## Long-Term Blood Pressure Regulation via Hormones Long-term blood pressure regulation (hours to days) depends on fluid volume and electrolyte balance, which are controlled by hormonal systems acting on the kidneys and blood vessels. ### Hormones That INCREASE Blood Pressure **Key Point:** Three major hormonal systems increase blood pressure: 1. **Renin-Angiotensin-Aldosterone System (RAAS)** - Angiotensin II: vasoconstriction + ↑ sympathetic activity + ↑ ADH release - Aldosterone: ↑ Na^+^ and H~2~O reabsorption → ↑ blood volume 2. **Antidiuretic Hormone (ADH/Vasopressin)** - ↑ Water reabsorption in collecting duct → ↑ blood volume - Direct vasoconstriction at high concentrations (V1 receptors) 3. **Sympathetic Nervous System** - ↑ Catecholamines (epinephrine, norepinephrine) - ↑ HR, contractility, vasoconstriction ### The Exception: Atrial Natriuretic Peptide (ANP) **High-Yield:** ANP is the **only major hormone that DECREASES blood pressure**: - Released by atrial myocytes in response to ↑ atrial stretch (high blood volume/pressure) - **Mechanisms of action:** - ↑ GFR (dilates afferent arteriole, constricts efferent arteriole) - ↑ Sodium and water excretion (inhibits Na^+^ reabsorption in collecting duct) - Inhibits renin and aldosterone release - Causes vasodilation - **Net effect:** ↓ Blood volume and ↓ Blood pressure **Warning:** ANP is a **pressure-lowering** hormone, not a pressure-raising hormone. The question asks which does NOT contribute to increasing blood pressure — ANP is the answer because it does the opposite. ### Comparison Table: Hormonal Effects on Blood Pressure | Hormone | Primary Site of Action | Effect on BP | Mechanism | | --- | --- | --- | --- | | Angiotensin II | Vessels, adrenal, kidney | ↑ BP | Vasoconstriction, Na^+^ reabsorption, ↑ ADH | | Aldosterone | Collecting duct | ↑ BP | ↑ Na^+^ and H~2~O reabsorption | | ADH/Vasopressin | Collecting duct, vessels | ↑ BP | ↑ H~2~O reabsorption, vasoconstriction | | ANP | Kidney, vessels | ↓ BP | ↑ Na^+^ and H~2~O excretion, vasodilation, ↓ RAAS | **Clinical Pearl:** ANP is released when blood pressure is too high. It acts as a natural "brake" on the RAAS and sympathetic nervous system. Patients with heart failure have elevated ANP levels, but the kidney becomes resistant to ANP (ANP resistance), contributing to fluid retention and hypertension.
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