Abstract:Angiotensin II receptor blockers could prevent the development of atherosclerosis beyond reducing blood pressure in monkeys fed a high-cholesterol diet. However, it has been unclear whether hypotensive effects improve atherosclerosis in primates. We investigated whether antihypertensive agents, an angiotensin II receptor antagonist, candesartan, and a calcium channel blocker, amlodipine, prevent areas of atherosclerotic lesions in the aorta of monkeys fed a high-cholesterol diet. Seventeen male monkeys fed a h… Show more
“…They reported that in the ApoEKO mice treated with streptozotocin, the vascular renin-angiotensin system plays a critical role in mediating acceleration of ath- erosclerosis, and this may explain why irbesartan was superior to amlodipine in reducing the diabetes-associated acceleration of atherosclerosis. Takai et al (23) reported that amlodipine tended to decrease the atherosclerotic area in monkeys fed a high-cholesterol diet, although this effect was not statistically significant. In contrast, others have reported that amlodipine inhibited atherosclerosis in non-diabetic animal models of atherosclerosis (24,25).…”
We examined whether amlodipine, an L-type calcium channel blocker (CCB), has an inhibitory effect on oxidative stress and inflammatory response, and thereby atherosclerosis, in apolipoprotein E-deficient
“…They reported that in the ApoEKO mice treated with streptozotocin, the vascular renin-angiotensin system plays a critical role in mediating acceleration of ath- erosclerosis, and this may explain why irbesartan was superior to amlodipine in reducing the diabetes-associated acceleration of atherosclerosis. Takai et al (23) reported that amlodipine tended to decrease the atherosclerotic area in monkeys fed a high-cholesterol diet, although this effect was not statistically significant. In contrast, others have reported that amlodipine inhibited atherosclerosis in non-diabetic animal models of atherosclerosis (24,25).…”
We examined whether amlodipine, an L-type calcium channel blocker (CCB), has an inhibitory effect on oxidative stress and inflammatory response, and thereby atherosclerosis, in apolipoprotein E-deficient
“…In particular, angiotensin II promotes hypertrophy of cardiovascular cells and aldosterone causes fibrosis of the cardiovascular tissues (12,13). Therefore, antihypertensive drugs that suppress RAAS, such as ARBs and ACE inhibitors, are expected to confer protection against hypertensive injuries in cardiovascular organs that goes beyond their hypotensive effects (32). Fibrosis and deposition of intercellular matrices such as collagen in the cardiac tissue cause reduction in left ventricular distensibility (33).…”
“…The AT1 receptor antagonists irbesartan and candesartan but not amlodipine treatment showed beneficial effects in diabetic apolipoprotein E-null mouse or monkeys. [31][32] …”
Section: Liu Et Al Increased Trpc3 In Shrmentioning
Abstract-We tested the hypothesis that transient receptor potential canonical type 3 (TRPC3) channels are increased in vascular smooth muscle cells and aortic tissue from spontaneously hypertensive rats (SHR) compared with normotensive Wistar Kyoto rats. Expression of TRPC3 was analyzed by immunohistochemistry and Western blotting. TRPC3 gene knockdown was performed by specific small interfering RNA and TRPC3 overexpression using the pAdEasy-1 system. Cytosolic calcium was measured using fluorescence spectrophotometry and vasoconstriction of aortic rings using a force transducer. In SHR, the expression of TRPC3 channel protein was significantly higher in aortic rings (
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