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dc.contributor.editorZicha, Josef
dc.contributor.editorVaněčková, Ivana
dc.date.accessioned2023-02-02T16:48:51Z
dc.date.available2023-02-02T16:48:51Z
dc.date.issued2023
dc.identifierONIX_20230202_9783036563183_167
dc.identifier.urihttps://directory.doabooks.org/handle/20.500.12854/96766
dc.description.abstractEssential hypertension is still an important health care problem. It is necessary to investigate its mechanisms in animal models. The potential clinical importance of such experimental research might be expected. This Special Issue concerned several important topics. First, several studies focused on the pathophysiological mechanisms responsible for blood pressure elevation during hypertension development, organ damage in chronic hypertension, and drugs targeting hypertension and/or its complications. Other studies were interested in the participation of central and peripheral blood pressure control, changes in vascular structure and function, and neural, humoral, and endocrine factors. Furthermore, the contribution of altered redox signaling, chronic inflammation, microbiome changes, and interactions of genetic and environmental factors were evaluated in multiple papers. Finally, special attention was paid to the progress in pharmacological tools for the control of hypertension and associated organ damage, genetic modifications to alter blood pressure levels, and non-pharmacological interventions attenuating hypertension or its complications. The original articles or reviews covered the interesting aspects of the pathophysiology of hypertension and associated end-organ damage, the use of various experimental hypertensive models, and the importance of specific environmental factors acting in distinct phases of the ontogeny. We especially appreciate the presentation of new ideas and the critical discussion of traditional theories.
dc.languageEnglish
dc.subject.classificationthema EDItEUR::M Medicine and Nursingen_US
dc.subject.classificationthema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJD Cardiovascular medicineen_US
dc.subject.otherdevelopmental origins of health and disease (DOHaD)
dc.subject.othergut microbiota
dc.subject.otherhypertension
dc.subject.othershort chain fatty acid
dc.subject.otheroxidative stress
dc.subject.otherprobiotics
dc.subject.otherprebiotics
dc.subject.otherrenin–angiotensin system
dc.subject.otherfibroblast growth factor-23
dc.subject.otherleft ventricular hypertrophy
dc.subject.otherrenin–angiotensin–aldosterone system
dc.subject.otherlosartan
dc.subject.othercanrenone
dc.subject.otherHyp mice
dc.subject.otherX-linked hypophosphatemia
dc.subject.otherhairless SHRM
dc.subject.othercold acclimation
dc.subject.othercardiac Cx43
dc.subject.otherextracellular matrix
dc.subject.otherthyroid hormones
dc.subject.otherSHR
dc.subject.othersacubitril/valsartan
dc.subject.otherARNI
dc.subject.otherivabradine
dc.subject.otherremodelling
dc.subject.othercardiac dysfunction
dc.subject.otherfibrosis
dc.subject.otherangiotensin II
dc.subject.otherangiotensin 1-7
dc.subject.otherknock-out
dc.subject.othergenome-editing
dc.subject.otherSHRSP
dc.subject.otherDahl SS
dc.subject.otherfoetal programming of hypertension
dc.subject.othersympathetic neurotransmission
dc.subject.othersympathetic innervation
dc.subject.othervascular remodelling
dc.subject.otherfoetal undernutrition
dc.subject.otherold SHR
dc.subject.otherantihypertensive therapy
dc.subject.otherblood pressure monitoring
dc.subject.otherLV hypertrophy
dc.subject.otherECM markers
dc.subject.othercardiac fibrosis
dc.subject.otherSHR-CRP
dc.subject.otherSGLT-2 inhibitor
dc.subject.othergene expression
dc.subject.otherage
dc.subject.otherlipid metabolism
dc.subject.othernitric oxide
dc.subject.otherl-NAME
dc.subject.otherrostral ventrolateral medulla
dc.subject.otheraging
dc.subject.otherreactive oxygen species
dc.subject.otherNADPH oxidase activator 1
dc.subject.othermitochondria
dc.subject.otherchloride
dc.subject.othercalcium-activated chloride channel
dc.subject.otherNa+–K+–2Cl− cotransporter 1
dc.subject.otherTMEM16A
dc.subject.othersmooth muscle
dc.subject.otherfetal undernutrition programming
dc.subject.othercross-fostering
dc.subject.otherlactation period
dc.subject.othercardiovascular hypertrophy
dc.subject.otheradipose tissue browning
dc.subject.othercardiovascular disease
dc.subject.othercatecholamines
dc.subject.otherliquid chromatography–tandem mass spectrometry
dc.subject.otherSGLT-2 inhibition
dc.subject.otherproteinuria
dc.subject.otheruninephrectomized salt-loaded
dc.subject.othertwo-kidney
dc.subject.otherone-clip hypertension
dc.subject.otherfawn-hooded hypertensive rat
dc.subject.otherApoE KO
dc.subject.otherapolipoprotein E knockout mice
dc.subject.otheratherosclerosis
dc.subject.otherNa,K-ATPase
dc.subject.otherTCTP
dc.subject.otherTCTP-overexpressing transgenic mice
dc.subject.othertranslationally controlled tumor protein
dc.subject.otherTCTP-TG
dc.subject.otherexperimental hypertension
dc.subject.otherbone
dc.subject.otherrats
dc.subject.othertaurine
dc.subject.othermagnesium
dc.subject.other24 h urine(24U)
dc.subject.otherstroke-prone spontaneously hypertensive rat
dc.subject.otheryoung SHR
dc.subject.othercombination therapy
dc.subject.othertreatment effect
dc.subject.othersystolic blood pressure
dc.titleAnimal Models for Study of Pathophysiological Mechanisms of Hypertension and Its Complications
dc.typebook
oapen.identifier.doi10.3390/books978-3-0365-6319-0
oapen.relation.isPublishedBy46cabcaa-dd94-4bfe-87b4-55023c1b36d0
oapen.relation.isbn9783036563183
oapen.relation.isbn9783036563190
oapen.pages296
oapen.place.publicationBasel


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