All of the following hormones contribute to long-term blood pressure regulation EXCEPT:
A. Aldosterone increases blood pressure by promoting sodium and water reabsorption in the collecting duct
B. Antidiuretic hormone (ADH/vasopressin) increases blood pressure by promoting water reabsorption and vasoconstriction
C. Atrial natriuretic peptide (ANP) increases blood pressure by promoting sodium and water excretion
D. Angiotensin II increases blood pressure by promoting vasoconstriction and sodium reabsorption
Explanation
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:
Aldosterone: ↑ Na+ and H2O 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-YieldNEET PG
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
Table
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 H2O reabsorption
ADH/Vasopressin
Collecting duct, vessels
↑ BP
↑ H2O reabsorption, vasoconstriction
ANP
Kidney, vessels
↓ BP
↑ Na+ and H2O 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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