Vasodilator responses of coronary resistance arteries of exercise-trained pigs.

Muller, Judy M.; Myers, Paul R.; Laughlin, M. Harold

doi:10.1161/01.cir.89.5.2308

Cited by 140 publications

(142 citation statements)

References 21 publications

Supporting

Mentioning

120

Contrasting

Unclassified

Order By: Relevance

“…EX animals entered a progressive treadmill running program for 16 weeks, and SED animals remained inactive by cage confinement during this period. The exercise program has been used extensively by Laughlin and colleagues 7,8,16,17 and is similar to that described by Tipton et al 18 In brief, during the first week of training, animals ran at 4 to 5 mph, 0% grade for 15 minutes (sprint) and 3 mph, 0% grade for 20 to 30 minutes (endurance). Speed and duration were progressively increased depending on the ability of the animal.…”

Section: Exercise-training Programmentioning

confidence: 99%

“…From each EX and SED animal, we isolated size-matched arterioles (Ϸ100 m ID) from both the collateral-dependent LCx region (distal to occlusion) and the nonoccluded LAD region; collateral-dependent arterioles were easily identified as arteriolar branches arising from LCx branch arteries distal to occlusion. Arterioles were evaluated as reported by Muller et al 8 Briefly, arterioles were placed into a Plexiglas chamber filled with Krebs solution (95% O 2 /5% CO 2 ; pH 7.4) and maintained at 4°C. Each end of the arteriole was cannulated with a glass micropipette (40-to 60-m ID) and secured with 10-0 Ethicon nylon suture.…”

Section: Isolation and Preparation Of Coronary Arteriolesmentioning

confidence: 99%

“…Significant evidence indicates that in normal hearts, exercise training increases coronary endothelium-dependent relaxation 7,8 ; these effects are associated with increases in nitric oxide (NO) [7][8][9][10] production and endothelial nitric oxide synthase (ecNOS) gene expression. 10,11 Conversely, canine and porcine hearts exposed to chronic coronary occlusion exhibit impaired endothelium-dependent vasorelaxation [12][13][14] and enhancement of selected vasoconstrictor responses.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Endothelium-Mediated Relaxation of Porcine Collateral-Dependent Arterioles Is Improved by Exercise Training

et al. 2001

View full text Add to dashboard Cite

Background-Endothelium-dependent modulation of coronary tone is impaired in the collateral-dependent coronary microcirculation. We used a porcine model of chronic coronary occlusion and collateral development to evaluate the hypothesis that exercise training enhances endothelium-mediated relaxation and increases endothelial nitric oxide synthase (ecNOS) mRNA levels of collateral-dependent microvasculature. Methods and Results-Adult female miniature swine were subjected to chronic, progressive ameroid occlusion of the proximal left circumflex coronary artery (LCx); after 2 months, animals were randomly exposed to 16-week exercise-training (EX group; treadmill running) or sedentary (SED group; cage confinement) protocols. After completion of EX or SED programs, coronary arterioles (Ϸ100 m in diameter) were isolated from collateral-dependent LCx (distal to occlusion) and nonoccluded left anterior descending coronary artery (LAD) regions of each heart. Arterioles were studied by in vitro videomicroscopy or frozen for ecNOS mRNA analysis (RT-PCR techniques). Relaxation to the endothelium-dependent vasodilator bradykinin was decreased (PϽ0.05) in arterioles isolated from collateral-dependent LCx versus nonoccluded LAD regions of SED animals. Bradykinin-mediated relaxation, however, was not different in LCx versus LAD arterioles isolated from EX animals. Nitroprusside-induced relaxation was unaffected by either chronic occlusion or exercise. Importantly, ecNOS mRNA expression was significantly decreased in arterioles isolated from LCx versus LAD regions of SED animals. After training, ecNOS mRNA expression was not different between LAD and LCx arterioles. Conclusions-These data indicate that exercise training enhances bradykinin-mediated relaxation of collateral-dependent LCx arterioles isolated after chronic coronary occlusion, most likely because of effects on ecNOS mRNA expression and increased production of NO.

show abstract

Section: Exercise-training Programmentioning

confidence: 99%

Section: Isolation and Preparation Of Coronary Arteriolesmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Endothelium-Mediated Relaxation of Porcine Collateral-Dependent Arterioles Is Improved by Exercise Training

et al. 2001

View full text Add to dashboard Cite

show abstract

“…Endothelium dysfunction, which can be evidenced by an impairment in endothelium-dependent relaxation, plays a pivotal role in the pathogenesis of cardiovascular diseases, such as arterial hypertension and coronary heart disease (54), as well as in diabetic angiopathy (13). Moreover, NO interferes with key events involved in the development of atherosclerosis, such as smooth muscle cell proliferation, platelet adhesion and vessel wall interaction, and monocyte and leucocyte adhesion (54).Several studies demonstrated that chronic aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO (15,38,59), EDHF (33,36), and prostanoid metabolites (21), mainly in resistance vessels of the cardiac and skeletal muscle vascular beds (36,47). It is suggested that increased vascular wall shear stress associated with acute bouts of aerobic exercise may represent the main stimulus for vascular adaptations induced by chronic aerobic exercise (3,39,41).…”

mentioning

confidence: 99%

“…Several studies demonstrated that chronic aerobic exercise alters endothelial function, improving vasodilating mechanisms mediated by NO (15,38,59), EDHF (33,36), and prostanoid metabolites (21), mainly in resistance vessels of the cardiac and skeletal muscle vascular beds (36,47). It is suggested that increased vascular wall shear stress associated with acute bouts of aerobic exercise may represent the main stimulus for vascular adaptations induced by chronic aerobic exercise (3,39,41).…”

