Released by stretched myocardium; they oppose the renin-angiotensin system
Mnemonic
“Stretch releases them, and they undo what the renin system does”:
- ANP from the atria, BNP from the ventricles, both released by wall stretch
- Effects: natriuresis and diuresis, vasodilatation, inhibition of renin, aldosterone and ADH
They are therefore the body’s own counter-regulation to the renin-angiotensin-aldosterone system, which is the basis of sacubitril, a neprilysin inhibitor that prevents their breakdown.
Clinical use is as a rule out test in heart failure, because of the high negative predictive value: a normal BNP or NT-proBNP makes heart failure very unlikely.
Raised without heart failure: age, female sex, renal impairment, atrial fibrillation, sepsis, pulmonary embolism, right heart strain and left ventricular hypertrophy. Falsely low: obesity, and treatment with diuretics, ACE inhibitors and beta blockers.
Expansion
- Atrial natriuretic peptide (ANP) - from atrial myocytes, in response to atrial stretch
- B-type natriuretic peptide (BNP) - from ventricular myocytes, in response to ventricular stretch and wall stress
Actions, all opposing volume overload:
- Natriuresis and diuresis
- Vasodilatation, arterial and venous
- Inhibition of renin, aldosterone and antidiuretic hormone
- Increased glomerular filtration, by dilating the afferent and constricting the efferent arteriole
- Increased capillary permeability, shifting fluid out of the circulation
BNP and its inactive fragment NT-proBNP are used clinically: a normal value has a high negative predictive value and effectively excludes heart failure as the cause of breathlessness.
Levels rise with age and renal impairment, and are lowered by obesity, which must be allowed for when interpreting them.