Remodelling of septal branch of coronary artery and carotid artery in L-NAME treated rats
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
9085358
Knihovny.cz E-resources
- MeSH
- Carotid Arteries drug effects pathology ultrastructure MeSH
- Hypertrophy, Left Ventricular pathology MeSH
- Enzyme Inhibitors pharmacology MeSH
- Coronary Vessels drug effects pathology ultrastructure MeSH
- Blood Pressure MeSH
- Rats MeSH
- NG-Nitroarginine Methyl Ester pharmacology MeSH
- Nitric Oxide metabolism MeSH
- Rats, Wistar MeSH
- Tunica Intima pathology MeSH
- Tunica Media pathology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Enzyme Inhibitors MeSH
- NG-Nitroarginine Methyl Ester MeSH
- Nitric Oxide MeSH
Coronary and carotid artery structure was studied in rats in order to analyze the processes in the cardiovascular system in NO-deficient hypertension model. Long-term inhibition of NO synthase was induced by L-nitro arginine methyl ester (L-NAME, 50 mg/kg/day p.o.) for a period of 8 weeks. An increase in blood pressure and heart/body weight ratio confirmed the reliability of the model. The wall thickness as well as the calculated wall area of the coronary artery increased by 70% and 50%, respectively, in comparison to control vessels. The wall thickness and the calculated wall area of the carotid artery increased by 73% and 70%, respectively. Further analysis indicated that both the tunica intima and tunica media in the coronary and the carotid artery increased quantitatively in a similar manner. Remarkable differences were found in the contribution of cellular and noncellular components in the tunica media of the coronary and carotid arteries of experimental animals. The calculated extracellular area increased by 116% in comparison to the control coronary artery and by 97% in comparison to the control carotid artery. The increase in extracellular matrix of the tunica media of coronary and carotid arteries seems to be basic cause of the remodelling of the vessels studied.
Age-dependent redox status in the brain stem of NO-deficient hypertensive rats