Endothelium-dependent relaxations in canine coronary arteries are enhanced in early heart failure and persist in recovery

1994 ◽  
Vol 72 (10) ◽  
pp. 1148-1154 ◽  
Author(s):  
Giulia Larosa ◽  
Paul W. Armstrong ◽  
Christine Forster
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Early Onset ◽  
Contractile Responses ◽  
Acetylcholine Sensitivity ◽  
Coronary Endothelium ◽  
Functional Relaxation

In vitro coronary artery responsiveness to noradrenaline, phenylephrine, and BHT-920 together with functional relaxation to acetylcholine was assessed in dogs at the early onset of pacing-induced heart failure (1 week) and in dogs recovered from heart failure (3 weeks paced, followed by 4 weeks discontinued pacing). α-Adrenoceptor stimulation produced contractile responses that were unaltered in early congestive heart failure and recovery. Contractions to noradrenaline and BHT-920 were always less than those produced by phenylephrine. Endothelium-intact arteries demonstrated relaxations in response to noradrenaline and BHT-920, but not phenylephrine. Relaxations to noradrenaline were enhanced 24% in early heart failure and 47% following recovery from heart failure, compared with control. BHT-920 produced relaxations that were augmented 21 and 76% in early heart failure and recovery, respectively. Contractile sensitivity to noradrenaline increased 5-fold in early heart failure and was not different in recovery, compared with control. Contractile sensitivity to BHT-920 and phenylephrine was unaltered throughout. Acetylcholine produced relaxations that were increased 21% in early heart failure and 13% after recovery from congestive heart failure. Furthermore, acetylcholine sensitivity was significantly enhanced in early heart failure and recovery. The current study reveals a progressive adaptation of the coronary endothelium in congestive heart failure, possibly directed towards protection against excessive vasoconstriction due to circulating catecholamines.Key words: endothelium, congestive heart failure, coronary arteries, α-adrenoceptors, noradrenaline, acetylcholine.

Altered reactivity of coronary arteries located distal to a chronic coronary occlusion

1997 ◽  
Vol 273 (4) ◽  
pp. H1879-H1887 ◽  
Author(s):  
Julie A. Rapps ◽  
Michael Sturek ◽  
Allan W. Jones ◽  
Janet L. Parker
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Adrenergic Receptor ◽  
Coronary Artery Occlusion ◽  
Canine Model ◽  
Contractile Responses ◽  
Chronic Occlusion ◽  
Chronic Coronary Occlusion

The coronary vasculature located distal to a chronic occlusion (collateral-dependent) has been shown to exhibit altered reactivity to vasoactive agonists. Thus we evaluated effects of chronic coronary artery occlusion on vasomotor responsiveness of collateral-dependent arteries isolated from a canine model of Ameroid occlusion of the left circumflex (LCX) coronary artery. We compared in vitro responses of large (∼1.3- to 1.4-mm-ID) and small (∼0.6-mm-ID) LCX arteries located distal to an occlusion with responses of similar-sized segments of the unoccluded left anterior descending (LAD) coronary artery. α-Adrenergic receptor-mediated contractile responses to norepinephrine (10−9–10−4M) and phenylephrine (10−9–10−4M) in the presence of propranolol were markedly enhanced in large LCX arteries compared with LAD arteries ( P< 0.001). Prazosin (1 μM), an α1-adrenergic receptor antagonist, abolished contractile responses of LCX and LAD arteries to norepinephrine. Inhibition of nitric oxide synthesis with N ω-nitro-l-arginine methyl ester (100 μM) enhanced norepinephrine-induced contractions of LAD arteries to a greater extent than contractions of LCX arteries. We simultaneously measured myoplasmic free Ca2+ (fura 2 fluorescence ratio) and contractile responses in LCX and LAD arteries denuded of endothelium; norepinephrine-induced increases in myoplasmic free Ca2+ and contractile tension were significantly enhanced in LCX arteries compared with LAD arteries. In addition, large and small LCX arteries exhibited impaired relaxation in response to adenosine (10−8–10−3M) compared with LAD arteries ( P < 0.05). In contrast, relaxation in response to the β-adrenergic agonist isoproterenol (10−9–10−4M) and sodium nitroprusside (10−10–10−4M) was not significantly different in LCX and LAD arteries. Thus collateral-dependent coronary arteries exhibit enhanced α-adrenergic vasoconstriction and impaired vasorelaxation in response to adenosine. The enhanced α-adrenergic contractile responsiveness involves at least two mechanisms: 1) enhanced α1-adrenergic reactivity of smooth muscle and 2) decreased α-adrenergic-induced synthesis of nitric oxide by the endothelium.

