کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9176673 | 1180351 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Role of Endothelin in the Pathogenesis of Hypertension
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کلمات کلیدی
RBFUltrafiltration coefficientIMCDGFRVSMCinositol triphosphatePKCAVPDOCAPUFIP3mRNAECe - ECAmessenger RNA - RNA messengerAngiotensin II - آنژیوتانسین دوendothelin - اندوتلینNeutral endopeptidase - اندوپپتیداز عصبیrenal blood flow - جریان خون کلیویSpontaneously Hypertensive Rat - خودآزمایی موش بالینیAng II - دومVascular smooth muscle cell - سلول عضله صاف عروقیShr - شریmean arterial pressure - فشار متوسط شریانیGlomerular filtration rate - نرخ فیلتراسیون گلومرولیmap - نقشهNEP - نپNitric oxide - نیتریک اکسیدarginine vasopressin - وازوپرسین آرژینینProtein kinase C - پروتئین کیناز سیinner medullary collecting duct - کانال جمع آوری مدولاری داخلی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
کاردیولوژی و پزشکی قلب و عروق
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چکیده انگلیسی
In 1985, investigators characterized a potent vasoconstrictor of endothelial origin called endothelin (ET). Subsequently, 3 peptides were recognized that had a comparable molecular structure but different receptors that mediate potent vasoconstrictive and mild vasodilative effects. The renal effects are characterized by natriuresis despite renal vasoconstriction. This effect, along with the stimulation of ET by high sodium intake, suggests that ET may be responsible for maintaining sodium balance when the reninangiotensin system is depressed. Endothelin is activated in desoxycorticosterone acetate salt hypertension models and salt-sensitive hypertension. However, ET involvement with spontaneous hypertension models and renovascular hypertension in rats appears minimal. In humans, the role of ET appears similar to that in experimental animals; in both, ET regulates salt metabolism. Salt-sensitive patients exhibit a blunted renal ET-1 response during sodium load. The role of ET in humans has been investigated using nonspecific ET receptor blockers that inhibit the vasoconstrictive and vasodilative components of ET. However, the effects of ET blockade should be investigated with ET subtype A receptor blockers that mediate vasoconstriction alone. Effects of ET blockade also should be evaluated with respect to stimulation of oxidative stress and tissue damage, important mechanisms responsible for tissue fibrosis. This review offers the clinician a balanced view on the hypertensive mechanisms involved with activation of ET and associated clinical implications.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mayo Clinic Proceedings - Volume 80, Issue 1, January 2005, Pages 84-96
Journal: Mayo Clinic Proceedings - Volume 80, Issue 1, January 2005, Pages 84-96
نویسندگان
Candelas Perez MD, Carlos Javier Garcia MD, Carlos A. MD, PhD, Luis A. MD, J. Carlos MD,