Animal Models for Study of Pathophysiological Mechanisms of Hypertension and Its Complications

Edited by
January 2023
296 pages
  • ISBN978-3-0365-6318-3 (Hardback)
  • ISBN978-3-0365-6319-0 (PDF)

This book is a reprint of the Special Issue Animal Models for Study of Pathophysiological Mechanisms of Hypertension and Its Complications that was published in

Biology & Life Sciences
Medicine & Pharmacology

Essential 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.

  • Hardback
License and Copyright
© 2022 by the authors; CC BY-NC-ND license
developmental origins of health and disease (DOHaD); gut microbiota; hypertension; short chain fatty acid; oxidative stress; probiotics; prebiotics; renin–angiotensin system; fibroblast growth factor-23; left ventricular hypertrophy; hypertension; renin–angiotensin–aldosterone system; losartan; canrenone; Hyp mice; X-linked hypophosphatemia; hairless SHRM; cold acclimation; cardiac Cx43; extracellular matrix; thyroid hormones; SHR; sacubitril/valsartan; ARNI; ivabradine; remodelling; cardiac dysfunction; fibrosis; renin–angiotensin–aldosterone system; angiotensin II; angiotensin 1-7; knock-out; genome-editing; SHR; SHRSP; Dahl SS; foetal programming of hypertension; sympathetic neurotransmission; sympathetic innervation; vascular remodelling; fibrosis; foetal undernutrition; old SHR; antihypertensive therapy; blood pressure monitoring; LV hypertrophy; ECM markers; cardiac fibrosis; SHR-CRP; SGLT-2 inhibitor; gene expression; age; lipid metabolism; nitric oxide; l-NAME; hypertension; rostral ventrolateral medulla; aging; reactive oxygen species; NADPH oxidase activator 1; mitochondria; chloride; calcium-activated chloride channel; hypertension; Na+–K+–2Cl cotransporter 1; TMEM16A; smooth muscle; fetal undernutrition programming; cross-fostering; lactation period; cardiovascular hypertrophy; adipose tissue browning; hypertension; left ventricular hypertrophy; renin–angiotensin–aldosterone system; cardiovascular disease; catecholamines; liquid chromatography–tandem mass spectrometry; SGLT-2 inhibition; proteinuria; uninephrectomized salt-loaded; two-kidney; one-clip hypertension; fawn-hooded hypertensive rat; ApoE KO; apolipoprotein E knockout mice; atherosclerosis; hypertension; Na,K-ATPase; TCTP; TCTP-overexpressing transgenic mice; translationally controlled tumor protein; TCTP-TG; angiotensin II; experimental hypertension; bone; rats; taurine; magnesium; 24 h urine(24U); stroke-prone spontaneously hypertensive rat; young SHR; old SHR; antihypertensive therapy; combination therapy; treatment effect; systolic blood pressure; LV hypertrophy; cardiac fibrosis