As shown in this diagram, increased blood osmolarity stimulates hypothalamic osmoreceptors. What happens next? (What goes in the yellow box?)

A. Glomerular filtration rate will increase: Vasoconstriction of the efferent arteriole increases resistance, raising glomerular pressure and increasing GFR.
B. Urine output will increase: Increased GFR results in more filtrate, which can lead to increased urine output.
C. Systemic blood pressure will go up: This is unlikely to be directly caused by local vasoconstriction of the efferent arteriole. Systemic BP is mainly influenced by overall vascular resistance and cardiac output.
D. Net filtration pressure will increase: Efferent arteriole constriction backs up pressure in the glomerulus, increasing net filtration pressure.

A. Posterior pituitary releases ADH: Dehydration increases blood osmolarity. This is sensed by hypothalamic osmoreceptors. In response, the hypothalamus signals the posterior pituitary to release antidiuretic hormone (ADH). ADH then acts on the distal convoluted tubules and collecting ducts of the kidney to promote water reabsorption, thereby concentrating the urine and reducing blood osmolarity.

B. Adrenal medulla releases aldosterone: Aldosterone is released from the adrenal cortex, not medulla, and is more responsive to low sodium or high potassium, not directly to osmolarity.

C. Kidneys release erythropoietin: Erythropoietin is released in response to hypoxia, not dehydration or osmolarity.

D. Anterior pituitary releases oxytocin: Oxytocin is released by the posterior pituitary, and it is not involved in osmolarity or water balance.

E. Adrenal cortex releases norepinephrine: Norepinephrine is released by the adrenal medulla, and is involved in fight-or-flight, not osmolarity regulation.