Which hormone causes vasoconstriction and stimulates aldosterone release, raising blood pressure?

Which hormone causes vasoconstriction and stimulates aldosterone release, raising blood pressure?

• A. Angiotensin II
• B. Atrial natriuretic peptide
• C. Antidiuretic hormone
• D. Cortisol

Answer: (A)

The main concept here is how a hormone system raises blood pressure by both narrowing vessels and increasing fluid volume. Angiotensin II fits best because it does two key things: it directly constricts small arteries, raising systemic vascular resistance, and it stimulates the adrenal cortex to release aldosterone. Aldosterone then promotes sodium (and water) reabsorption in the kidneys, increasing blood volume and further elevating blood pressure. This duo—vasoconstriction plus aldosterone-driven volume expansion—drives the BP rise described. Understanding the pathway helps: when blood pressure or sodium delivery to the kidneys falls, renin is released and converts angiotensinogen to Angiotensin I. Angiotensin-converting enzyme transforms that into Angiotensin II, which acts on blood vessels to constrict them and on the adrenal glands to boost aldosterone production. The increased aldosterone makes the kidneys reclaim more sodium, with water following, so blood volume goes up. Other options don’t fit both actions. Atrial natriuretic peptide causes vasodilation and promotes sodium loss, which lowers BP rather than raises it. Antidiuretic hormone mainly promotes water retention (and can cause some vasoconstriction at high levels) but does not stimulate aldosterone release. Cortisol has broad metabolic effects and limited mineralocorticoid action, not the targeted combination described.

The main concept here is how a hormone system raises blood pressure by both narrowing vessels and increasing fluid volume. Angiotensin II fits best because it does two key things: it directly constricts small arteries, raising systemic vascular resistance, and it stimulates the adrenal cortex to release aldosterone. Aldosterone then promotes sodium (and water) reabsorption in the kidneys, increasing blood volume and further elevating blood pressure. This duo—vasoconstriction plus aldosterone-driven volume expansion—drives the BP rise described.

Understanding the pathway helps: when blood pressure or sodium delivery to the kidneys falls, renin is released and converts angiotensinogen to Angiotensin I. Angiotensin-converting enzyme transforms that into Angiotensin II, which acts on blood vessels to constrict them and on the adrenal glands to boost aldosterone production. The increased aldosterone makes the kidneys reclaim more sodium, with water following, so blood volume goes up.

Other options don’t fit both actions. Atrial natriuretic peptide causes vasodilation and promotes sodium loss, which lowers BP rather than raises it. Antidiuretic hormone mainly promotes water retention (and can cause some vasoconstriction at high levels) but does not stimulate aldosterone release. Cortisol has broad metabolic effects and limited mineralocorticoid action, not the targeted combination described.