BNP, ANP and troponin release from stretched or damaged heart muscle
Stretched heart muscle cells with intact membranes release natriuretic peptides (hormones that promote loss of salt and water), whereas damaged cells leak troponin (a protein that helps regulate contraction).
Remember
Stretched cells with intact membranes secrete natriuretic peptides: brain natriuretic peptide (BNP) from the ventricles and atrial natriuretic peptide (ANP) from the atria, while damaged cells leak troponin.
Memory aid
torn cells leak troponin, stretched cells secrete natriuretic peptides
Cells that are torn leak troponin, whereas cells that are only stretched secrete natriuretic peptides.
Cardiac muscle cells release chemicals depending on their state, whether stretched or damaged.
When heart muscle cells are stretched, but their cell membrane (the sarcolemma) is still intact, as in heart failure, they release natriuretic peptides. These hormones promote loss of salt and water in the urine and widen blood vessels. They lower blood volume and vascular resistance (the resistance the heart pumps against), which takes some of the stretch off the heart.
The peptides are split by chamber. When the atria are stretched, as in mitral valve stenosis (a narrowing of the mitral valve), atrial natriuretic peptide (ANP) is released. When the ventricles are stretched, as in heart failure, brain natriuretic peptide (BNP) is released. The name is a misnomer: BNP was first isolated in brain tissue, but it is released from the ventricular wall. BNP, or NT-proBNP (a longer-lived fragment of the same precursor, the molecule that both are made from), is raised in heart failure and helps in assessing it.
In a heart attack, ischaemia (a shortage of blood supply) damages cardiac muscle cells, and they leak troponin, a protein that helps regulate contraction. A troponin blood test is used to detect damage to the heart muscle.
Key facts
- Stretch with intact membrane
- Stretched cardiac muscle cells with an intact cell membrane (sarcolemma) release natriuretic peptides, as in heart failure.
- Atrial stretch
- Stretched atria release atrial natriuretic peptide (ANP), as in mitral valve stenosis.
- Ventricular stretch
- Stretched ventricles release brain natriuretic peptide (BNP), as in heart failure.
- Damage
- Damaged cardiac muscle cells, for example in a heart attack, leak troponin, so a troponin blood test is used to detect damage to the heart muscle.
- Other injury markers
- Creatine kinase MB, an enzyme inside muscle cells, and myoglobin, an oxygen-carrying protein of muscle cells, enter the blood after injury and mark damage rather than stretch.
- Clinical use
- BNP, or NT-proBNP (a longer-lived fragment of the same precursor, the molecule that both are made from), is raised in heart failure and helps in assessing it.
Exam traps
- Troponin is not the molecule of the stretch response of heart muscle: it leaks into the blood when cardiac muscle cells are damaged, for example in a heart attack.
- ANP is not the peptide of stretched ventricles, as in heart failure: it is released when the atria are stretched, as in mitral valve stenosis, but the ventricles release BNP.
- BNP is also released when heart muscle is stretched, but it is tied to ventricular stretch, as in heart failure, so stretch of the atria, as in mitral valve stenosis, releases ANP instead.
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