Excretion

• Mechanisms of Medullary Hyperosmolarity:
• The renal medullary osmotic gradient ($300\text{ up to }1200\text{ mOsm/kg}$) is established and maintained by:
• Active NaCl reabsorption by the thick ascending limb of Henle's loop into the medullary interstitium.
• Recirculation and medullary trapping of urea from inner medullary collecting ducts via UT-A1/UT-A3 transporters.
• Sluggish medullary blood flow through the hairpin vasa recta (countercurrent exchangers) preventing solute washout.
• Calcium Exclusion: Medullary $Ca^{2+}$ concentration plays NO role in generating the hyperosmotic gradient [Option 4].

Correct option: (4) Increased medullary Ca?*

• Insulin-Dependent Glucose Transporter: Insulin specifically promotes the exocytotic translocation and cell-surface expression of GLUT4 (Glucose Transporter Type 4).
• Target Tissues: Resides in intracellular tubulovesicular endosomes in skeletal muscle, cardiac muscle, and adipose tissue. Binding of insulin to its tyrosine kinase receptor triggers IRS-1/PI3K/Akt activation, mobilizing GLUT4 vesicles to the plasma membrane to facilitate glucose uptake.

Correct option: (3) GLUT4

• Pancreatic Receptor Ligands: Cholecystokinin (CCK), Secretin, and Acetylcholine are natural physiological ligands binding specific acinar cell receptors to stimulate pancreatic enzyme and fluid secretion. Gastrin is not a primary natural regulatory ligand for pancreatic acinar secretion [Option 2].

Correct option: (2) Gastrin