In the absence of ADH, aquaporin channels are still inserted in the DCT and collecting ducts.

A. It promotes ADH release: Alcohol acts as a pharmacological inhibitor of antidiuretic hormone secretion from the posterior pituitary. Promoting ADH would result in water retention and concentrated urine, which is the opposite of the diuresis observed after ethanol consumption. It would decrease free water clearance.

B. It causes vasodilation in afferent arterioles: Ethanol has direct and indirect vasodilatory effects on the renal microvasculature. By reducing the resistance of the afferent arteriole, it increases the glomerular hydrostatic pressure. This hemodynamic shift directly elevates the rate of filtrate production across the glomerulus.

C. It inhibits aldosterone secretion: While alcohol can interfere with various hormonal axes, its primary acute effect on urine volume is not mediated by aldosterone inhibition. Aldosterone primarily regulates long-term sodium and potassium balance. The immediate increase in GFR is driven by hemodynamic changes.

D. It inhibits ADH release, reducing water reabsorption: This statement describes the mechanism for increased urine volume (polyuria), but it does not explain an increase in the filtration rate itself. ADH inhibition affects the collecting duct's permeability. GFR is an upstream process determined by glomerular pressures.

B. False: The insertion of aquaporin-2 channels into the apical membrane is strictly dependent on the presence of antidiuretic hormone. Without this hormonal signal, the channels are internalized into endosomes, making the membrane impermeable to water. This allows for the excretion of large volumes of dilute urine.