Adaptation to short-term stress prevents post-infarction hyperactivation of the endothelium and decrease in blood pressure in rats.

Abstract

The aim of the study was to elucidate the possibility of preventing the decrease in blood pressure (BP) and the endothelial hyperactivation that are induced by experimental myocardial infarction in rats. The endothelial hyperactivation manifested itself in potentiated endothelium-dependent relaxation and in attenuated contractile responses to noradrenaline in isolated rat aortas. Furthermore, the postinfarction changes in BP showed a negative correlation with the endothelium-dependent relaxation. Preliminary adaptation of rats to short-term nondamaging stress exposures or pretreatment with the antioxidant, ionol, prevented to a great extent both the postinfarction decrease in BP and the disturbances in endothelium-mediated responses of smooth muscle. Since, according to the literature, infarction-concomitant stress strongly activates free-radical processes which may result in a hyperproduction of endothelium-derived relaxing factor, it is suggested that the increased potency of anti-oxidant systems is the mechanism common to the protective effects both of adaptation and of ionol.

• Authors: F Z Meerson, E B Manukhina, A V Lapshin
• Journal: Biomedical science (Biomed Sci) Vol. 2 Issue 6 Pg. 623-8 ( 1991) ISSN: 0955-9701 [Print] England
• PMID: 1841631 (Publication Type: Journal Article)

Chemical References

• Butylated Hydroxytoluene
• Acetylcholine
• Norepinephrine

Topics

• Acetylcholine (pharmacology)
• Adaptation, Physiological (physiology)
• Animals
• Blood Pressure
• Butylated Hydroxytoluene (pharmacology)
• Endothelium, Vascular (physiopathology)
• Male
• Myocardial Infarction (physiopathology)
• Norepinephrine (pharmacology)
• Rats
• Rats, Wistar
• Stress, Physiological (physiopathology)
• Vasoconstriction (drug effects)
• Vasodilation (drug effects)