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

Area of Science:

• Cardiovascular Physiology
• Biochemistry

Background:

• Nitric oxide (NO) plays a crucial role in regulating blood pressure and vascular function.
• NO deficiency can lead to hypertension and may impact myocardial and vascular tissue synthesis.

Purpose of the Study:

• To investigate the effect of short-term NO deficiency on proteosynthesis in the myocardium and coronary arteries.
• To explore the potential role of ornithine decarboxylase in polyamine synthesis during NO deficiency-induced pressure overload.

Main Methods:

• Administered N(G)-nitro-L-arginine-methyl ester (L-NAME) to anesthetized dogs to induce NO synthase inhibition and NO deficiency.
• Monitored blood pressure and heart rate.
• Measured total RNA concentration and [14C]leucine incorporation to assess proteosynthesis.
• Assessed ornithine decarboxylase activity in myocardial and coronary artery tissues.

Main Results:

• L-NAME administration increased diastolic blood pressure and initially affected systolic blood pressure and heart rate.
• Total RNA concentrations and [14C]leucine incorporation significantly increased in the left ventricle, LADCA, and LCCA, indicating enhanced proteosynthesis.
• Ornithine decarboxylase activity in the left ventricle decreased significantly, while changes in coronary arteries were not significant.

Conclusions:

• Short-term NO deficiency enhances proteosynthesis in the myocardium and coronary arteries, likely as an adaptive response to increased blood pressure.
• The observed decrease in ornithine decarboxylase activity suggests that polyamines may not play a supporting role in this increased proteosynthesis.
• Further research is needed to elucidate the mechanisms underlying proteosynthesis regulation during NO deficiency-induced hypertension.