2009
DOI: 10.1210/jc.2009-1588
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Hypertrophic Remodeling of Subcutaneous Small Resistance Arteries in Patients with Cushing’s Syndrome

Abstract: Our results suggest the presence of hypertrophic remodeling in sc small resistance arteries of CS, probably as a consequence of growth-promoting properties of circulating cortisol and/or increased vascular oxidative stress.

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Cited by 42 publications
(27 citation statements)
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“…The cross-sectional media area of subcutaneous small resistance arteries was significantly greater in CS compared to hypertensive patients and controls, while the media to lumen ratio was greater in hypertensive and CS patients compared to controls (168). MR activation by GCs can mediate vascular damage, since mineralocorticoids have growth promoting and profibrotic activities, which lead to remodelling and fibrosis of small vessels (169).…”
Section: European Journal Of Endocrinologymentioning
confidence: 99%
“…The cross-sectional media area of subcutaneous small resistance arteries was significantly greater in CS compared to hypertensive patients and controls, while the media to lumen ratio was greater in hypertensive and CS patients compared to controls (168). MR activation by GCs can mediate vascular damage, since mineralocorticoids have growth promoting and profibrotic activities, which lead to remodelling and fibrosis of small vessels (169).…”
Section: European Journal Of Endocrinologymentioning
confidence: 99%
“…Both these observations when taken together would indicate an impaired myogenic regulation of vascular smooth muscle tone in CS leading to a diminished myogenic relaxation during the period of occlusion and a delay in the recovery of myogenic vasoconstrictor tone following the release of arterial occlusion and restoration of stretch on the vessel walls. This impairment in myogenic regulation of vascular tone could possibly be a pathophysiologic manifestation of the hypertrophic remodelling of blood vessels in patients with CS which has been shown by previous micromyographic studies [12]. The diminished vasorelaxation during the period of occlusion could also be due to endothelial dysfunction as it has been shown by in vitro studies that, deformation of endothelial cells resulting from the collapse of vessel intima during the period of arterial occlusion induces endothelial nitric oxide release and contributes to the maximal vasorelaxation response observed at the time of release of occlusion [30].…”
Section: Declaration Of Interestmentioning
confidence: 56%
“…In both these studies patients and subjects were shown to be free of any of the clinical or biochemical features of glucocorticoid induced metabolic syndrome suggesting that excess glucocorticoid levels can per se affect vascular endothelial function. Pathological changes in vascular structure and function in patients with excess circulating glucocorticoid levels due to an endogenous or exogenous cause have also been linked to an increased oxidative stress in them [10,12].…”
Section: Assessment Of Vascular Functionmentioning
confidence: 99%
“…As a consequence of growth-promoting properties of circulating cortisol and/or increased vascular oxidative stress there is a hypertrophic remodeling in subcutaneous small resistance arteries (23). Persistently elevated cardiovascular risk in CS despite remission of hypercortisolism has been shown in a study using multi-detector CT coronary angiogram.…”
Section: Atherosclerosis and Endothelial Dysfunctionmentioning
confidence: 97%