Heart failure in an elderly man: where is that coronary?

2021 ◽  
pp. 1-4
Author(s):  
Charlie J. Sang ◽  
Stephen A. Clarkson ◽  
Elizabeth A. Jackson ◽  
Firas Al Solaiman ◽  
Marc G. Cribbs
Keyword(s):  
Heart Failure ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Medical Therapy ◽  
Coronary Arteries ◽  
Right Coronary Artery ◽  
Adult Population ◽  
Anomalous Coronary ◽  
Anomalous Coronary Arteries

Abstract Anomalous coronary arteries from the pulmonary artery are uncommon causes of heart failure in the adult population. This case demonstrates the unusual presentation in a patient with anomalous right coronary artery from the pulmonary artery and discusses the complex pathophysiology of this lesion and the role of guideline-directed medical therapy in the management of these patients.

scholarly journals A novel role for miR-133a in centrally mediated activation of the renin-angiotensin system in congestive heart failure

2017 ◽  
Vol 312 (5) ◽  
pp. H968-H979 ◽  
Author(s):  
Neeru M. Sharma ◽  
Shyam S. Nandi ◽  
Hong Zheng ◽  
Paras K. Mishra ◽  
Kaushik P. Patel
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Paraventricular Nucleus ◽  
Renin Angiotensin System ◽  
Luciferase Reporter ◽  
Mrna Levels ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin

An activated renin-angiotensin system (RAS) within the central nervous system has been implicated in sympathoexcitation during various disease conditions including congestive heart failure (CHF). In particular, activation of the RAS in the paraventricular nucleus (PVN) of the hypothalamus has been recognized to augment sympathoexcitation in CHF. We observed a 2.6-fold increase in angiotensinogen (AGT) in the PVN of CHF. To elucidate the molecular mechanism for increased expression of AGT, we performed in silico analysis of the 3′-untranslated region (3′-UTR) of AGT and found a potential binding site for microRNA (miR)-133a. We hypothesized that decreased miR-133a might contribute to increased AGT in the PVN of CHF rats. Overexpression of miR-133a in NG108 cells resulted in 1.4- and 1.5-fold decreases in AGT and angiotensin type II (ANG II) type 1 receptor (AT1R) mRNA levels, respectively. A luciferase reporter assay performed on NG108 cells confirmed miR-133a binding to the 3′-UTR of AGT. Consistent with these in vitro data, we observed a 1.9-fold decrease in miR-133a expression with a concomitant increase in AGT and AT1R expression within the PVN of CHF rats. Furthermore, restoring the levels of miR-133a within the PVN of CHF rats with viral transduction resulted in a significant reduction of AGT (1.4-fold) and AT1R (1.5-fold) levels with a concomitant decrease in basal renal sympathetic nerve activity (RSNA). Restoration of miR-133a also abrogated the enhanced RSNA responses to microinjected ANG II within the PVN of CHF rats. These results reveal a novel and potentially unique role for miR-133a in the regulation of ANG II within the PVN of CHF rats, which may potentially contribute to the commonly observed sympathoexcitation in CHF. NEW & NOTEWORTHY Angiotensinogen (AGT) expression is upregulated in the paraventricular nucleus of the hypothalamus through posttranscriptional mechanism interceded by microRNA-133a in heart failure. Understanding the mechanism of increased expression of AGT in pathological conditions leading to increased sympathoexcitation may provide the basis for the possible development of new therapeutic agents with enhanced specificity.

