Effects of Aldosterone on the Vasculature

Schiffrin, Ernesto L.

doi:10.1161/01.hyp.0000201443.63240.a7

Cited by 259 publications

(200 citation statements)

References 83 publications

(75 reference statements)

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“…[23][24][25] Moreover, aldosterone induces oxidative stress in vascular cells through NADPH oxidase activation, which has a central role in endothelial dysfunction and atherosclerotic vascular disease. 13,26 Therefore, targeting aldosterone synthesis and release may be clinically important in preventing cardiovascular disease. Ca 2+ ions are transported via T-type calcium channels to mitochondria, where they activate aldosterone synthesis, which in turn stimulates T-type calcium channel expression, 27,28 creating a positive feedback loop of aldosterone biosynthesis in adrenal cells.…”

Section: Discussionmentioning

confidence: 99%

“…11,12 In addition, aldosterone induces oxidative stress in vascular cells through NADPH oxidase activation, which has a central role in endothelial dysfunction and atherosclerotic vascular disease. 13 Recently, some calcium channel blockers (CCBs) have been demonstrated to exhibit an organ protection effect that is independent of their antihypertensive action. Azelnidipine attenuates angiotensin IIinduced peritubular ischemia and has antioxidative properties that may be involved in its beneficial effect on renal injury.…”

Section: Introductionmentioning

confidence: 99%

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Additive antioxidative effects of azelnidipine on angiotensin receptor blocker olmesartan treatment for type 2 diabetic patients with albuminuria

et al. 2011

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The present study aimed to determine whether either of two calcium channel blockers affected urinary albumin excretion or urinary levels of 8-hydroxy-2¢-deoxyguanosine (8-OHdG) and liver-type fatty acid-binding protein (L-FABP) in hypertensive diabetic patients with chronic kidney disease (CKD) who were already being treated with maximum doses of the angiotensin II receptor blocker olmesartan. We conducted an open-label, randomized, parallel-controlled study on type 2 diabetic patients with stable glycemic control who were receiving fixed doses of antidiabetic agents. The patients received either 8 mg per day azelnidipine, which was increased up to 16 mg per day (azelnidipine group; n¼34), or 2.5 mg per day amlodipine, which was increased up to 5 mg per day (amlodipine group; n¼33), over a 24-week period. Mean systolic and diastolic blood pressure decreased significantly in both groups, but there was no significant difference between the two groups at the end of the study. Serum creatinine levels and estimated glomerular filtration rate did not differ significantly between the two groups, whereas the urinary albumin/creatinine ratio and 8-OHdG and L-FABP levels decreased significantly in the azelnidipine group compared with the amlodipine group. Plasma aldosterone level was significantly decreased in the azelnidipine group, and its changes correlated significantly with those of urinary 8-OHdG and L-FABP. Our results suggest that the addition of azelnidipine to the maximal recommended dose of olmesartan was more effective in reducing albuminuria and oxidant stress in hypertensive diabetic patients with CKD than the addition of amlodipine. Hypertension Research (2011) 34, 935-941; doi:10.1038/hr.2011.67; published online 9 June 2011 Keywords: aldosterone; calcium channel blocker; chronic kidney disease; diabetic nephropathy; oxidant stress INTRODUCTIONThe importance of strict blood pressure (BP) control in patients with chronic kidney disease (CKD) was emphasized by the Japanese Society of Hypertension recommendations of a target BP of o130/ 80 mm Hg for hypertensive patients with CKD. This target is further reduced to o125/75 mm Hg for diabetic nephropathy patients whose urinary protein excretion is 41 g per day. 1 Reduction in proteinuria using suitable therapeutic interventions, similar to renin-angiotensin system (RAS) blockade an antihypertensive treatment regimen, is associated with a slower decline in renal function compared with other treatment groups with similar BPs. 2,3 RAS blockade with angiotensin-converting enzyme inhibitors or angiotensin II type-1 receptor blockers (ARBs) is currently considered the most effective pharmacological approach for renoprotection. These agents reduce proteinuria more effectively than other antihypertensive drugs, and therefore, RAS inhibitors should be titrated to maximal recommended doses. 1,4 However, it is difficult to control BP with mono-

