In the kidney filtration experiment, the results suggest that cells, proteins, and large molecules were too large to diffuse through the semi-permeable membrane.

A. Aldosterone: This steroid hormone primarily stimulates the reabsorption of sodium and the secretion of potassium in the distal tubule. While water follows sodium osmotically, aldosterone does not directly regulate the water permeability of the collecting duct. Its primary target is the monovalent cation.

B. Antidiuretic hormone (ADH): Also known as vasopressin, this peptide binds to V2 receptors on principal cells to induce the apical insertion of aquaporin-2 channels. This directly increases the water permeability of the collecting ducts. It is the most potent regulator of free water recovery.

C. Atrial natriuretic peptide (ANP): This hormone is secreted by the atria in response to high blood volume and functions as a diuretic. It inhibits sodium reabsorption and suppresses ADH release to increase urine output. It decreases water reabsorption to lower systemic blood pressure.

D. Cortisol: While glucocorticoids have some weak mineralocorticoid activity, their primary metabolic role is unrelated to the regulation of water channels in the kidney. Excessive cortisol can interfere with water balance, but it is not a physiological promoter of collecting duct water recovery.

B. False: Antidiuretic hormone is synthesized in the hypothalamus and released by the posterior pituitary gland. Its primary function is to decrease urine output by increasing water reabsorption in the renal collecting ducts. This process conserves systemic water and concentrates the final urine.