Integrative control of coronary resistance vessel tone by endothelin and angiotensin II is altered in swine with a recent myocardial infarction

Beer, Vincent J. de; Sorop, Oana; Pijnappels, Daniël A.; Dekkers, Dick H. W.; Boomsma, Frans; Lamers, Jos M. J.; Duncker, Dirk J.; Merkus, Daphne

doi:10.1152/ajpheart.01163.2007

Cited by 12 publications

(14 citation statements)

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“…These observations are similar to our previous reports in normotensive female and male rats (Santos et al 2004). It has been shown that there are gender differences in components of the reninangiotensin system that may play a role in the control of coronary tone (de Beer et al 2008). through an interaction with the renin-angiotensin system (Xu et al 2008).…”

Section: Discussionsupporting

confidence: 92%

Sex differences in the coronary vasodilation induced by 17 β‐oestradiol in the isolated perfused heart from spontaneously hypertensive rats

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Section: Discussionsupporting

confidence: 92%

Sex differences in the coronary vasodilation induced by 17 β‐oestradiol in the isolated perfused heart from spontaneously hypertensive rats

et al. 2010

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“…Flow probes were placed around the proximal left anterior descending coronary artery (2.5-3 mm; Transonic Systems) for measurement of coronary blood flow and the aorta (14 -16 mm; Skalar) for measurement of both cardiac output and stroke volume (33). Finally, in all animals the proximal part of the left coronary circumflex artery (LCx) was exposed, but only in 17 swine that were designated to the MI group the LCx was permanently occluded with a silk suture (7). Three MI swine died during surgery, due to recurrent fibrillation.…”

Section: Surgical Proceduresmentioning

confidence: 99%

“…Coronary vasomotor tone is tightly regulated by a multitude of vasodilator and vasoconstrictor influences, which, in addition to any direct effects on the vascular smooth muscle, can also impact each others expression, secretion, and receptor activation (7,9,37). After MI, endothelial and neurohumoral control of coronary vasomotor tone is altered (12).…”

Section: Perspective and Conclusionmentioning

confidence: 99%

“…After MI, endothelial and neurohumoral control of coronary vasomotor tone is altered (12). To maintain perfusion of the hypertrophied remote myocardium after MI in the presence of endothelial dysfunction (reduced NO vasodilation), coronary flow reserve is recruited not only by increasing metabolic vasodilation via K ATP channel activation (35) but surprisingly also by suppression of endogenous vasoconstrictor influences of ET (7,34) and angiotensin II (7,32). The present study shows that the suppression of the vasoconstrictor influences of ET on the coronary resistance vessels in the remote remodeled myocardium is not due to NO, of which the overall vasodilator influence and the inhibition of ET influence were blunted.…”

Section: Perspective and Conclusionmentioning

confidence: 99%

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Prostanoids suppress the coronary vasoconstrictor influence of endothelin after myocardial infarction

