The heart releases a few different hormones that play important roles in regulating cardiovascular function. The main hormone released by the heart is called atrial natriuretic peptide (ANP). This hormone is secreted by cells in the atria (upper chambers) of the heart in response to high blood volume and pressure.
What is atrial natriuretic peptide (ANP)?
Atrial natriuretic peptide (ANP) is a hormone produced and secreted by heart muscle cells in the upper chambers (atria) of the heart. It was first discovered in 1981 by researchers studying rat hearts. They found that extracting fluid from rat atria caused a diuretic and blood pressure-lowering response when injected into rats, indicating a hormone was present. Further study isolated a 28 amino acid peptide as the active agent, which was named atrial natriuretic factor or ANF. The name was later changed to atrial natriuretic peptide.
In humans, ANP is secreted by heart muscle cells in the right atrium in response to high blood volume or pressure. Specific cells called cardiomyocytes contain storage granules of proANP, an inactive precursor form. When the atria are stretched due to increased blood volume, proANP is cleaved by an enzyme called corin to produce active ANP, which is then released into the bloodstream. ANP levels can also be increased by certain hormones like endothelin and angiotensin II.
Actions of ANP
Once released into circulation, ANP works systemically to counterbalance the effects of volume and pressure overload in the heart and blood vessels. Its main actions include:
- Promoting sodium and water excretion by the kidneys – ANP acts on kidney tubule cells to inhibit sodium reabsorption, leading to increased sodium and water excretion in the urine. This helps reduce blood volume and pressure.
- Vasodilation – ANP relaxes vascular smooth muscle cells, causing vasodilation to reduce blood pressure.
- Suppressing renin-angiotensin-aldosterone system (RAAS) – ANP inhibits renin release, thereby reducing production of angiotensin II and aldosterone. This system is normally activated to retain sodium and water.
- Inhibiting fibrosis – ANP appears to inhibit cardiac fibrosis and remodeling in response to high blood pressure and other cardiac insults.
Overall, the actions of ANP work together to promote sodium excretion, relax blood vessels, counter RAAS activation, and inhibit pathological cardiac remodeling – all effects that reduce blood volume and pressure. This forms a key hormonal system for regulating fluid balance and cardiovascular function.
Other Heart Hormones
In addition to ANP, a few other hormones are secreted directly by the heart that have regulatory effects on the cardiovascular system:
B-type Natriuretic Peptide (BNP)
Like ANP, BNP is produced and secreted by cardiomyocytes in the heart ventricles. BNP has a similar structure to ANP and exerts comparable effects on sodium excretion, vasodilation, and RAAS inhibition. BNP secretion is stimulated by ventricular stretch from pressure or volume overload. Plasma BNP levels are often measured clinically as an indicator of heart failure severity.
C-type Natriuretic Peptide (CNP)
CNP is the third and most widespread natriuretic peptide produced in the body. However, CNP is only produced in very small amounts by the heart. It acts locally as a paracrine regulator in the vascular system to cause vasodilation and inhibit cell growth. Plasma CNP levels do not change significantly in cardiovascular disease.
Neuregulin-1 (NRG-1)
NRG-1 is a growth factor secreted by microvascular endothelial cells in the heart. It acts on cardiomyocytes and stem cells to induce regeneration, growth, and survival mechanisms. NRG-1 may help limit cardiac cell death and improve recovery after ischemic injury or heart failure.
Adrenomedullin
Adrenomedullin is a vasoactive peptide produced in numerous tissues, including cardiomyocytes in the heart. Like ANP, it causes vasodilation, natriuresis, and RAAS inhibition. Adrenomedullin production is increased in certain heart conditions like hypertension, heart failure, and myocardial infarction.
Regulation of Heart Hormone Secretion
The major stimuli for heart hormone secretion are increased mechanical stretch and stress on the heart chambers and cells:
- Stretching of the atria stimulates ANP release
- Ventricular stretch increases BNP secretion
- Cellular stress and ischemia can elevate adrenomedullin levels
These increases in heart hormones form an important systemic response to reduce cardiac workload by decreasing blood volume, pressure, and RAAS activity. Heart hormones are also regulated by certain other factors:
- Angiotensin II and endothelin-1 stimulate ANP and BNP release
- Inflammatory cytokines like IL-1B and TNF-alpha increase ANP secretion
- Sympathetic nervous stimulation inhibits ANP release
Blood levels of ANP and BNP often correlate with severity of heart failure – higher levels are associated with greater ventricular dysfunction and poorer prognosis.
Summary of Key Points
- The main hormone secreted by the heart is atrial natriuretic peptide (ANP)
- ANP is produced by atrial muscle cells and released in response to high blood volume/pressure
- Actions of ANP: vasodilation, sodium excretion, suppresses RAAS, and inhibits cardiac fibrosis
- Other heart hormones: BNP, CNP, neuregulin-1, and adrenomedullin
- Major regulators of heart hormone secretion are mechanical stretch and cellular stress on the heart
Frequently Asked Questions
What stimulates ANP release from the heart?
The main stimulus for ANP release is stretching of the atrial walls due to increased blood volume and pressure. This causes the cardiomyocytes to deform and release stored ANP granules into the circulation. Hormones like angiotensin II and endothelin-1 as well as inflammatory cytokines can also stimulate ANP secretion.
Does the heart produce adrenaline?
No, the heart does not produce adrenaline (epinephrine). Adrenaline is synthesized and secreted by the adrenal medulla gland as part of the sympathetic nervous system. It acts as a “fight or flight” hormone, increasing heart rate, blood pressure, and respiratory rate to prepare the body for stress. The heart responds to adrenaline but does not produce it directly.
What does ANP do to blood pressure?
ANP acts to reduce blood pressure through a few mechanisms:
1) It induces vasodilation of vascular smooth muscle, causing dilation of veins and arteries.
2) It increases sodium and water excretion by the kidneys, reducing blood plasma volume.
3) It inhibits the renin-angiotensin-aldosterone system, preventing retention of sodium and water.
Together, these ANP actions work to counteract mechanisms that increase blood pressure. It provides an important hormonal system to regulate cardiovascular function.
Is BNP better than ANP for heart failure?
BNP and ANP have very similar effects in promoting sodium excretion, vasodilation and RAAS inhibition. BNP levels more closely correlate with ventricular function than ANP levels, so BNP measurement is preferred clinically for diagnosing heart failure and assessing severity. However, there is no clear evidence showing BNP is substantially more beneficial than ANP for treatment of heart failure. Synthetic versions of both peptides are used to improve outcomes in certain heart failure patients.
Conclusion
The heart plays a key role in cardiovascular homeostasis through secretion of regulatory hormones in response to changing conditions. Stretch-activated release of ANP and BNP from heart muscle cells provides an elegant feedback mechanism to counteract the detrimental effects of high blood volume and pressure on the heart and circulation. Along with other local hormones like adrenomedullin, these natriuretic peptides help maintain fluid balance, vascular tone, and cardiac structure. Dysregulation of this hormonal system contributes to common diseases like hypertension and heart failure.