Comparison of Nitric Oxide Production in Response to Carbachol Between Macrovascular and Microvascular Cardiac Endothelial Cells
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概要
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Cardiac microvascular endothelial cells (EC) play an important role in the physiological regulation of coronary blood flow, but their function has not been rigorously examined, because suitable in vitro models have not been available. Cardiac macrovascular and microvascular BC were isolated and cultured from 14-16-week-old Sprague-Dawley rats to examine the pharmacological responses of carbachol-induced nitric oxide (NO) production using a Griess method. Carbachol-induced NO production was only detected in cardiac macrovascular EC, which suggests that endothelial production of NO differs between macrovascular and microvascular BC. Next, cardiac microvascular BC was treated with either vehicle, angiotensin-converting enzyme (ACE) inhibitor (captopril, 10μmol/L) or angiotensin II type 1 (AT1) receptor antagonist (CV1 1974, 10μmol/L) for 4 days. Carbachol-induced NO production was improved by captopril (136±45 nmol, p<0.01 vs vehicle) and CV1 1974 (146±30nmol, p<0.01 vs vehicle). Angiotensin II concentration in the culture medium and protein expressions of endothelial nitric oxide synthase and AT1 receptor in the BC were similar among the 3 groups. Interestingly, the level of muscarmnic subtype 3 (M_3) receptor was significantly increased in the EC treated with captopril (214%, p<0.01) and CV1 1974 (296%, p<0.01). When cardiac microvascular EC were treated with neomycin (non-selective phospholipase C inhibitor), carbachol-induced NO production was also improved (146±35nmol, p<0.01, neomycin 1 mmol/L) together with increased expression of M_3 receptor (p<0.01). These data suggest that the upregulation of the M_3 receptor by captopril or CV1 1974 occurs via a phospholipase C-dependent pathway. Cardiac microvascular EC also produced NO constitutively, as did the macrovascular EC, but carbachol-induced NO production was decreased. The present data suggest that the upregulation of the M_3 receptor by the ACE inhibitor and AT1 receptor antagonist is a new beneficial effect of these drugs on microvascular endothelial function.
- 社団法人日本循環器学会の論文
- 2002-04-20
著者
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Takeishi Yasuchika
First department of internal medicine, Fukushima Medical University
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Tomoike Hitonobu
National Cardiovascular Center
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TAKAHASHI Hiroki
First Department of Internal Medicine, Sapporo Medical University, School of Medicine
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Kubota Isao
First Department of Internal Medicine Yamagata University School of Medicine
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Miyamoto Takuya
First Department of Internal Medicine, Yamagata University
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Takeishi Yasuchika
First Department Of Internal Medicine Fukushima Medical University
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Miyashita Takehiko
山形大学 医学部循環･呼吸･腎臓内科学
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Kato Shuichi
Department Of Cardiology Pulmonology Nephrology Yamagata University School Of Medicine
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Katoh Shigehiko
山形大学 医学部循環･呼吸･腎臓内科学
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Kawashima Sukehiko
Department Of Cardiology Pulmonology And Nephrology Yamagata University School Of Medicine
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Miyamoto Takuya
Department Of Cardiology Pulmonology And Nephrology Yamagata University School Of Medicine
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Miyamoto Takuya
山形大学 医学部循環･呼吸･腎臓内科学
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MIYASHITA Takehiko
First Department of Internal Medicine and Division of Radiology, Yamagata University School of Medic
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Fujii Satoshi
The Institute for Life Support Technology, Yamagata Technopolis Foundation
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Yoshimura Tetsuhiko
The Institute for Life Support Technology, Yamagata Technopolis Foundation
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Kato Shuichi
Public Okitama General Hospital
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Takahashi Hiroki
Department Of Cardiology Pulmonology And Nephrology Yamagata University School Of Medicine
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Tomoike Hitonobu
First Department Of Internal Medicine Yamagata University School Of Medicine
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Takahashi Hiroki
First Department Of Internal Medicine Sapporo Medical University
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Yoshimura Tetsuhiko
The Institute For Life Support Technology Yamagata Technopolis Foundation
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Takahashi Hiroki
First Department Of Internal Medicine Gunma University School Of Medicine
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Fujii Satoshi
The Institute For Life Support Technology Yamagata Technopolis Foundation
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