💡 Atrial Natriuretic Peptide (ANP): A peptide hormone that acts as a vasodilator 🫀, diuretic 💧, and natriuretic (Na⁺-excreting) agent.
It suppresses sympathetic tone and the RAAS, playing a key role in blood pressure and fluid balance regulation.
📍 About
- Source: Secreted mainly by atrial myocytes (RA > LA) in response to stretch/↑ blood volume. Ventricles contribute in severe overload (HF).
- Structure: 28-amino acid peptide, acts via ↑ intracellular cGMP.
- Degradation: Broken down by neutral endopeptidases.
⚙️ Effects
- Renal:
- ↑ GFR by dilating afferent & constricting efferent arterioles.
- ↓ Na⁺ reabsorption (via ENaC inhibition in distal nephron).
- ↑ Diuresis + natriuresis → ↓ circulating volume.
- Vascular: Potent vasodilation → ↓ systemic vascular resistance & BP.
- Systemic: Suppresses sympathetic activity + RAAS. Regulates Na⁺, K⁺, fluid & adipose metabolism.
🧬 Mechanism of Action
- ANP binds to natriuretic peptide receptor-A (NPR-A).
- Activates guanylyl cyclase → ↑ cGMP →
- Relaxed vascular smooth muscle.
- Inhibition of Na⁺ reabsorption in renal tubules.
- ↓ Aldosterone secretion (adrenal cortex).
🩺 Clinical Relevance
- Elevated ANP: Seen in hypervolemia → Heart Failure ❤️, CKD, Liver Cirrhosis (ascites).
- Marker: ANP & BNP are used as biomarkers of HF severity & fluid overload.
- Exam Pearl: BNP is more commonly measured, but both rise in HF → helpful in dyspnoea differentials.
💊 Uses
- ANP analogues/related drugs under study for:
- Acute decompensated heart failure.
- Refractory hypertension.
- Renal disorders with volume overload.
📝 References