Beer

Taverne

Kuster

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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de Beer VJ, Taverne YJ, Kuster DW, Najafi A, Duncker DJ, Merkus D. Prostanoids suppress the coronary vasoconstrictor influence of endothelin after myocardial infarction. Am J Physiol Heart Circ Physiol 301: H1080 -H1089, 2011. First published June 17, 2011 doi:10.1152/ajpheart.01307.2010 is associated with endothelial dysfunction resulting in an imbalance in endothelium-derived vasodilators and vasoconstrictors. We have previously shown that despite increased endothelin (ET) plasma levels, the coronary vasoconstrictor effect of endogenous ET is abolished after MI. In normal swine, nitric oxide (NO) and prostanoids modulate the vasoconstrictor effect of ET. In light of the interaction among NO, prostanoids, and ET combined with endothelial dysfunction present after MI, we investigated this interaction in control of coronary vasomotor tone in the remote noninfarcted myocardium after MI. Studies were performed in chronically instrumented swine (18 normal swine; 13 swine with MI) at rest and during treadmill exercise. Furthermore, endothelial nitric oxide synthase (eNOS) and cyclooxygenase protein levels were measured in the anterior (noninfarcted) wall of six normal and six swine with MI. eNOS inhibition with N -nitro-L-arginine (L-NNA) and cyclooxygenase inhibition with indomethacin each resulted in coronary vasoconstriction at rest and during exercise, as evidenced by a decrease in coronary venous oxygen levels. The effect of L-NNA was slightly decreased in swine with MI, although eNOS expression was not altered. Conversely, in accordance with the unaltered expression of cyclooxygenase-1 after MI, the effect of indomethacin was similar in normal and MI swine. L-NNA enhanced the vasodilator effect of the ETA/B receptor blocker tezosentan but exclusively during exercise in both normal and MI swine. Interestingly, this effect of L-NNA was blunted in MI compared with normal swine. In contrast, whereas indomethacin increased the vasodilator effect of tezosentan only during exercise in normal swine, indomethacin unmasked a coronary vasodilator effect of tezosentan in MI swine both at rest and during exercise. In conclusion, the present study shows that endothelial control of the coronary vasculature is altered in post-MI remodeled myocardium. Thus the overall vasodilator influences of NO as well as its inhibition of the vasoconstrictor influence of ET on the coronary resistance vessels were reduced after MI. In contrast, while the overall prostanoid vasodilator influence was maintained, its inhibition of ET vasoconstrictor influences was enhanced in post-MI remote myocardium. endothelin; nitric oxide; prostacyclin CONGESTIVE HEART FAILURE IS the only major cardiovascular disorder of which the incidence has increased over the past decade, which is principally due to a reduction in mortality associated with acute myocardial infarction (MI). Consequently, MI has become an increasingly important risk factor for the development of congestive heart failure (5). The loss of viable myocardial tissue and the consequent left ve...

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“…It is mainly produced in endothelial cells through cleavage from its inactive precursor, Big ET, primarily by ET converting enzyme (ECE) and, to a lesser degree, by chymase, in concert with neutral endopeptidase (NEP) (31). Several studies have shown that ET receptor blockade results in systemic and coronary vasodilation (3,21,32), and hence that ET contributes to basal vascular tone in the systemic vasculature, as well as the coronary circulation. Our laboratory (21) has previously demonstrated that recruitment of coronary flow reserve during exercise is mediated, at least in part, through withdrawal of the vasoconstrictor effect of ET on the coronary vasculature.…”

mentioning

confidence: 99%

Exercise limits the production of endothelin in the coronary vasculature

Beer

Bender

Taverne

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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We previously demonstrated that endothelin (ET)-mediated coronary vasoconstriction wanes with increasing exercise intensity via a nitric oxide- and prostacyclin-dependent mechanism (Ref. 23). Therefore, we hypothesized that the waning of ET coronary vasoconstriction during exercise is the result of decreased production of ET and/or decreased ET receptor sensitivity. We investigated coronary ET receptor sensitivity using intravenous infusion of ET and coronary ET production using intravenous infusion of the ET precursor Big ET, at rest and during continuous treadmill exercise at 3 km/h in 16 chronically instrumented swine. In the systemic vasculature, Big ET and ET induced similar changes in hemodynamic parameters at rest and during continuous exercise at 3 km/h, indicating that exercise does not alter ET production or receptor sensitivity in the systemic vasculature. In the coronary vasculature, infusion of ET resulted in similar dose-dependent decreases in coronary blood flow and coronary venous oxygen tension and saturation at rest and during exercise. In contrast, administration of Big ET resulted in dose-dependent decreases in coronary blood flow, as well as coronary venous oxygen tension and saturation at rest. These effects of Big ET were significantly reduced during exercise. Altogether, our data indicate that continuous exercise at 3 km/h attenuates ET-mediated coronary vasoconstriction through reduced production of ET from Big ET rather than through reduced ET sensitivity of the coronary vasculature. The decreased ET production during exercise likely contributes to metabolic coronary vasodilation.

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Integrative control of coronary resistance vessel tone by endothelin and angiotensin II is altered in swine with a recent myocardial infarction

Cited by 12 publications

References 55 publications

Sex differences in the coronary vasodilation induced by 17 β‐oestradiol in the isolated perfused heart from spontaneously hypertensive rats

Sex differences in the coronary vasodilation induced by 17 β‐oestradiol in the isolated perfused heart from spontaneously hypertensive rats

Prostanoids suppress the coronary vasoconstrictor influence of endothelin after myocardial infarction

Exercise limits the production of endothelin in the coronary vasculature

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