Effect of behavioral stress on coronary artery relaxation altered with aging in BHR

Citation
Ad. Giulumian et al., Effect of behavioral stress on coronary artery relaxation altered with aging in BHR, AM J P-REG, 45(2), 1999, pp. R435-R440
Citations number
42
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
45
Issue
2
Year of publication
1999
Pages
R435 - R440
Database
ISI
SICI code
0363-6119(199902)45:2<R435:EOBSOC>2.0.ZU;2-V
Abstract
Behavioral stress and aging are associated with an increase in vascular dis ease. This study determined the mechanisms contributing to changes in endot helium-dependent relaxation of isolated coronary arteries (300-350 mu m) in duced by exposure to 10 days of air-jet stress (2 h/day) in young (3 mo) an d old (18 mo) male borderline hypertensive rats (BHR). Aging, alone, did no t alter endothelium-dependent relaxation to acetylcholine (ACh) quantitativ ely but did alter the mechanisms contributing to relaxation to ACh, which w as largely dependent on nitric oxide synthase (NOS) in vessels from old, bu t not young, BHR. Behavioral stress resulted in an enhanced relaxation to A Ch that was dependent on NOS in vessels from young stressed compared with y oung control BHR. Conversely, relaxation to ACh was reduced in coronary art eries from old stressed compared with old control BHR. In vessels from old control BHR, there was an NOS-independent component of relaxation mediated by opening of K+ channels that was absent in vessels from old stressed BHR. The superoxide anion scavenger, tiron, partially restored relaxation, and inhibition of cyclooxygenase largely restored relaxation to ACh in vessels from old stressed BHR. In summary, the effect of behavioral stress was age dependent. ACh-induced relaxation of coronary arteries was enhanced in an N OS-dependent manner in young BHR and was impaired in old BHR due to superox ide anions, vasoconstrictor cyclooxygenase products, and a loss of K+ chann el-mediated relaxation.