Vascular Alterations in Mental Disorders: Focus in Angiotensin II Role

Mental disorders have high prevalence and long duration, affecting the quality of life and generating elevated economic costs in public health. Approximately 25% of population worldwide will develop any mental illness at some moment of its lifetime. These disorders are the result of complex processes involving the interaction of many pathological changes. Although, each psychiatric disease has well-defined characteristics, some of their neurobiological processes, like inflammation and vascular alterations, seem to be common. Since microvasculature is involved in essential functions as oxygen delivery, waste product removal, and transvascular exchange, any brain vessel alteration could promote a pathological state. In this sense, capillary ultrastructural abnormalities, deficient perfusion, and blood-brain barrier disruption have been described in schizophrenia, depression, and Parkinson?s and Alzheimer?s diseases. These vascular dysfunctions could be related to angiogenic factor deregulations. The abovementioned evidences point out to evaluate the vasculature as a future pharmacological target for the treatment of mental disorders. Among the several factors involved in the regulation of angiogenesis, this chapter will focus on the upstream angiogenic mediator Angiotensin II. This peptide is produced at peripheral and brain level and exerts its principal effects acting through AT1 receptors. Considering that the available treatments for mental illnesses have low efficacy and high incidence of side effects, new pharmacological tools become necessary. The present chapter will be focused in the evidences that support Angiotensin II as a key factor in the understanding and therapy of these pathologies.Fil: Delgado Marín, Leticia Ester. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones Biológicas y Tecnológicas. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Instituto de Investigaciones Biológicas y Tecnológicas; ArgentinaFil: Basmadjian, Osvaldo Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Occhieppo, Victoria Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Marchese, Natalia Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Bregonzio Diaz, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Baiardi, Gustavo Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones Biológicas y Tecnológicas. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Instituto de Investigaciones Biológicas y Tecnológicas; Argentin

Glial Cells in the Schizophrenia Puzzle: Angiotensin II Role

Schizophrenia is a neuropsychiatric disease with 1% worldwide prevalence and characterized by a deep distortion in thought and perception, cognitive dysfunction, and social behavioral deficits. After the discovery of the antipsychotic effects of chlorpromazine, a large body of evidence pointed out to the neurotransmission misbalance as the main factor in the development of this pathology. Nowadays, it is known that schizophrenia is related to a pluri-factorial etiopathogenesis where gene factors, neuroinflammation, and brain microenvironment?s alterations are taken into account as well. In this sense, glial cells (oligodendrocytes, astrocytes, and microglial cells) are essential pieces in brain microenvironment with crucial roles in synaptic establishment and function, neuroinflammation, and metabolic and ion homeostasis, among others. Currently, glial cells are the target of numerous researches on the race to puzzle out the schizophrenia etiopathology.Among the multiplicity of regulatory substances involved in glial cell functionality, it becomes outstanding the newly described roles for brain angiotensin II (Ang II). This neuropeptide, through its AT1 receptors (AT1-R), expressed in neurons and glial cells modulates brain homeostasis and several neurotransmission systems (dopaminergic, glutamatergic, and GABAergic) and has a pro-inflammatory role in pathological conditions. In this way, Ang II has been involved in cognition processes, stress responses, and mental disorders such as schizophrenia, addiction, Parkinson?s, and Alzheimer?s diseases.In this chapter, we aimed to summarize the role of the glial cells in the schizophrenia with a special reference to AT1-R involvement in this complex scenario.Fil: Occhieppo, Victoria Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Basmadjian, Osvaldo Martin. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Marchese, Natalia Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Rodríguez, Anahí. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Jaime, Andrea del Valle. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Herrera Lopez, Malena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; ArgentinaFil: Bregonzio Diaz, Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; Argentin