Renin secretion is increased by

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: 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.

Correct Answer: D

Rationale: T4 increases cardiovascular β-receptors, enhancing catecholamine sensitivity metabolic/cardiac boost. It's regulated by negative feedback (TSH, TRH). Most T4 binds TBG (~70%), not albumin (~10%). T4 lowers LDL by increasing clearance, not raising it. β-receptor increase distinguishes T4's action, critical for heart response, unlike feedback, transport, or lipid errors.

Correct Answer: D

Rationale: Hormones regulate internal environment (e.g., ADH for water), metabolism (e.g., thyroxine), glandular secretions (e.g., TSH), and growth (e.g., GH), but they don't produce electrolytes ions like sodium or potassium are managed by kidneys or diet, not synthesized by hormones. 'Produces electrolytes' is incorrect as hormones modulate existing substances, not create them. This distinction highlights hormones' role as signaling molecules, not producers of biochemical raw materials, critical for understanding endocrine specificity versus metabolic processes.

Correct Answer: A

Rationale: Luteinizing hormone (LH) from the anterior pituitary triggers gonadal secretion of progesterone (ovaries) and testosterone (testes), not TSH (thyroid), corticotropin (adrenals), MSH, or GH. LH's reproductive role distinguishes it, essential for sex hormone cycles, contrasting with metabolic or pigment regulators.