Deoxycorticosterone acetate (DOCA) is a steroid hormone produced by the adrenal gland that possesses mineralocorticoid activity and acts as a precursor to aldosterone. Myocardial stiffness was increased and left ventricular compliance significantly diminished in the DOCA control group, and these changes were attenuated by epicatechin treatment[3]. The systolic blood pressure of non-treated 6-week-old Sprague-Dawley strain rats was gradually increased by DOCA-salt treatment from 137±2 mmHg to 195±7 mmHg at 10 weeks of age[4]. DOCA-escape in the rat is associated with specific alteration of sodium transport in the collecting duct system[5].
Deoxycorticosterone Acetate/乙酸去氧皮质酮 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
DOCA-salt hypertension model
Subcutaneous implantation
50 mg
Single implantation, lasting 21 days
To evaluate the relative contributions of the mitochondrial respiratory chain and NADPH oxidase in DOCA-salt hypertension. Results showed that mitochondrial respiratory chain inhibitors (e.g., rotenone) significantly lowered blood pressure, while NADPH oxidase-deficient mice exhibited only partial blood pressure reduction in the early stages of hypertension.
Kidney Int. 2011 Jul;80(1):51-60
Sprague-Dawley rats
DOCA-salt hypertension model
Subcutaneous injection
10 mg/kg
Twice a week for 2 weeks
DOCA-salt treatment significantly increased the mean blood pressure in rats, and inhibition of CPY-like kininase partially prevented the development of hypertension.
Br J Pharmacol. 2000 Oct;131(4):820-6
Mice
DOCA/HS model
Subcutaneous implantation
150 mg
Daily 1% NaCl in drinking water
To investigate the effect of intrarenal dopamine on the development of hypertension in the DOCA/HS model. Results showed that the blood pressure elevation was significantly attenuated in COMT ?/? mice, with increased urinary sodium excretion and significantly reduced renal oxidative stress.
Hypertension. 2009 Nov;54(5):1077-83
C57BL/6J mice
DOCA-salt hypertension model
Subcutaneous implantation
50 mg
21 days
To investigate the effects of DOCA-salt on metabolic rate, results showed that DOCA-salt treatment caused a significant increase (20%) in basal metabolic rate, independent of blood pressure elevation.
Hypertension. 2011 Mar;57(3):600-7
Sprague-Dawley rats and C57BL/6 mice
DOCA/salt-induced hypertension model
Subcutaneous implantation
150 mg/rat or 50 mg/mouse
3 weeks
To investigate the role of ELA in DOCA/salt-induced hypertension and renal injury. Results showed that ELA overexpression significantly reduced blood pressure, improved glomerular morphological damage, decreased serum blood urea nitrogen (BUN), and blocked the accumulation of fibrotic markers. Additionally, ELA inhibited renal NADPH oxidase activity and subsequent ROS production, thereby blocking the formation and activation of NLRP3 inflammasome.
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