Endogenous and Exogenous Coronary Vasodilatation are Attenuated in Cardiac Hypertrophy: a Morphological Defect?

• Published in: Journal of molecular and cellular cardiology 2000-03, Vol.32 (3), p.527-538
• Main Authors: Kingsbury, Martyn P., Turner, Mark A., Flores, Nicholas A., Bovill, Esta, Sheridan, Desmond J.
• Format: Article
• Language: English
• Subjects: Adenosine; Animals; Coronary Circulation; Coronary Vessels - drug effects; Coronary Vessels - pathology; Coronary Vessels - physiopathology; Endothelial-derived factors; Guinea Pigs; Hyperemia - metabolism; Hyperemia - pathology; Hyperemia - physiopathology; Hypertrophy; Hypertrophy, Left Ventricular - metabolism; Hypertrophy, Left Ventricular - pathology; Hypertrophy, Left Ventricular - physiopathology; Male; Microcirculation; Nitrates - metabolism; Nitric oxide; Purines - metabolism; Reactive hyperaemia; Vasodilatation; Vasodilation; Ventricular Dysfunction, Left - metabolism; Ventricular Dysfunction, Left - pathology; Ventricular Dysfunction, Left - physiopathology
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1006/jmcc.1999.1097

Reactive hyperaemia (RH) following brief ischaemia is reduced in hypertrophied hearts, and this may contribute to reduced coronary flow reserve. We studied vasodilatation during RH and in response to exogenous stimuli in control and hypertrophied hearts and explored the mechanisms underlying RH. Vascular reactivity was assessed in isolated hypertrophied hearts (55±3 days after aortic banding or sham operation) by constructing dose–response curves to acetylcholine (ACh), sodium nitroprusside (SNP) and adenosine. Reactive hyperaemic vasodilatation was assessed after global ischaemia (5–120 s) in the presence/absence of L -NAME, 8-phenyltheophylline (8-PT) and glibenclamide. Purine release and NO overflow in the coronary perfusate were analysed. Aortic constriction increased heart/body weight ratio (47%), myocyte size (19%) and arteriolar wall thickness (51%), all P