Cross talk between prostacyclin and nitric oxide under shear in smooth muscle cell: role in monocyte adhesion

Second Department of Internal Medicine, Hirosaki University School of Medicine, Hirosaki, 036-8562 Japan We tested the hypothesis that at sites of vascular damage, vessel homeostasis is maintained through the cross talk of shear-induced production of prostacyclin and nitric oxide (NO) in vascular sm...

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Published in:American journal of physiology. Heart and circulatory physiology 2001-07, Vol.281 (1), p.H177-H182
Main Authors: Osanai, Tomohiro, Akutsu, Noriyuki, Fujita, Norio, Nakano, Takao, Takahashi, Koki, Guan, Weiping, Okumura, Ken
Format: Article
Language:English
Subjects:
Animals
Blotting, Western
Cell Adhesion - physiology
Epoprostenol - biosynthesis
Epoprostenol - physiology
Mesenteric Veins - cytology
Mesenteric Veins - metabolism
Monocytes - physiology
Muscle, Smooth, Vascular - physiology
Nitric Oxide - biosynthesis
Nitric Oxide - physiology
Rats
Rats, Inbred WKY
Stress, Mechanical
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Summary:Second Department of Internal Medicine, Hirosaki University School of Medicine, Hirosaki, 036-8562 Japan We tested the hypothesis that at sites of vascular damage, vessel homeostasis is maintained through the cross talk of shear-induced production of prostacyclin and nitric oxide (NO) in vascular smooth muscle cells (VSMC). Confluent A7r5 cells derived from rat aortic VSMC and mesenteric VSMC were exposed to shear stress at 15 dyn/cm 2 for 90 min with the use of a cone-plate device, and productions of prostacyclin and NO were examined. Shear stress increased cumulative production of prostacyclin by 3- to 3.5-fold and that of NO by 6- to 7.5-fold. Western blot analysis showed that inducible NO synthase protein was expressed after shear stress in both types of VSMC. Inhibition of NO synthase enhanced the shear-induced production of prostacyclin from 40 to 60%. Shear-induced production of NO was suppressed by 70% after treatment with 10 4 M of indomethacin. A7r5 cells adhesiveness for monocytes was suppressed by 50% after shear stress. This suppression was abolished by pretreatment with 10 4 M of indomethacin, whereas inhibition of NO synthase only minimally inhibited it. We conclude that there is a cross talk of shear-induced production of prostacyclin and NO in VSMC. At sites of vascular damage, prostacyclin synthesis may prevent monocyte adhesiveness for VSMC through the concomitant enhancement of NO production. shear stress; vascular smooth muscle cells
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.2001.281.1.h177