Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic, as well as acute emotional arousal, is a consequence of various types of social interaction, i.e., those between mother and infant and between controlling dominant and less effective subordinate. The neurohumoral accompaniments of this social stress include the sympathetic adrenal medullary and hypothalamic pituitary adrenal responses. A common ensuing pathophysiological state involves a chronic increase of blood pressure. Although Selye's General Adaptation Syndrome presupposed the same response to a variety of stimuli; recent work shows that specific perceptions of control result in different patterns of neuroendocrine activation. A challenge perceived as easy to handle will elicit an active coping response and release of the neurosympathetic system's norepinephrine. Testosterone will rise as the subject savors success. With increasing anxiety this active coping shifts to a more passive mode and the behavior becomes less assured as the animal loses control. The norepinephrine/epinephrine ratio decreases as epinephrine, prolactin, renin and fatty acids rise. As the outcome becomes still less certain and distress grows, adrenocorticotropic hormone and cortisol levels arise. Thus, the effort required on the one hand and the degree of frustration conflict and uncertainty on the other, determine the ratio of catecholamines to corticoids. With severe emotional trauma, brain dysfunction may occur. These effects can be lasting, and corticoids paradoxically return to normal as the behavior changes to that of post-traumatic stress disorder. Repression and denial set in and the organism responds with decreased concern of impaired attachment and increased irritability.
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PMID:Biological basis of the stress response. 157 90

The kallikrein-kinin system (KKS) is an intricate endogenous pathway involved in several physiological and pathological cascades in the brain. Due to the pathological effects of kinins in blood vessels and tissues, their formation and degradation are tightly controlled. Their components have been related to several central nervous system diseases such as stroke, Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy and others. Bradykinin and its receptors (B1R and B2R) may have a role in the pathophysiology of certain central nervous system diseases. It has been suggested that kinin B1R is up-regulated in pathological conditions and has a neurodegenerative pattern, while kinin B2R is constitutive and can act as a neuroprotective factor in many neurological conditions. The renin angiotensin system (RAS) is an important blood pressure regulator and controls both sodium and water intake. AngII is a potent vasoconstrictor molecule and angiotensin converting enzyme is the major enzyme responsible for its release. AngII acts mainly on the AT1 receptor, with involvement in several systemic and neurological disorders. Brain RAS has been associated with physiological pathways, but is also associated with brain disorders. This review describes topics relating to the involvement of both systems in several forms of brain dysfunction and indicates components of the KKS and RAS that have been used as targets in several pharmacological approaches.
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PMID:What have we learned about the kallikrein-kinin and renin-angiotensin systems in neurological disorders? 2492 Oct 4