mentioning

confidence: 99%

Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

Moraes¹,

Gioseffi²,

Nóbrega³

et al. 2004

Journal of Applied Physiology

View full text Add to dashboard Cite

is known to improve vasodilating mechanisms mediated by endothelium-dependent relaxing factors in the cardiac and skeletal muscle vascular beds. However, the effects of exercise training on visceral vascular reactivity, including the renal circulation, are still unclear. We used the experimental model of the isolated perfused rabbit kidney, which involves both the renal macro-and microcirculation, to test the hypothesis that exercise training improves vasodilator mechanisms in the entire renal circulation. New Zealand White rabbits were pen confined (Sed; n ϭ 24) or treadmill trained (0% grade) for 5 days/wk at a speed of 18 m/min during 60 min over a 12-wk period (ExT; n ϭ 24). Kidneys isolated from Sed and ExT rabbits were continuously perfused in a nonrecirculating system under conditions of constant flow and precontracted with norepinephrine (NE). We assessed the effects of exercise training on renal vascular reactivity using endothelial-dependent [acetylcholine (ACh) and bradykinin (BK)] and -independent [sodium nitroprusside (SNP)] vasodilators. ACh induced marked and dose-related vasodilator responses in kidneys from Sed rabbits, the reduction in perfusion pressure reaching 41 Ϯ 8% (n ϭ 6; P Ͻ 0.05). In the kidneys from ExT rabbits, vasodilation induced by ACh was significantly enhanced to 54 Ϯ 6% (n ϭ 6; P Ͻ 0.05). In contrast, BK-induced renal vasodilation was not enhanced by training [19 Ϯ 8 and 13 Ϯ 4% reduction in perfusion pressure for Sed and ExT rabbits, respectively (n ϭ 6; P Ͼ 0.05)]. Continuous perfusion of isolated kidneys from ExT animals with N -nitro-L-arginine methyl ester (L-NAME; 300 M), an inhibitor of nitric oxide (NO) biosynthesis, completely blunted the additional vasodilation elicited by ACh [reduction in perfusion pressure of 54 Ϯ 6 and 38 Ϯ 5% for ExT and L-NAME ϩ ExT, respectively (n ϭ 6; P Ͻ 0.05)]. On the other hand, L-NAME infusion did not affect ACh-induced vasodilation in Sed animals. Exercise training also increased renal vasodilation induced by SNP [36 Ϯ 7 and 45 Ϯ 10% reduction in perfusion pressure for Sed and ExT rabbits, respectively (n ϭ 6; P Ͻ 0.05)]. It is concluded that exercise training alters the rabbit kidney vascular reactivity, enhancing endothelium-dependent and -independent renal vasodilation. This effect seems to be related not only to an increased bioavailability of NO but also to the enhanced responsiveness of the renal vascular smooth muscle to NO. chronic exercise; endothelial dysfunction; isolated perfused rabbit kidney IT IS WELL KNOWN THAT THE endothelium plays a role of paramount importance in the regulation of the vasomotor tone (for review, see Ref. 26). The endothelial cells synthesize and release several relaxing and contracting diffusible substances that interact with the underlying vascular smooth muscle, thus contributing to the continuous modulation of vascular reactivity (26). The best-characterized endothelium-derived relaxing factors are nitric oxide (NO) and prostacyclin (PGI 2 ), which can be released by physical (shear stress by the fl...

show abstract

Peripheral Circulation

Laughlin

Davis

Secher

et al. 2012

Comprehensive Physiology

219

234

View full text Add to dashboard Cite

Blood flow (BF) increases with increasing exercise intensity in skeletal, respiratory, and cardiac muscle. In humans during maximal exercise intensities, 85% to 90% of total cardiac output is distributed to skeletal and cardiac muscle. During exercise BF increases modestly and heterogeneously to brain and decreases in gastrointestinal, reproductive, and renal tissues and shows little to no change in skin. If the duration of exercise is sufficient to increase body/core temperature, skin BF is also increased in humans. Because blood pressure changes little during exercise, changes in distribution of BF with incremental exercise result from changes in vascular conductance. These changes in distribution of BF throughout the body contribute to decreases in mixed venous oxygen content, serve to supply adequate oxygen to the active skeletal muscles, and support metabolism of other tissues while maintaining homeostasis. This review discusses the response of the peripheral circulation of humans to acute and chronic dynamic exercise and mechanisms responsible for these responses. This is accomplished in the context of leading the reader on a tour through the peripheral circulation during dynamic exercise. During this tour, we consider what is known about how each vascular bed controls BF during exercise and how these control mechanisms are modified by chronic physical activity/exercise training. The tour ends by comparing responses of the systemic circulation to those of the pulmonary circulation relative to the effects of exercise on the regional distribution of BF and mechanisms responsible for control of resistance/conductance in the systemic and pulmonary circulations.

show abstract

Vasodilator responses of coronary resistance arteries of exercise-trained pigs.

Abstract: These results suggest that exercise training enhances bradykinin-induced vasodilation through increased endothelium-derived relaxing factor/nitric oxide production by the L-arginine/nitric oxide synthase pathway.

Cited by 140 publications

References 21 publications

Endothelium-Mediated Relaxation of Porcine Collateral-Dependent Arterioles Is Improved by Exercise Training

Endothelium-Mediated Relaxation of Porcine Collateral-Dependent Arterioles Is Improved by Exercise Training

Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

Peripheral Circulation

Contact Info

Product

Resources

About