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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; 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; angiotensin II; angiotensin 1-7; knock-out; genome-editing; SHRSP; Dahl SS; foetal programming of hypertension; sympathetic neurotransmission; sympathetic innervation; vascular remodelling; 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; rostral ventrolateral medulla; aging; reactive oxygen species; NADPH oxidase activator 1; mitochondria; chloride; calcium-activated chloride channel; Na+–K+–2Cl− cotransporter 1; TMEM16A; smooth muscle; fetal undernutrition programming; cross-fostering; lactation period; cardiovascular hypertrophy; adipose tissue browning; 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; Na,K-ATPase; TCTP; TCTP-overexpressing transgenic mice; translationally controlled tumor protein; TCTP-TG; experimental hypertension; bone; rats; taurine; magnesium; 24 h urine(24U); stroke-prone spontaneously hypertensive rat; young SHR; combination therapy; treatment effect; systolic blood pressure