| | Experimental model | Description |
| Genetic hypertension
(i) SHR
(ii) Dahl salt-sensitive
(iii) Transgenic | (i) SHR is developed by inbreeding Wistar rats (brother-to-sister) with the highest BP [28]. The BP increases at week 4 to week 6 and reach systolic BP of 180–200 mmHg [28]. SHR may develop cardiac hypertrophy, cardiac failure, renal dysfunction, and impaired endothelium-dependent relaxations [60–62].
(ii) Dahl salt-sensitive rats derived from Sprague-Dawley rats on the basis of administering high NaCl diet. Salt-sensitive rats become hypertensive when given normal salt diets; however these rats develop severe and fatal hypertension with high salt diet (8% NaCl) [32]. These rats may develop cardiac hypertrophy, severe cardiac failure, hypertensive nephropathy, impaired endothelium-dependent relaxations [63–65].
(iii) Transgenic model can be generated by overexpression of a specific gene, for example, the mouse Ren-2 gene, and TGR(mREN2)27 [66]. Manifestations include marked cardiac hypertrophy, moderate proteinuria, and impaired endothelium-dependent relaxations [67, 68]. |
| | Endocrine hypertension | (i) Administration of DOCA in a combination with high salt diet and unilateral nephrectomy [69].
(ii) DOCA-induced hypertension induces a low renin model of hypertension [70].
(iii) Increased cardiac weight, proteinuria, glomerulosclerosis, and impaired endothelium-dependent relaxations [71, 72]. |
| | Environmental hypertension | (i) Stress-induced hypertension using flashing lights, loud noise, restraint cage, and cold or hot stimuli [73, 74].
(ii) Activation of sympathetic nervous system and RAAS may contribute to the initiation of stress-induced hypertension [75, 76]. |
| | Pharmacological hypertension | (i) Nitric oxide-deficient model by administering NOS inhibitors such as L-NAME [77].
(ii) Increase in BP was reported during long-term oral treatment with NOS inhibitors [78, 79].
(iii) Development of endothelial dysfunction is gradually with increased of BP [80]. |
| | Renal hypertension | (i) This includes two-kidney one-clip hypertension (2K1C; constriction of one renal artery while the contralateral kidney is left intact), one-kidney one-clip hypertension (1K1C; one renal artery is constricted and the contralateral kidney is removed), and two-kidney two-clip hypertension (2K2C; constriction of aorta or both renal arteries) [81, 82].
(ii) In the two-kidney model, circulating renin and aldosterone levels are increased [83], which are most notably in the early phase of hypertension [84]. |
|
|
