Abstract
The acute and prolonged diuretic effects of coconut water (CW) and the underlying mechanism were investigated with a saline-loaded rat model. In an acute diuretic experiment, CW could significantly increase urine excretion. In addition, the treatment of CW significantly increased urinary sodium and chloride ions, thereby considerably increasing the excretion of NaCl. However, the calcium concentration and pH value were not affected. In the prolonged diuretic experiment, CW dramatically increased the urine output and urine electrolyte concentrations (Na+, K+, and Cl–). Furthermore, CW could suppress the activation of renin–angiotensin–aldosterone system by decreasing serum antidiuretic hormone, angiotensin II, and aldosterone levels, and significantly increasing the serum atriopeptin level. CW treatment significantly reduced the mRNA expressions and protein levels of aquaporin 1 (AQP1), AQP2, and AQP 3. This report provided basic data for explaining the natural tropical beverage of CW as an alternative diuretic agent.
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