Publisher's Synopsis
The book is organized into sections/chapters. Section I, The Renin-Angiotensin-Aldosterone System (RAAS) in health and disease, conveys topics like an overview and history of RAAS discovery and its significance in cardiovascular physiology, the RAAS in the cardiovascular system, including the cardiorenal axis, and other RAAS endocrine systems (in the liver, lungs, adrenal glands, and testes). RAAS pathways and second messengers (Cyclic AMP, Calcium), and receptors [AT1R, AT2R, MasR binding to the vasodilator angiotensin-(1-7)], medications targeting the RAAS, and effects of the RAAS on inflammation. Oxidative stress, vascular smooth muscle contraction, endothelial dysfunction, fibrosis, and the hypertrophic, anti-apoptotic, and pro-mitogenic effects of Angiotensin II. RAAS local brain systems and pleiotropic effects, including neuroinflammation, autophagy, endoplasmic reticulum stress, and mitochondrial dysfunction. Section II, the Renin-Angiotensin System (RAS) in Parkinson's disease, deals with general considerations, pathogeny and pharmacotherapeutics, the RAS and Alzheimer's disease and other neurodegenerative diseases, neuroprotective and anti-inflammatory properties of AT2 in motor neuron disease treatment, Amyotrophic Lateral Sclerosis (ALS) and Spinal Muscular Atrophy (SMA); RAS modulation of dopaminergic neurotransmission: effects on Parkinson's disease motor symptoms, motor fluctuations, memory, cognition and mood; ACEIs and ARBs' therapeutic benefits on mood and depressive symptoms; brain RAS as a potential therapeutic target in psychiatric disorders; the risk of Parkinson's disease and the use of Renin-angiotensin modulators; brain RAS regulation of stress and neuroinflammation, and participation of the hypothalamic-pituitary-adrenal axis; risk of Parkinson's disease and the use of RAS modulators; the relationship between RAS, COVID-19, and Parkinson's disease; RAS, Parkinson, and COVID-19: ACE2 and post COVID-19 parkinsonism; the relationship between RAS and other pathological conditions that increase PD risk. RAS role in the pathophysiology of diabetes and complications - nephropathy and retinopathy; gut microbiota and local gastrointestinal RAS two-way interaction; gut dysbiosis and impaired renin-angiotensin system (RAS) function in cognitive decline and neurodegeneration; gut microbiota impact on RAS-related disorders; gastrointestinal dopaminergic and renin-angiotensin systems; gut ACE2, probiotics supplementation, and diabetic retinopathy in type 1 diabetes; Ang-(1-7) protection in diabetes and diabetic retinopathy; ACE2 gene therapy improvement of glycemic control in diabetic mice.
