| Nitric oxide and H2O2 contribute to reactive dilation of isolated coronary arterioles. | |
| | |
MedLine Citation:
|
PMID: 15319207 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
The role of metabolic factors derived from cardiac muscle in the development of reactive hyperemia after brief occlusions of the coronary circulation seems to be well established. However, the contribution of occlusion-induced changes in hemodynamic forces to eliciting reactive hyperemia is less known. We hypothesized that in isolated coronary arterioles changes in intraluminal pressure and flow, during and after release of occlusion (O/R), themselves via activating intrinsic mechanosensitive mechanisms, elicit release of vasoactive factors resulting in reactive dilations. Thus in isolated coronary arterioles (diameter: 88 +/- 8 microm) changes in diameter to changes in pressure or pressure plus flow (P+F) during and after a brief period (30, 60, and 120 s) of O/R of cannulating tube were measured by videomicroscopy. In response to both types of O/R, diameter first decreased, then, subsequently increased during occlusions. When only pressure was changed (from 80-10-80 mmHg), after release of occlusion, peak dilations increased as a function of the duration of occlusions. After flow was established (30 microl/min), O/R elicited changes in both pressure and flow (from 80-10-80 mmHg and from 0 to 30 microl/min). In these conditions, after the release of occlusions, not only the peak but also the duration of reactive dilation increased significantly as a function of the length of occlusions. The dilations during, and peak dilations after occlusions both in pressure and P+F protocols were significantly reduced by the inhibition of NO synthase with Nomega-nitro-L-arginine-methyl-ester (L-NAME) or by endothelium removal, whereas duration of postocclusion dilations were reduced by L-NAME or by endothelium removal only in P+F protocols. Furthermore, in both protocols, catalase significantly reduced the peak but not the duration of reactive dilations. Thus, mechanosensitive mechanisms that are sensitive to deformation, pressure, stretch, and wall shear stress elicit release of NO and H2O2, resulting in reactive dilation of isolated coronary arterioles. |
| | |
Authors:
|
Akos Koller; Zsolt Bagi |
Related Documents
:
|
8462157 - Experimental basis of determining maximum coronary, myocardial, and collateral blood fl... 10676677 - Coronary microcirculatory vasoconstriction during ischemia in patients with unstable an... 7295927 - Comparison of radiotelemetry of blood pressure and standard exercise tests. 1182727 - Mechanical effects of heart contraction on coronary flow. 15876787 - Anesthetic and cardiovascular effects of balanced anesthesia using constant rate infusi... 17078157 - Characterization of insomnia in patients with essential hypertension. |
Publication Detail:
|
Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2004-08-19 |
Journal Detail:
|
Title: American journal of physiology. Heart and circulatory physiology Volume: 287 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2004 Dec |
Date Detail:
|
Created Date: 2004-11-19 Completed Date: 2005-01-03 Revised Date: 2007-11-14 |
Medline Journal Info:
|
Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
|
Languages: eng Pagination: H2461-7 Citation Subset: IM |
Affiliation:
|
Dept. of Physiology, New York Medical College, Valhalla, NY 10595, USA. koller@nymc.edu |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Arterioles / physiology Blood Flow Velocity / physiology Blood Pressure / physiology Catalase / pharmacology Coronary Vessels / physiology* Endothelium, Vascular / physiology Enzyme Inhibitors / pharmacology Hydrogen Peroxide / metabolism* Male NG-Nitroarginine Methyl Ester / pharmacology Nitric Oxide / metabolism* Perfusion Rats Rats, Wistar Stress, Mechanical Vasodilation / drug effects, physiology* |
| Grant Support | |
ID/Acronym/Agency:
|
HL-43023/HL/NHLBI NIH HHS; HL-46813/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
|
0/Enzyme Inhibitors; 10102-43-9/Nitric Oxide; 50903-99-6/NG-Nitroarginine Methyl Ester; 7722-84-1/Hydrogen Peroxide; EC 1.11.1.6/Catalase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Renal blood flow in heart failure patients during exercise.
Next Document: Sex modifies exercise and cardiac adaptation in mice.