2017
DOI: 10.4172/2324-8602.1000305
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Angiotensin II as an Indicator of Left ventricular Hypertrophy in Uncontrolled Treated Hypertensive Patients

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“…Angiotensin-II mediates vasoconstriction within the acute phase of exposure in hypertension [37], while chronicity eventually results in hypertrophy and intimal anatomical aberrations [38]. Vascular angiotensin-II is derived from circulating angiotensin-II produced by ACE [39], while the local angiotensin-II in the vessel is produced by both the ACE and Chymase [40]. Chymase activity is significant in the blood vessels following vascular injury [41].…”
Section: Distribution and Activity Of Chymase In Vascular Tissuesmentioning
confidence: 99%
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“…Angiotensin-II mediates vasoconstriction within the acute phase of exposure in hypertension [37], while chronicity eventually results in hypertrophy and intimal anatomical aberrations [38]. Vascular angiotensin-II is derived from circulating angiotensin-II produced by ACE [39], while the local angiotensin-II in the vessel is produced by both the ACE and Chymase [40]. Chymase activity is significant in the blood vessels following vascular injury [41].…”
Section: Distribution and Activity Of Chymase In Vascular Tissuesmentioning
confidence: 99%
“…Angiotensin-II plays a key role in homeostasis by regulating arterial tone and fluid balance [5], but becomes toxic to tissues in pathological states [6]. Angiotensin-II is the main biochemical mediator involved in LVH [7], although its inhibitors do not reduce blood pressure significantly compared to calcium channel blockers, diuretics and vasodilators [8]. This stresses on the impact of biochemical mediators causing left ventricular hypertrophy independent of the level of blood pressure.…”
Section: Introductionmentioning
confidence: 99%
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