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Additive antioxidative effects of azelnidipine on angiotensin receptor blocker olmesartan treatment for type 2 diabetic patients with albuminuria

et al. 2011

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“…Aldosterone is a mineralocorticoid synthesised by the adrenal cortex and perhaps also in blood vessels 144,145 . It exerts blood pressure elevating effects through interactions with the kidney that influence salt and water balance and may have additional direct effects on blood vessels 56,145,146 .…”

Section: Mineralocorticoid Receptor Antagonistsmentioning

confidence: 99%

“…It exerts blood pressure elevating effects through interactions with the kidney that influence salt and water balance and may have additional direct effects on blood vessels 56,145,146 . Mineralocorticoid receptor activation may contribute to cardiovascular dysfunction, inflammation and fibrosis 56 .…”

Section: Mineralocorticoid Receptor Antagonistsmentioning

confidence: 99%

Drug Treatment of Hypertension: Focus on Vascular Health

Cameron

Lang

Touyz

2016

Drugs

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Hypertension, the most common preventable risk factor for cardiovascular disease and death, is a growing health burden. Serious cardiovascular complications result from target organ damage including cerebrovascular disease, heart failure, ischaemic heart disease and renal failure. While many systems contribute to blood pressure elevation, the vascular system is particularly important, because vascular dysfunction is a cause and consequence of hypertension. Hypertension is characterised by a vascular phenotype of endothelial dysfunction, arterial remodelling, vascular inflammation and increased stiffness. Antihypertensive drugs that influence vascular changes associated with high blood pressure have greater efficacy for reducing cardiovascular risk than drugs that reduce blood pressure but have little or no effect on the adverse vascular phenotype. Angiotensin converting enzyme Key Points• Hypertension is characterized by a vascular phenotype of endothelial dysfunction and structural remodeling.• Anti-hypertensive drugs that target the vascular changes associated with hypertension appear to be most efficacious• New anti-hypertensive drugs should promote vascular health as well as reducing blood pressure 3

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“…18 Moreover, both angiotensin II and NE are secretagogues for aldosterone biosynthesis. 19 As the increase in SVR from summer to winter was accompanied by a profound increase in PA and because of the current interest in the effects of aldosterone on the vasculature, [20][21][22] we were interested in determining the independent contribution of PA, as well as the other hormones, age, and BMI to MAP and its haemodynamic components, CO and SVR. Thus, we proceeded to do MRA in 16 subjects matched on all variables.…”

Section: Discussionmentioning

confidence: 99%

Seasonal variation in haemodynamics and blood pressure-regulating hormones

Radke

2009

J Hum Hypertens

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Seasonal variation in blood pressure (BP) has been described in some people, although the variation is small for both systolic and diastolic BPs. The aim of this study was to elucidate underlying haemodynamic and hormonal mechanisms that may occur to defend seasonal changes in BP. Participants were 27 men and 7 women with either normal BP or early hypertension. Measurements of haemodynamics (cardiac output by dual-gas rebreathing) and hormones (resting catecholamines, renin activity, and aldosterone by radioenzymatic assay or radioimmunoassay) were performed during the summer, fall, winter, and spring seasons. Student's paired t-test with Bonferroni modification and regression analyses were used to examine the data with a significance level of Po0.05. Systolic and diastolic BP remained relatively constant across seasons. Cardiac output and stroke volume significantly decreased 10 and 15%, respectively, from summer to winter, whereas heart rate and systemic vascular resistance significantly increased 5 and 11%, respectively. Plasma aldosterone (PA) significantly increased 59% from summer to winter, whereas plasma norepinephrine (PNE), plasma epinephrine, and plasma renin activity (PRA) increased 19, 2, and 17%, respectively (pNS for each). Across the four seasons, mean arterial pressure significantly correlated with PRA and PA, whereas systemic vascular resistance significantly correlated with PNE and PRA. There are dramatic counterregulatory haemodynamic and hormonal adaptations to maintain a relatively constant BP. Norepinephrine, PRA, and aldosterone have a function in mediating the changes in haemodynamics.

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Effects of Aldosterone on the Vasculature

Cited by 259 publications

References 83 publications

Additive antioxidative effects of azelnidipine on angiotensin receptor blocker olmesartan treatment for type 2 diabetic patients with albuminuria

Additive antioxidative effects of azelnidipine on angiotensin receptor blocker olmesartan treatment for type 2 diabetic patients with albuminuria

Drug Treatment of Hypertension: Focus on Vascular Health

Seasonal variation in haemodynamics and blood pressure-regulating hormones

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