Target cells for hypothalamic releasing hormones are in the

Correct Answer: C

Rationale: Hypothalamic releasing hormones (e.g., TRH, GnRH) target anterior pituitary cells, stimulating hormone release (e.g., TSH, FSH). Thyroid responds to TSH, hypothalamus produces, posterior pituitary stores ADH/oxytocin. Anterior pituitary targeting distinguishes this axis, vital for endocrine regulation, contrasting with storage or effector glands.

Correct Answer: D

Rationale: The pituitary gland, dubbed the 'master gland,' controls other endocrine glands (e.g., thyroid via TSH, adrenals via ACTH) through tropic hormones. Thyroid regulates metabolism, pineal sleep, adrenals stress not others. Pituitary's anterior/posterior lobes orchestrate this, distinguishing its hierarchical role, vital for endocrine harmony, contrasting with effector glands.

Correct Answer: C

Rationale: Prostaglandins (e.g., PGE2) increase renin secretion from juxtaglomerular cells, boosting RAAS during inflammation or low perfusion. High Na/Cl at macula densa or high arteriole pressure (stretch) suppress renin negative feedback signals adequacy. ADH conserves water, not directly affecting renin. Prostaglandins' stimulatory role distinguishes them, critical for RAAS activation in stress, unlike inhibitory or unrelated factors.

Correct Answer: A

Rationale: Glucagon raises glucose via glycogenolysis without increasing lactate gluconeogenesis (lactate source) is secondary. Insulin uses GLUT2 in liver, not GLUT4 (muscle/adipose). Cortisol boosts gluconeogenesis, not glycogenolysis primarily. Glucagon stimulates insulin short-term, not inhibits. Glucagon's lactate-free glucose rise distinguishes it, key to its hepatic action, unlike transporter, cortisol, or insulin errors.

Correct Answer: A

Rationale: α-adrenergic stimulation (e.g., norepinephrine) inhibits insulin secretion via α2-receptors, reducing glucose uptake in stress. Theophylline enhances insulin by increasing cAMP, not inhibits. Insulin's half-life is ~5-10 minutes, not 30. Somatostatin inhibits insulin, not stimulates. α-adrenergic inhibition distinguishes it, key to sympathetic-glucose balance, unlike cAMP, kinetics, or somatostatin errors.