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1 Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan; Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
2 Cardiovascular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
3 Physiology, Kawasaki Medical School, Kurashiki, Okayama, Japan
4 Department of Medical Engineering and Systems Cardiology, Kawasaki Medical School, Kurashiki, Japan
5 Medical Engineering and Systems Cardiology, Kawasaki Medical School, Kurashiki, Okayama, Japan
6 Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Okayama, Japan
* To whom correspondence should be addressed. E-mail: mkajiya{at}md.okayama-u.ac.jp.
Pulmonary hypertension (PH) causes right ventricular hypertrophy (RVH) and, according to the extent of pressure overload, eventual heart failure. We tested the hypothesis that the mechanical stress in PH-RV impairs the vasoreactivity of the RV coronary microvessels of different sizes with increased superoxide levels. Five-week-old male Sprague Dawley rats were injected with monocrotaline (n=126) to induce PH, or with saline as controls (n=114). After 3 weeks, coronary arterioles (diameter = 30-100 µm) and small arteries (SAs; diameter = 100-200 µm) in the RV were visualized using intravital videomicroscopy. We evaluated ACh-induced vasodilation alone, in the presence of N
-nitro-L-arginine methyl ester (L-NAME), in the presence of tetraethylammonium (TEA) or catalase with or without L-NAME, and in the presence of SOD. The degree of suppression in vasodilation by L-NAME and TEA was used as indices of the contributions of endothelial nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), respectively. In PH rats, ACh-induced vasodilation was significantly attenuated in both arterioles and SAs, especially in arterioles. This decreased vasodilation was largely attributable to reduced NO-mediated vasoreactivity, while the EDHF-mediated vasodilation was relatively robust. The suppressive effect on arteriolar vasodilation by catalase was similar to TEA in both groups. Superoxide, as measured by lucigenin chemiluminescence, was significantly elevated in the RV tissues in PH. SOD ameliorated significantly the impairment of ACh-induced vasodilation in PH. Robust EDHF function will play a protective role in preserving coronary microvascular homeostasis in the event of NO dysfunction with increased superoxide levels.
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