scholarly journals Elevated plasma levels of human urotensin-II immunoreactivity in congestive heart failure

2003 ◽  
Vol 285 (4) ◽  
pp. H1576-H1581 ◽  
Author(s):  
Fraser D. Russell ◽  
Deborah Meyers ◽  
Andrew J. Galbraith ◽  
Nick Bett ◽  
Istvan Toth ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Artery Disease ◽  
Congestive Heart Failure ◽  
Coronary Artery ◽  
Pulmonary Artery ◽  
Femoral Artery ◽  
Aortic Root ◽  
Femoral Vein ◽  
Urotensin Ii ◽  
Artery Disease

Human urotensin-II (hU-II) is the most potent endogenous cardiostimulant identified to date. We therefore determined whether hU-II has a possible pathological role by investigating its levels in patients with congestive heart failure (CHF). Blood samples were obtained from the aortic root, femoral artery, femoral vein, and pulmonary artery from CHF patients undergoing cardiac catheterization and the aortic root from patients undergoing investigative angiography for chest pain who were not in heart failure. Immunoreactive hU-II (hU-II-ir) levels were determined with radioimmunoassay. hU-II-ir was elevated in the aortic root of CHF patients (230.9 ± 68.7 pg/ml, n = 21; P < 0.001) vs. patients with nonfailing hearts (22.7 ± 6.1 pg/ml, n = 18). This increase was attributed to cardiopulmonary production of hU-II-ir because levels were lower in the pulmonary artery (38.2 ± 6.1 pg/ml, n = 21; P < 0.001) than in the aortic root. hU-II-ir was elevated in the aortic root of CHF patients with nonischemic cardiomyopathy (142.1 ± 51.5 pg/ml, n = 10; P < 0.05) vs. patients with nonfailing hearts without coronary artery disease (27.3 ± 12.4 pg/ml, n = 7) and CHF patients with ischemic cardiomyopathy (311.6 ± 120.4 pg/ml, n = 11; P < 0.001) vs. patients with nonfailing hearts and coronary artery disease (19.8 ± 6.6 pg/ml, n = 11). hU-II-ir was significantly higher in the aortic root than in the pulmonary artery and femoral vein, with a nonsignificant trend for higher levels in the aortic root than in the femoral artery. The findings indicated that hU-II-ir is elevated in the aortic root of CHF patients and that hU-II-ir is cleared at least in part from the microcirculation.

scholarly journals Right coronary artery fistula with congestive heart failure in the neonate. Doppler echocardiographic diagnosis and closure with detachable balloon

2000 ◽  
Vol 74 (3) ◽  
Author(s):  
Ivan Romero Rivera ◽  
Valdir Ambrósio Moises ◽  
Antonio Sergio Tebexreni ◽  
Celia Camelo Silva ◽  
José Lázaro Andrade ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Coronary Artery ◽  
Right Coronary Artery ◽  
Coronary Artery Fistula ◽  
Detachable Balloon

An Infant With Mucolipidosis-II And an Atretic orifice of the Left Coronary Artery

2009 ◽  
Vol 20 (1) ◽  
pp. 97-99 ◽  
Author(s):  
Ana Siles ◽  
Grant A. Mitchell ◽  
Nagib S. Dahdah
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Coronary Artery ◽  
Left Coronary Artery ◽  
Color Doppler ◽  
Type Ii ◽  
Retrograde Flow ◽  
Cardiac Enzymes ◽  
Selective Coronary Angiography ◽  
Mucolipidosis Ii

AbstractA one-month-old boy, with type-II mucolipidosis, presented with congestive heart failure and elevated cardiac enzymes. The atretic nature of the orifice of the left coronary artery was revealed by retrograde flow on color Doppler and selective coronary angiography. Type-II mucolipidosis and atresia of the left coronary artery are rare. To the best of our knowledge, this is the first report of their combined occurence, suggesting a possible causal relationship.

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