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• W4313445401 abstract "HypertensionHypertension, which affects more than one billion people, is the major modifiable risk factor for cardiovascular diseaseCardiovascular disease death. Although the pathophysiology of hypertensionHypertension is not entirely understood, disruption of the renin angiotensin systemRenin angiotensin system (RAS), which includes the systemic and brain RAS, has been identified as one of the key causes of numerous forms of hypertensionHypertension. As a result, developing a solid understanding of the fundamental science of RASRenin angiotensin system and the underlying processes of the signalling pathways associated with RASRenin angiotensin system may aid in the development of new therapeutic targets for the treatment of patients with cardiovascular and renal illnesses. Four kinds of angiotensin IIAngiotensin II receptors (AT1RAT4R) have been found, with AT1R playing an essential function in vasoconstriction and receiving the most attention. It has been discovered in numerous areas of the brain, and its distribution is closely related to that of angiotensin-like immunoreactivity in nerve terminals. The impact of AT1R includes the activation of various media and signalling pathways, the most prominent of which are the AT1R/JAK/STAT and Ras/Raf/MAPK pathways. Furthermore, the impact of ATR1 is linked to the regulation of the nuclear factor light-chain enhancer of activated B cells (NFB) and cyclic AMP response element-binding (CREB) pathways. Their action mechanisms are associated with proinflammatory and sympathetic excitatory effects. At1R is involved in nearly every type of hypertensionHypertension, including spontaneous hypertensionHypertension, obesityObesity-induced hypertensionHypertension, renovascular hypertensionHypertension, diabetic hypertensionHypertension, L-NAME-induced hypertensionHypertension, stress-induced hypertensionHypertension, and angiotensin IIAngiotensin II-induced hypertensionHypertension. Acute and chronic central AT1R inhibition are the two forms of central AT1R blockade. The latter is possible by chemical blockage or geneticGenetics modification. This chapter study aimed to emphasize the prevalence, functions, interactions, and modulation methods of central AT1R to treat a variety of clinical disorders. The discovery of angiotensin-derived peptides and the creation of AT2R agonists may give a more comprehensive understanding of RASRenin angiotensin system and innovative treatment methods." @default.
• W4313445401 created "2023-01-06" @default.
• W4313445401 creator A5047456988 @default.
• W4313445401 date "2023-01-01" @default.
• W4313445401 modified "2023-10-18" @default.
• W4313445401 title "Role Renin Angiotensin System in Hypertension" @default.
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• W4313445401 cites W1964816832 @default.
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• W4313445401 cites W1981935901 @default.
• W4313445401 cites W1989434611 @default.
• W4313445401 cites W1990891118 @default.
• W4313445401 cites W1991182836 @default.
• W4313445401 cites W2008087295 @default.
• W4313445401 cites W2014138378 @default.
• W4313445401 cites W2024040351 @default.
• W4313445401 cites W2031083476 @default.
• W4313445401 cites W2032171017 @default.
• W4313445401 cites W2036369270 @default.
• W4313445401 cites W2040054030 @default.
• W4313445401 cites W2041880968 @default.
• W4313445401 cites W2044834588 @default.
• W4313445401 cites W2054640522 @default.
• W4313445401 cites W2054715005 @default.
• W4313445401 cites W2057087149 @default.
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• W4313445401 cites W2123779772 @default.
• W4313445401 cites W2124242252 @default.
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• W4313445401 cites W2133088349 @default.
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• W4313445401 doi "https://doi.org/10.1007/978-3-031-14952-8_12" @default.
• W4313445401 hasPublicationYear "2023" @default.
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