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. 2021 Aug 20;12:734917. doi: 10.3389/fphar.2021.734917

TABLE 3.

Studies of effect of angiotensin II in in-vivo and in-vitro studies.

Model Dose, Route, Duration of Ang II Result Limitations Ref.
Sprague-Dawley rats and cardiomyocytes 20 μM, 2 h Short-term treatment with Ang II attenuates the transversal YM in isolated adult rat cardiomyocytes acting via an AT1 R High sample indentation in direct contact mode or lack of selectivity or that makes it difficult to assess the sample–probe interaction Swiatlowska et al. (2020)
Long exposure time to high-intensity light affecting cell enzymatic reactions, difficulty in manufacturing instruments, time-consuming measurements
C57BL/6J mice & Primary cardiomyocytes from C57BL/6J mice 2.5 mg/kg/day, s.c., 2 weeks. 100 nM, 24 h Administration of Ang II increases the expression of miR-154-5p and cardiac remodeling concurrently. miR-154-5p interacts with 3′ UTR and inhibits arylsulfatase B to trigger cardiomyocyte apoptosis and hypertrophy associated with oxidative stress The hypothesis of miR-154-5p promoting hypertrophy needs further testing in the near future Wang Q. et al. (2019)
HEK293T, HEK293-AT1R, and HEK293T-SIN1−/− cells 200 nM SGK1 activation occurs at a distinct subcellular compartment from that of Akt The use of SIN1 and SGK1 overexpression since overexpression of these proteins might influence their subcellular localization. Gleason et al. (2019)
ApoE−/− mice 750 µg/kg/day, s. c. Ang II increases the expression of EMMPRIN in atherosclerotic plaque Further research is required to elucidate details of the mechanism involved Zhang Y. et al. (2019)
Amniotic fluid mesenchymal stem cells 0.1 and 1 μM Ang II and TGF-β1 are efficient cardiomyogenic inducers of human AF-MSCs; They initiate protein expression, alterations at the gene and epigenetic levels in stem cells leading towards cardiomyocyte-like phenotype formation. Gasiūnienė et al. (2019)
Male silent information regulator 1 (SIRT1) flox/flox and cardiomyocyte-specific inducible SIRT1 knockout mice (SIRT1-iKO) 1.1 mg/kg/day for 4 weeks FGF21 improves cardiac function and alleviates Ang II-induced cardiac hypertrophy in a SIRT1-dependent manner Presence of a small number of animals in a group Li et al. (2019)
CRFK cells (feline kidney epithelial cell line) - Ang II shows a similar result to TGF-β1 if the AT1 R was expressed more in CRFK cells The experiment could have involved other cells. van Beusekom and Zimmering, (2019)
C57BL/6J mice 1.5 μg/min/kg, s.c., 4 weeks Soluble receptors for advanced glycation end-products were evidenced to attenuate Ang II-induced LV hypertrophy using a 9.4T pre-clinical magnetic resonance imaging instrument Since they didn’t perform electrocardiography, they were unable to confirm the superiority of MRI in assessing cardiac remodeling Gao Q. et al. (2020)
Thromboxane A2 (TP) knockout (Tp−/−) mice 1,000 ng/kg/min, s.c., 28 days TP receptors may contribute to cardiac hypertrophy but not, proteinuria and are responsible for thepathogenesis of Ang II induced hypertension and hypertrophy As thromboxane production was not analyzed in Cox1−/− mice, they were unable to assure the reduction caused by TXA2 Heo et al. (2019)
Sprague-Dawley rats 200 ng/kg/min, micro-infusion Ghrelin inhibited Ang II-induced cardiac fibrosisin a PPAR-dependent manner The study was performed on young male rats which restricts the extrapolation of results for females and older cohorts. Zhong et al. (2018)
Also, the age and sex-mediated effects of ghrelin need to be explored.
Rat tubular epithelial cell line NRK52E 1 mM for 0–24 h Inhibition of HMGB1 and gene silencing of TLR4 decreases Ang II-mediated inflammation in the kidney Future in-vivo studies will be required for elucidating the role of TLR4 signaling in Ang II-induced renal injury on the AT1 R knock out model Nair et al. (2015)
The existence of HMGB1-TLR4 signaling is a development of hypertensive renal injury
Mouse Neuro-2a cells - Involvement of HMGB1 in the PVN for development of Ang II-induced hypertension Further research depicting the involvement of Mas will be necessary Nair and Philips, (2015)
Sprague-Dawley rats 120 ng/kg/min, s.c.,2 weeks Activation of brain RAS and PPAR-γ to reduce central inflammation may be used as a strategy in the management of Ang II-induced hypertension Studies need to be performed to evaluate the relative role of individual types of cell Yu et al. (2015)
Sprague-Dawley rats 100 ng/kg, i. c. v., before and after a 1 h ICV infusion of inhibitor Role of brain p44/42 MAPK signaling cascade in the maintenance of renal sympathetic excitation in HF rats. They evaluated the involvement of p44/42 MAPK signaling in the brain containing presympathetic neurons of PVN neurons only and did not evidence the contribution of p44/42 MAPK signaling in other nuclei of brain-like RVLM or other neurons in cardiovascular and autonomic centers, including organum vasculosum of the lamina terminalis, median preoptic nucleus, and the subfornical organ. Shinohara et al. (2015)
Alteration in brain p44/42 MAPK can increase adverse effects of brain RAS on renal and cardiovascular functions during HF progression.
Attenuation in Fra-LI–positive PVN neurons in p44/42 MAPK inhibitors treated rats suffering from HF.
Sprague-Dawley rats 800 ng/kg/min, s.c., 1 week Association of NO-mediated mechanisms with presence of female sex hormones to be protective against sympathetically mediated Ang II-induced hypertension in female mice - Wattanapitayakul et al. (2000)