Components of flow-induced dilation in rat perfused coronary artery |
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Authors: | P Véquaud J L Freslon |
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Institution: | (1) Department of Pharmacology, Faculty of Pharmacy, University of Bordeaux II, Bordeaux Cedex, France;(2) Department of Pharmacology, Faculty of Pharmacy, University of Bordeaux II, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France |
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Abstract: | This study was undertaken to determine the endothelial factors involved in the flow-induced dilation of a rat perfused coronary artery. Segments of the right interventricular coronary artery were taken from 10–15-week-old male Wistar rats. Vessels were mounted in an arteriograph where internal diameter was continuously monitored while intraluminal pressure was controlled. Vessels were preconstricted with serotonin (10 mol/L), and the dilation induced by flow (0–800 l/min) was quantified. This dilator effect was measured in control conditions, after incubation with L-NAME (100 mol/L), with indomethacin (100µmol/L), and after mechanical destruction of the endothelium (–E). Dilations were expressed as percentage of the serotonin-induced constriction, and wall shear stress due to the physical forces exerted on the wall of the vessel was calculated and expressed in dyn/cm2.In control conditions, raising the flow up to 800 l/min led to an increase in dilation (maximal dilation 63% ± 4%) and in sheer stress (maximal shear stress 76 ±4dyn/cm2). With indomethacin, maximal dilation was 69% ± 4% and maximal shear stress was 81 ± 6 dyn/cm2. With L-NAME or after destruction of endothelium, dilation was greatly reduced (39% ± 3% and 40% ± 2%, respectively) whereas shear stress values were greatly increased (173 ± 14 and 150 ± 13 dyn/cm2, respectively).These results confirm the viability of this model for the study of flow-dependent dilation. This dilation seems to be greatly dependent on NO release. In contrast, results do not favor a significant involvement of prostanoid vasodilating substance. Without endothelium, a dilation was still observed and showed the persistence of an endothelium-independent component of flow-induced dilation in this preparation that remains to be determined.Abbreviations Ach
acetylcholine
- BSA
bovine serum albumin
- EDRF
endothelium-derived relaxing factor
- EDHF
endothelium-derived hyperpolarizing factor
- L-NAME
N
-nitro-L-arginine-methyl ester
- NO
nitric oxide
- PSS
physiological salt solution
- PGI2
prostacyclin
- 5-HT
serotonin
- SNP
sodium nitroprusside
- TXA2
thromboxane A2 |
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Keywords: | coronary artery endothelium EDRF flow shear stress |
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