated eNOS (pS1179), determined by immunoblot, was elevated in arterioles from exercise-trained animals with the greatest effect in collateral-dependent vasculature. Taken together, we demonstrate the interaction of opposing exercise training-enhanced arteriolar basal active tone, nitric oxide production, and K+ channel activity in chronic coronary occlusion, potentially enhancing the capacity to regulate blood flow to collateral-dependent myocardium.

scholarly journals Exercise Training Increases Basal Nitric Oxide Production From the Forearm in Hypercholesterolemic Patients

1999 ◽  
Vol 19 (11) ◽  
pp. 2782-2787 ◽  
Author(s):  
Tamara V. Lewis ◽  
Anthony M. Dart ◽  
Jaye P. F. Chin-Dusting ◽  
Bronwyn A. Kingwell
Keyword(s):  
Nitric Oxide ◽  
Exercise Training ◽  
Nitric Oxide Production ◽  
Oxide Production

Exercise training restores adenosine-induced relaxation in coronary arteries distal to chronic occlusion

2000 ◽  
Vol 278 (6) ◽  
pp. H1984-H1992 ◽  
Author(s):  
Cristine L. Heaps ◽  
Michael Sturek ◽  
Julie A. Rapps ◽  
M. Harold Laughlin ◽  
Janet L. Parker
Keyword(s):  
Coronary Artery ◽  
Exercise Training ◽  
Sodium Nitroprusside ◽  
Coronary Arteries ◽  
Coronary Occlusion ◽  
Circumflex Coronary Artery ◽  
Miniature Swine ◽  
Chronic Occlusion ◽  
Chronic Coronary Occlusion ◽  
Camp And Cgmp

We previously reported that canine collateral-dependent coronary arteries exhibit impaired relaxation to adenosine but not sodium nitroprusside. In contrast, exercise training enhances adenosine sensitivity of normal porcine coronary arteries. These results stimulated the hypothesis that chronic coronary occlusion and exercise training produce differential effects on cAMP- versus cGMP-mediated relaxation. To test this hypothesis, Ameroid occluders were surgically placed around the proximal left circumflex coronary artery (LCx) of female Yucatan miniature swine 8 wk before initiating sedentary or exercise training (treadmill run, 16 wk) protocols. Relaxation to the cAMP-dependent vasodilators adenosine (10− 7 to 10− 3 M) and isoproterenol (3 × 10− 8 to 3 × 10− 5 M) were impaired in collateral-dependent LCx versus nonoccluded left anterior descending (LAD) arterial rings isolated from sedentary but not exercise-trained pigs. Furthermore, adenosine-mediated reductions in simultaneous tension and myoplasmic free Ca2+ were impaired in LCx versus LAD arteries isolated from sedentary but not exercise-trained pigs. In contrast, relaxation in response to the cAMP-dependent vasodilator forskolin (10− 9 to 10− 5 M) and the cGMP-dependent vasodilator sodium nitroprusside (10− 9 to 10− 4 M) was not different in LCx versus LAD arteries of sedentary or exercise-trained animals. These data suggest that chronic occlusion impairs receptor-dependent, cAMP-mediated relaxation; receptor-independent cAMP- and cGMP-mediated relaxation were unimpaired. Importantly, exercise training restores cAMP-mediated relaxation of collateral-dependent coronary arteries.

CHRONIC CORONARY OCCLUSION, EXERCISE TRAINING, AND PLASMA LIPIDS IN MINIATURE SWINE

2001 ◽  
Vol 33 (5) ◽  
pp. S214
Author(s):  
K Wooten ◽  
S E. Martin ◽  
J L. Parker ◽  
M Mattox ◽  
J Fogarty ◽  
...  
Keyword(s):  
Exercise Training ◽  
Coronary Occlusion ◽  
Plasma Lipids ◽  
Miniature Swine ◽  
Chronic Coronary Occlusion

scholarly journals Effect of exercise training on nitric oxide and superoxide/H2O2 signaling pathways in collateral-dependent porcine coronary arterioles

2012 ◽  
Vol 112 (9) ◽  
pp. 1546-1555 ◽  
Author(s):  
Wei Xie ◽  
Janet L. Parker ◽  
Cristine L. Heaps
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Exercise Training ◽  
Vascular Function ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Miniature Swine ◽  
Protein Levels ◽  
Endothelial Nitric Oxide ◽  
Coronary Arterioles

