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  • In addition enhanced AT receptor function abnormally increas

    2023-01-16

    In addition, enhanced AT1 receptor function abnormally increases central and sympathetic activity, contributing to cardiac and renal disease, which in turn alters homeostasis, increases vulnerability to stress, and further injures the brain, and that AT1 receptor blockade ameliorates excessive sympathetic responses and peripheral organ damage [42], [43], [44], [45], [46].
    The use of ARBs for the treatment of stroke Hypertension affects cerebrovascular flow and is a major risk factor for stroke. The mechanisms include pathological remodeling of the cerebral arteries, diminished cerebrovascular autoregulation and cerebrovascular inflammation. This reduces the capacity of the flumethasone to adjust its regional blood flow to energy requirements, oxygen and nutrient supply, eventually leading to chronic hypoxia and cellular injury [47], [48], [49], [50], [51]. Chronic hypoxia and cerebrovascular inflammation have also been described in type II diabetes, another major factor of vulnerability to stroke [52], [53], [54]. Enhanced AT1 receptor activity is a major factor in the hypertension-induced cerebrovascular pathology. ARB treatment reverses these changes, reducing arterial remodeling and inflammation, improving autoregulation and normalizing oxygen and nutrient supply to the brain [27], [28], [47], [50], [55]. The therapeutic effects of ARB administration in stroke, first demonstrated in animal models, have strong clinical correlates. In many controlled randomized studies, ARBs have been demonstrated not only to reduce high blood pressure but also, in both preventive and corrective manners, ameliorate stroke pathology and protect brain function [29], [33]. Similar cerebrovascular neuroprotective effects of ARBs have been described in animal models of diabetes [56]. The many clinical studies demonstrating beneficial effects of ARB administration in stroke, hypertension and diabetes have been described elsewhere [27], [28], [33], [57], [58], [59], [60], [61], [62], [63], [64], [65], [66], [67]. There are multiple ongoing and recruiting clinical trials to assess the effect of ARB treatment on brain ischemia and stroke (https://clinicaltrials.gov/)
    Neurodegenerative disorders
    Traumatic brain injury Traumatic brain injury (TBI), a major cause of death and disability, was replicated in preclinical injury rodent models of controlled cortical impact [127], [128] . In this model, ARB administration within a reasonable therapeutic window of several hours after the injury decreased the volume of the lesion, strongly reduced the associated inflammatory response, and protected cognition and motor performance [33], [127], [128]. This is important because most frequently TBI is unpredictable and not expected, and post-trauma treatment must be applied within a few hours of the injury. Acute and repeated TBI are recognized risk factors for neurodegenerative disorders with progressive loss of cognitive and motor function and related behavioral alterations. These include Alzheimer’s and Parkinson’s disease as well as other dementias. The risk is not only associated with major single brain trauma, but with iterative traumatic experiences such as those linked with contact sports [129], [130], [131], [132]. Testing the effects of ARB therapy in clinical studies with patients suffering from acute and repeated TBI will clarify if these compounds may also be proposed not only to ameliorate the immediate consequences of brain trauma but also to prevent development of related neurodegenerative disorders.
    Radiation-induced brain damage Fractioned whole brain irradiation as treatment of primary or metastatic brain cancer chronically and progressively reduces cognition in 50% of the patients [133], [134] . In a rat model, AT1 receptor blockade prevented and reversed cognitive deficits [133], [134]. In addition, radiation- induced lung injury is reduced in response to ACE inhibitors, compounds that by decreasing Angiotensin II production also reduce AT1 receptor stimulation [135].