about
Perivascular adipose tissue and coronary vascular diseaseLeptin augments coronary vasoconstriction and smooth muscle proliferation via a Rho-kinase-dependent pathwayContribution of electromechanical coupling between Kv and Ca v1.2 channels to coronary dysfunction in obesity.Contribution of BK(Ca) channels to local metabolic coronary vasodilation: Effects of metabolic syndrome.Cardiovascular and hemodynamic effects of glucagon-like peptide-1.Mechanisms underlying capsaicin effects in canine coronary artery: implications for coronary spasm.Control of coronary blood flow during exercise.Glucagon-like peptide-1 (7-36) but not (9-36) augments cardiac output during myocardial ischemia via a Frank-Starling mechanism.Comparison of isoflurane and α-chloralose in an anesthetized swine model of acute pulmonary embolism producing right ventricular dysfunctionFunctional contribution of P2Y1 receptors to the control of coronary blood flow.Lean and Obese Coronary Perivascular Adipose Tissue Impairs Vasodilation via Differential Inhibition of Vascular Smooth Muscle K+ Channels.Matching coronary blood flow to myocardial oxygen consumption.The effect of aging on adrenergic and nonadrenergic receptor expression and responsiveness in canine skeletal muscleEpicardial perivascular adipose tissue as a therapeutic target in obesity-related coronary artery diseaseEffects of leptin on cardiovascular physiologyBiphasic alterations in coronary smooth muscle Ca(2+) regulation in a repeat cross-sectional study of coronary artery disease severity in metabolic syndrome.Impaired cardiometabolic responses to glucagon-like peptide 1 in obesity and type 2 diabetes mellitusPeriadventitial adipose tissue impairs coronary endothelial function via PKC-beta-dependent phosphorylation of nitric oxide synthase.Leptin and mechanisms of endothelial dysfunction and cardiovascular disease.Regulation of 130-kDa smooth muscle myosin light chain kinase expression by an intronic CArG element.Impaired function of coronary BK(Ca) channels in metabolic syndromeObesity alters molecular and functional cardiac responses to ischemia/reperfusion and glucagon-like peptide-1 receptor agonism.Contribution of hydrogen sulfide to the control of coronary blood flow.Mutual reinforcement of pathophysiological host-microbe interactions in intestinal stasis models.Leptin-induced endothelial dysfunction: a target for therapeutic interventions.Glucagon-Like Peptide 1 Receptor Activation Augments Cardiac Output and Improves Cardiac Efficiency in Obese Swine After Myocardial Infarction.Cardiovascular consequences of metabolic syndrome.Critical contribution of KV1 channels to the regulation of coronary blood flow.Contribution of voltage-dependent K+ and Ca2+ channels to coronary pressure-flow autoregulation.Intracoronary glucagon-like peptide 1 preferentially augments glucose uptake in ischemic myocardium independent of changes in coronary flow.Contribution of IKCa channels to the control of coronary blood flow.Voltage-dependent K+ channels regulate the duration of reactive hyperemia in the canine coronary circulation.Insulin improves cardiac contractile function and oxygen utilization efficiency during moderate ischemia without compromising myocardial energetics.Regulation of myocardial oxygen delivery in response to graded reductions in hematocrit: role of K+ channels.Nitric oxide modulates right ventricular flow and oxygen consumption during norepinephrine infusion.ATP-dependent K(+) channels contribute to local metabolic coronary vasodilation in experimental diabetes.Coronary blood flow regulation in the prediabetic metabolic syndrome.Alpha-adrenergic vasoconstrictor tone limits right coronary blood flow in exercising dogs.Intermittent hypoxic training protects canine myocardium from infarction.Nitric oxide contributes to right coronary vasodilation during systemic hypoxia.
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P50
description
researcher
@en
wetenschapper
@nl
name
Johnathan D Tune
@en
Johnathan D Tune
@nl
type
label
Johnathan D Tune
@en
Johnathan D Tune
@nl
prefLabel
Johnathan D Tune
@en
Johnathan D Tune
@nl
P106
P31
P496
0000-0003-2959-0801