Activation of the angiotensin II (AT₁) receptor causes which of the following: vasodilation, cellular growth, aldosterone secretion, or catecholamine release?

Angiotensin II AT₁ Receptor Activation Effects

Activation of the angiotensin II type 1 (AT₁) receptor leads to aldosterone secretion, cellular growth, and catecholamine release—but causes vasoconstriction, not vasodilation. 1

Multiple Physiological Effects of AT₁ Receptor Activation

Aldosterone Secretion

• AT₁ receptor activation directly stimulates aldosterone synthesis and release from the adrenal zona glomerulosa. 1
• The American Heart Association guidelines explicitly state that angiotensin II has "direct effects on aldosterone synthesis and release" through AT₁ receptor activation. 1
• Research confirms that AT₁ receptors, not AT₂ receptors, are the predominant mediators of aldosterone secretion in adrenocortical cells. 2, 3
• AT₁ receptor antagonists (ARBs) completely suppress angiotensin II-stimulated aldosterone secretion, while AT₂ receptor antagonists have no effect on this pathway. 2

Cellular Growth and Hypertrophy

• Angiotensin II promotes cardiac and vascular smooth muscle cell hypertrophy directly via AT₁ receptor activation. 1
• The growth-promoting effects occur through stimulation of multiple growth factors including platelet-derived growth factor, basic fibroblast growth factor, insulin-like growth factor-1, and transforming growth factor-β. 1
• AT₁ receptors mediate DNA synthesis and cell proliferation in adrenocortical cells, with complete suppression by AT₁ antagonists but no effect from AT₂ antagonists. 2

Catecholamine Release

• AT₁ receptor activation facilitates catecholamine release from both the adrenal medulla and peripheral sympathetic nerve terminals. 1
• The American Heart Association guidelines specify that angiotensin II enhances "sympathetic outflow from the brain" and facilitates "catecholamine release from the adrenals and peripheral sympathetic nerve terminals." 1
• AT₂ receptors may also contribute to catecholamine release in intact adrenal tissue, which then potentiates aldosterone secretion through β-adrenoceptor activation in a paracrine manner. 4

Vasoconstriction (NOT Vasodilation)

• AT₁ receptor activation causes potent vasoconstriction, particularly of the efferent arteriole in the kidney, not vasodilation. 5
• The vasoconstrictor effects are mediated through AT₁ receptors expressed in afferent and efferent arterioles, glomeruli, and proximal tubules. 5
• This is a critical distinction: angiotensin II causes constriction and remodeling of resistance vessels through AT₁ receptors. 1

Clinical Implications

Therapeutic Targeting

• ACE inhibitors and ARBs block AT₁ receptor-mediated effects, providing vasoprotective benefits beyond blood pressure lowering by preventing aldosterone secretion, cellular hypertrophy, and excessive catecholamine release. 1
• These medications cause efferent arteriolar vasodilation by blocking the vasoconstrictor effects of angiotensin II on AT₁ receptors. 5

Common Pitfall

• Do not confuse AT₁ receptor effects with vasodilation—this is incorrect. AT₁ activation causes vasoconstriction, while AT₂ receptor activation (a different receptor subtype) may mediate vasodilatory effects. 1