Endothelial nitric oxide (NO) synthase (NOS) has been shown to contribute to enhanced vascular function after exercise training. Recent studies have revealed that relatively low concentrations of reactive oxygen species can contribute to endothelium-dependent vasodilation under physiological conditions. We tested the hypothesis that exercise training enhances endothelial function via endothelium-derived vasodilators, NO and superoxide/H2O2, in the underlying setting of chronic coronary artery occlusion. An ameroid constrictor was placed around the proximal left circumflex coronary artery to induce gradual occlusion in Yucatan miniature swine. At 8 wk postoperatively, pigs were randomly assigned to sedentary (pen-confined) or exercise-training (treadmill-run: 5 days/wk for 14 wk) regimens. Exercise training significantly enhanced concentration-dependent, bradykinin-mediated dilation in cannulated collateral-dependent arterioles (∼130 μm diameter) compared with sedentary pigs. NOS inhibition reversed training-enhanced dilation at low bradykinin concentrations in collateral-dependent arterioles, although increased dilation persisted at higher bradykinin concentrations. Total and phosphorylated (Ser1179) endothelial NOS protein levels were significantly increased in arterioles from collateral-dependent compared with the nonoccluded region, independent of exercise. The H2O2 scavenger polyethylene glycol-catalase abolished the training-enhanced bradykinin-mediated dilation in collateral-dependent arterioles; similar results were observed with the SOD inhibitor diethyldithiocarbamate. Fluorescence measures of bradykinin-stimulated H2O2 levels were significantly increased by exercise training, independent of occlusion. The NADPH inhibitor apocynin significantly attenuated bradykinin-mediated dilation in arterioles of exercise-trained, but not sedentary, pigs and was associated with significantly increased protein levels of the NADPH subunit p67phox. These data provide evidence that, in addition to NO, the superoxide/H2O2 signaling pathway significantly contributes to exercise training-enhanced endothelium-mediated dilation in collateral-dependent coronary arterioles.

Gender-specific K+-channel contribution to adenosine-induced relaxation in coronary arterioles

2002 ◽  
Vol 92 (2) ◽  
pp. 550-558 ◽  
Author(s):  
Cristine L. Heaps ◽  
Douglas K. Bowles
Keyword(s):  
Nitric Oxide ◽  
Intraluminal Pressure ◽  
K Channel ◽  
Apical Region ◽  
Channel Blockers ◽  
Miniature Swine ◽  
Basal Diameter ◽  
Male And Female ◽  
Basal Tone ◽  
Coronary Arterioles

We examined the contribution of K+-channel activity on basal tone and adenosine-mediated relaxation of coronary arterioles isolated from sexually mature male and female miniature swine. Arterioles (∼100–200 μm ID) isolated from the apical region of the heart were cannulated and studied using videodimensional analysis under constant intraluminal pressure. Coronary arterioles from male and female pigs demonstrated similar levels of basal tone and reductions in basal diameter in response to the K+-channel blockers 4-aminopyridine (4-AP; 1 mM), tetraethylammonium (1 mM), and glibenclamide (Glib; 10 μM), with 4-AP producing significantly greater constriction than tetraethylammonium or Glib. After endothelin-induced preconstriction, relaxation responses to adenosine were not significantly different between coronary arterioles of male and female pigs. Inhibition of 4-AP-sensitive channels significantly impaired adenosine-mediated relaxation in arterioles from male but not female pigs. However, inhibition of K+ channels with iberiotoxin (100 nM) or Glib had no effect on adenosine-induced relaxation in either sex. Results obtained in the presence of nitric oxide synthase inhibition suggest a potential interaction of 4-AP-sensitive channels and nitric oxide at low adenosine concentrations. In conclusion, our data indicate that 4-AP-sensitive channels 1) contribute significantly to basal tone in coronary arterioles of both male and female pigs, 2) contribute to adenosine-mediated relaxation in male but not female pigs, and 3) can contribute to adenosine-induced relaxation independent of nitric oxide production in male pigs. These data are consistent with a significant role for voltage-dependent K+channels in adenosine-mediated relaxation of coronary arterioles from males.

Exercise training improves endothelium-mediated vasorelaxation after chronic coronary occlusion

1999 ◽  
Vol 87 (5) ◽  
pp. 1948-1956 ◽  
Author(s):  
Kawanza L. Griffin ◽  
M. Harold Laughlin ◽  
Janet L. Parker
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Nitric Oxide Synthase ◽  
Exercise Training ◽  
Coronary Occlusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Chronic Coronary Occlusion ◽  
Enhanced Production ◽  
Oxide Synthase

The present study evaluated combined effects of chronic coronary occlusion and exercise training on endothelial function. Gradual occlusion was produced by placement of an ameroid constrictor around the proximal left circumflex (LCX) coronary artery of female swine. Two months after placement of the ameroid, animals were restricted to their pens or exercise trained for 16 wk. Epicardial arteries (>500 μm ID) were isolated from the collateral-dependent LCX coronary artery distal to the occlusion and the nonoccluded left anterior descending (LAD) coronary artery. Bradykinin- and ADP-mediated relaxation of LCX and LAD coronary arteries was enhanced after exercise training. Inhibition of nitric oxide synthase with N G-nitro-l-arginine methyl ester decreased bradykinin- and ADP-mediated relaxation in LCX and LAD myocardial regions. Importantly, combined inhibition of effects of endothelium-derived hyperpolarizing factor with increased extracellular K+ (20–30 mM) and nitric oxide synthase completely abolished coronary LAD and LCX relaxation to bradykinin. Our data indicate that exercise training improves endothelium-mediated relaxation of arteries isolated after chronic coronary artery occlusion, likely as a result of enhanced production of nitric oxide and endothelium-derived hyperpolarizing factor.

Sign in / Sign up

Export Citation Format

Share Document