지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
이용수
초록· 키워드
오류제보하기
Nitric oxide (NO) is synthesized by a family of NO synthases (NOS), including neuronal,inducible, and endothelial NOS (n/i/eNOS). NO-mediated effects can be beneficial orharmful depending on the specific risk factors affecting the disease. In hypertension,the vascular relaxation response to acetylcholine is blunted, and that to direct NO donorsis maintained. A reduction in the activity of eNOS is mainly responsible for theelevation of blood pressure, and an abnormal expression of iNOS is likely to be relatedto the progression of vascular dysfunction. While eNOS/nNOS-derived NO is protectiveagainst the development of atherosclerosis, iNOS-derived NO may be proatherogenic. eNOS-derived NO may prevent the progression of myocardial infarction. Myocardialischemia/reperfusion injury is significantly enhanced in eNOS-deficient animals. Animportant component of heart failure is the loss of coronary vascular eNOS activity. A pressure-overload may cause severer left ventricular hypertrophy and dysfunctionin eNOS null mice than in wild-type mice. iNOS-derived NO has detrimental effectson the myocardium. NO plays an important role in regulating the angiogenesis andslowing the interstitial fibrosis of the obstructed kidney. In unilateral ureteral obstruction,the expression of eNOS was decreased in the affected kidney. In triplyn/i/eNOS null mice, nephrogenic diabetes insipidus developed along with reducedaquaporin-2 abundance. In chronic kidney disease model of subtotal-nephrectomizedrats, treatment with NOS inhibitors decreased systemic NO production and inducedleft ventricular systolic dysfunction (renocardiac syndrome).
목차
등록된 정보가 없습니다.
참고문헌 (99)
참고문헌 신청
Chou TC / 1998 / Alterations of nitric oxide synthase expression with aging and hypertension in rats / Hypertension 31:643~648
Bennai F / 1999 / Normalizing the expression of nitric oxide synthase by low-dose AT1 receptor antagonism parallels improved vascular morphology in hypertensive rats / J Am Soc Nephrol 10(Suppl 11):S104~S115
Kim IK / 1999 / Altered vascular expression of nitric oxide synthase isozymes in hypertension / Korean J Thorac Cardiovasc Surg 32:138~143
Tsutsui M / 2015 / Significance of nitric oxide synthases:Lessons from triple nitric oxide synthases null mice / J Pharmacol Sci 127:42~52
Morishita T / 2005 / Nephrogenic diabetes insipidus in mice lacking all nitric oxide synthase isoforms / Proc Natl Acad Sci USA 102:10616~10621
Bennai F / 1999 / Normalizing the expression of nitric oxide synthase by low-dose AT1 receptor antagonism parallels improved vascular morphology in hypertensive rats / J Am Soc Nephrol 10(Suppl 11):S104~S115
Kim IK / 1999 / Altered vascular expression of nitric oxide synthase isozymes in hypertension / Korean J Thorac Cardiovasc Surg 32:138~143
Tsutsui M / 2015 / Significance of nitric oxide synthases:Lessons from triple nitric oxide synthases null mice / J Pharmacol Sci 127:42~52
Morishita T / 2005 / Nephrogenic diabetes insipidus in mice lacking all nitric oxide synthase isoforms / Proc Natl Acad Sci USA 102:10616~10621
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