<p>Olmesartan Medoxomil, An Angiotensin II-Receptor Blocker, Ameliorates Renal Injury In db/db Mice</p>

Abstract

BackgroundDiabetic nephropathy (DN) is a common complication of diabetes mellitus (DM) and also a major cause of end-stage renal disease (ESRD). Olmesartan medoxomil (OM) is an angiotensin II receptor blocker (ARB) and has been shown to exhibit renoprotective effects on a streptozotocin (STZ)-induced diabetic rat model. Yet, whether OM affects DN progression and renal injury in db/db mice, a type 2 diabetic murine model, has not been established.MethodsWild-type (n = 15) and db/db mice (n = 15) were treated with control saline or OM via oral gavage. The physiological and biochemical parameters were evaluated and histological examinations of kidney specimens were performed.ResultsCompared with saline-treated db/db mice, db/db mice administered with OM showed ameliorated diabetic physiological and biochemical parameters. In addition, OM decreased urinary albumin excretion and plasma creatinine level in db/db mice. Moreover, histologically, OM reduced glomerular hypertrophy and injury, and also ameliorated tubular injury, thus suggesting that OM improves renal function and minimizes renal pathological deterioration in db/db mice.ConclusionOur study reveals a beneficial role of OM in ameliorating DN in db/db mice, which is associated with its renoprotective function.

Novel antihypertensive action of rutin is mediated via inhibition of angiotensin converting enzyme/mineralocorticoid receptor/angiotensin 2 type 1 receptor (ATR1) signaling pathways in uninephrectomized hypertensive rats

“…Therefore, uninephrectomized subjects are at greater risk of becoming hypertensive as reported elsewhere (Zohdi et al, 2012). Angiotensin II, because of its potent vasoconstrictor activity, increases disease progression in renal/ cardiovascular injury (Costantino et al, 2019;Zhu et al, 2019).…”

“…The rennin-angiotensin-aldosterone system (RAAS) has been well documented and reported for the regulation of blood pressure, fluid volume, and sodium balance (Zhang et al, 2019). Therefore, over activity of RAAS has been reported to promote both systemic and regional glomerular capillary hypertension leading to renal damage, vasoconstriction, endothelial dysfunction, thrombosis, inflammation, and fibrosis via proinflammatory pathways (Gromotowicz-Poplawska et al, 2016;Zhang et al, 2019).…”

“…The rennin-angiotensin-aldosterone system (RAAS) has been well documented and reported for the regulation of blood pressure, fluid volume, and sodium balance (Zhang et al, 2019). Therefore, over activity of RAAS has been reported to promote both systemic and regional glomerular capillary hypertension leading to renal damage, vasoconstriction, endothelial dysfunction, thrombosis, inflammation, and fibrosis via proinflammatory pathways (Gromotowicz-Poplawska et al, 2016;Zhang et al, 2019). Angiotensin-converting enzyme (ACE) inhibitors prevent the formation of more physiologically active angiotensin II from its precursor angiotensin I, and are, therefore, effective for the management of hypertension due to excessive generalized vasoconstriction in the cardiovascular system (Bhandari & Chadburn, 2019;Podzolkov & Tarzimanova, 2018).…”

Oxymatrine Inhibits Twist-Mediated Renal Tubulointerstitial Fibrosis by Upregulating Id2 Expression

“…The pathogenesis of hyperglycemia was very similar to that of patients with type 2 diabetes mellitus. It is also an ideal animal model for the experimental study of type 2 DN in the world (Lutz and Woods, 2012;Zar Kalai et al, 2014;Zhu et al, 2019). Our previous study found that oxymatrine played an antifibrotic effect in renal tubular epithelial cells (Liu et al, 2016).…”

The Influence of Hypertensive Therapies on Circulating Factors: Clinical Implications for SCFAs, FGF21, TNFSF14 and TNF-α

“…It has been shown that controlling BP with inhibitors of the RAAS is associated with renoprotection [ 44 ]. However, when we measured serum creatinine levels, we found no decrease in creatinine levels in the treated hypertensive patients, even though most were on RAAS inhibitors.…”