Early changes of protein synthesis in myocardium and coronary arteries induced by NO synthase inhibition

The question was addressed whether short-term (4 hour) NO deficiency, induc ing an increase in blood pressure in anaesthetized dogs, does influence pro teosynthesis in the myocardium and coronary arteries. A potentially positiv e answer was to be followed by the study of the supporting role of ornithin e decarboxylase for the polyamines pathway. NG-nitro-L-arginine-methyl eate r (L-NAME) (50 mg/kg per hour) was administered i.v. to inhibit NO synthase . After the first L-NAME dose diastolic blood pressure increased from 131.8 +/- 2.0 to 149.4 +/- 3.9 mm Hg (p < 0.001) and was maintained at about thi s level till the end of the experiment. Systolic blood pressure only increa sed after the first dose (from 150.8 +/- 1.1 to 175.0 +/- 5.8 mm Hg, p < 0. 01), returning thereafter to the control level. Similarly, the heart rate d eclined only after the first dose (from 190.4 +/- 5.3 to 147.6 +/- 4.5 beat s/min, p < 0.01). Total RNA concentrations increased in the left cardiac ve ntricle (LV), the left anterior descending coronary artery (LADCA) and left circumflex coronary artery (LCCA) by 15.9 +/- 0.7, 29.7 +/- 1.3 and 17.6 /- 1.0 %, p < 0.05, respectively. The same applied to [C-14]leucine incorpo ration (by 86.5 +/- 5.0, 33.5 +/- 2.6, 29.3 +/- 4.1%, p < 0.05, respectivel y). The above parameters indicated an increase of proteosynthesis in the LV myocardium and both coronary arteries LADCA and LCCA after short-term NO d eficiency. Surprisingly, the ornithine decarboxylase activity in the LV myo cardium decreased significantly by 40.2 +/- 1.6 % (p < 0.01) but the change s were not significant in the coronary arteries. This unexpected finding ma kes the role of polyamines in increasing proteosynthesis during a pressure overload due to NO deficiency questionable.