Latest research on Losartan

Losartan is an angiotensin-receptor blocker (ARB) that may be used alone or with other agents to treat hypertension. Losartan and its longer acting metabolite, E-3174, lower blood pressure by antagonizing the renin-angiotensin-aldosterone system (RAAS); they compete with angiotensin II for binding to the type-1 angiotensin II receptor (AT1) subtype and prevents the blood pressure increasing effects of angiotensin II. Unlike angiotensin-converting enzyme (ACE) inhibitors, ARBs do not have the adverse effect of dry cough. Losartan may be used to treat hypertension, isolated systolic hypertension, left ventricular hypertrophy and diabetic nephropathy. It may also be used as an alternative agent for the treatment of systolic dysfunction, myocardial infarction, coronary artery disease, and heart failure.

Latest findings

Losartan was able to significantly ameliorate this tendency for all Th1-mediated cytokines, and was able to decrease the expression levels of the Th17-mediated cytokines but not significantly (Fig. 2). [source, 2016]
Since Losartan had been demonstrated to have an anti-apoptotic effect in vitro (11), the present study investigated whether the protective effect of Losartan on TNBS-induced colitis was associated with its anti-apoptotic effect on IECs in vivo. [source, 2016]
An abundance of apoptotic IECs were observed following TNBS administration, whereas the number of apoptotic epithelial cells was markedly reduced in the TNBS + Losartan mice (Fig. 3A and B). [source, 2016]
Concordantly, treatment with Losartan partly alleviated the FD4 leak by decreasing intestinal permeability (Fig. 3C). [source, 2016]
These results indicate that Losartan may preserve the intestinal epithelial barrier and decrease gut permeability by inhibiting the apoptosis of IECs. [source, 2016]
The mechanism underlying the anti-apoptotic effect of Losartan on IECs was further investigated. [source, 2016]
There was a significant decrease in the protein expression levels of Bax, but not of Bcl-2, in the TNBS + Losartan group, as compared with the TNBS + Water group (Fig. 4A and B), which suggests that Losartan treatment may increase the Bcl-2/Bax ratio. [source, 2016]
Concordantly, the expression levels of cleaved caspase-3 were markedly inhibited in the TNBS + Losartan group. [source, 2016]
These data indicate that the anti-apoptotic mechanism of Losartan was, at least in part, attributed to the inhibition of caspase-3 induction through upregulation of the Bcl-2/Bax ratio. [source, 2016]
The results of the present study revealed the protective role of the AT1R blocker Losartan in TNBS-induced colitis. [source, 2016]