Long-term NO synthase inhibition affects heart weight and geometry of coronary and carotid arteries.
The heart weight and the structure of coronary and carotid arteries were studied in NO-deficient hypertension. Wistar rats were administered L-NAME (50 mg/kg/day) in drinking water for a period of 8 weeks. The blood pressure and heart rate were recorded weekly. In one group of control and experimental animals the heart weight was assessed and the heart/body weight ratio (relative heart weight) was calculated. In the other group of control and experimental animals, the cardiovascular system was perfused by a fixative under constant perfusion pressure. The inner circumference and the wall thickness (tunica intima and tunica media) of the coronary (septal branch) and carotid artery were measured using light microscopy and the wall/diameter ratio was calculated. Inhibition of NO synthase induced a significant increase in blood pressure (187.2 +/- 4.2 mm Hg compared to 131.4 +/- 1.9 mm Hg in the controls, p < 0.01). The heart rate decreased (334.4 +/- 7.0 beats/min compared to 352.6 +/- 4.1 beats/min in the controls, p < 0.05). The heart weight increased in NO-deficient rats (1.32 +/- 0.08 g versus 1.10 +/- 0.03 g, p < 0.05); the heart/body weight index increased remarkably (3.09 +/- 0.15 compared to 2.10 +/- 0.04 in the controls, p < 0.01). Morphometry of the septal branch of the left coronary artery indicated a decrease of the inner circumference (664 +/- 24 microns versus 832 +/- 30 microns, p < 0.01), the increased wall thickness (21.15 +/- 0.84 microns compared to 12.47 +/- 0.62 microns in the controls, p < 0.01) and the remarkably changed wall/diameter ratio (1:10 versus 1:21 in the controls). Similar alterations were found in the carotid arteries: the inner circumference was decreased (2456 +/- 39 microns versus 2732 +/- 66 microns, p < 0.01), the wall thickness increased (45.14 +/- 0.41 microns compared to 26.08 +/- 1.23 microns, p < 0.01) and the wall/diameter ratio was changed to 1:17 in comparison with 1:33 in the controls. In conclusion, cardiac hypertrophy and structural alterations of the coronary artery and carotid artery accompany NO-deficient hypertension.
Kristek
F
F
Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Gerová
M
M
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002339:Carotid Arteries / Q000033:anatomy & histology / Q000187:drug effects*; D003331:Coronary Vessels / Q000033:anatomy & histology / Q000187:drug effects*; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar
D004791:Enzyme Inhibitors; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester