In respiratory acidosis, the equation (CO2 + H2O↔ H2CO3 ↔ HCO3- +H+) shifts to the right because CO: retention increases H2CO3 levels, leading to more H production and a lower pH.

A. PTH, calcitriol, and calcitonin: Parathyroid hormone raises serum calcium, while calcitriol (active Vitamin D) increases intestinal absorption. Calcitonin serves as a minor antagonist to PTH by promoting bone deposition. Together, they regulate the flux of ions between bone, gut, and kidneys.

B. Thyroxine, epinephrine, and norepinephrine: These hormones regulate basal metabolic rate and the sympathetic "fight or flight" response. While they influence overall physiology, they do not possess specific receptors or mechanisms for mineral homeostasis. They do not directly control calcium or phosphate concentrations.

C. Estrogen, testosterone, and aldosterone: Sex steroids influence bone density over time, but they do not provide the acute regulation of mineral balance. Aldosterone is strictly a regulator of sodium and potassium. They lack the rapid feedback loops required to maintain ionized calcium levels.

D. Insulin, glucagon, and cortisol: These hormones are primarily involved in the regulation of carbohydrate, lipid, and protein metabolism. Cortisol can lead to bone loss in chronic excess, but it is not a primary homeostatic regulator. They do not manage the day-to-day phosphate balance.

True: Sodium is the primary extracellular cation, while chloride is the major extracellular anion, maintaining osmotic balance outside the cell. Active transport by the sodium-potassium pump ensures these ions remain at low concentrations within the cytoplasm. This distribution is critical for cellular hydration and electrical signaling.