Enter your Email address:
Wolters Kluwer Health may email you for journal alerts and information, but is committed
to maintaining your privacy and will not share your personal information without
Fogarty, J A.1; Parker, J L.1
1Dept. of Med. Phys. and Cardiovasc. Res. Ctr, TAMUS HSC, College Station, TX
Our lab and others have demonstrated that experimental coronary disease established with chronic coronary occlusion (CCO) is punctuated by impaired agonist-stimulated dilation in porcine coronary vasculature.
We hypothesized that nitric oxide (NO)-mediated vasodilation responses to bradykinin (BK) and vascular endothelial growth factor-165 (VEGF) are compromised by CCO; furthermore, vascular impairment is improved by exercise training (EX).
The proximal left circumflex coronary artery (LCx) of female Yucatan mini-swine was surgically instrumented with an ameroid occluder to induce CCO and collateral development; 8 wks post-surgery animals were randomized into sedentary(SED) or EX(treadmill; 5dys/wk) protocols for 14 wks. Coronary arterioles (< 150μm) and arteries (> 500μm) were isolated from collateral-dependent (LCx) and non-occluded (left anterior descending;LAD)-perfused myocardium of SED and EX animals.
Coronary arteries exposed to CCO did not demonstrate impaired responses to BK; however, EX significantly enhanced BK-stimulated relaxation of both LAD and LCx arteries. In contrast, vasodilation responses to BK in LCx arterioles were significantly diminished in association with reduction in NO synthase (NOS) mRNA; impairments were reversed by EX. Responses to VEGF also differentiated by vessel size. LAD and LCx arteries from SED and EX animals responded similarly to VEGF. Interestingly, EX markedly enhanced VEGF-induced vasodilation of LCx arterioles. Furthermore, vasodilation of EX LCx arterioles exceeded that of EX or SED LAD arterioles in response to VEGF. Enhanced responses of LCx arterioles due to EX was abolished by inhibition of NOS and tyrosine kinase activity. This EX-induced enhanced vasodilation was not demonstrated by use of other isoforms of VEGF and required the activation of a non-tyrosine kinase VEGF receptor, neuropilin-1.
These data indicate that EX enhances endothelial-dependent, NO-mediated responses in coronary arteries and arterioles from hearts exposed to CCO, potentially via multiple mechanisms and pathways.
©2003The American College of Sports Medicine
Colleague's E-mail is Invalid
Your Name: (optional)
Separate multiple e-mails with a (;).
Thought you might appreciate this item(s) I saw at Medicine & Science in Sports & Exercise.
Send a copy to your email
Your message has been successfully sent to your colleague.
Some error has occurred while processing your request. Please try after some time.
An Existing Folder
A New Folder
The item(s) has been successfully added to "".
Login with your LWW Journals username and password.
Username or Email:
Enter and submit the email address you registered with. An email with instructions to reset your password will be sent to that address.
Link to reset your password has been sent to specified email address.
What does "Remember me" mean?
By checking this box, you'll stay logged in until you logout. You'll get easier access to your articles, collections,
media, and all your other content, even if you close your browser or shut down your
To protect your most sensitive data and activities (like changing your password),
we'll ask you to re-enter your password when you access these services.
What if I'm on a computer that I share with others?
If you're using a public computer or you share this computer with others, we recommend
that you uncheck the "Remember me" box.
Save my selection
Article Level Metrics