Synonym |
ANF |
Species |
Human |
Protein Accession |
P01ACD |
Purity |
Greater than 95% as determined by SDS-PAGE |
Endotoxin Level |
Less than 1.0 EU per μg of the protein |
Biological Activity |
Measured by its ability to stimulate cGMP production in A-10 cells. The ED50 is typically
0.5-2.5 ng/mL |
Expression System |
E. coli |
Fusion Tag |
None |
Predicted Molecular Mass |
3.5 kDa |
Formulation |
Lyophilized from a 0.2 μm filtered solution of 20 mM Tris, 500 mM NaCl, pH 8.0 |
Reconstitution |
Centrifuge the vial prior to opening. Reconstitute in 5mM HCl to a concentration of 0.1-1.0
mg/mL. |
Storage & Stability |
Store at -80°C. Avoid repeated freeze-thaw cycles. |
FAQ
What is Thr-Ala-Pro-Arg-Atrial Natriuretic Factor (1-28) and how does it work in the
body?
Thr-Ala-Pro-Arg-Atrial Natriuretic Factor (1-28), also known as ANF or ANP, is a peptide
hormone involved in the regulation of blood pressure and fluid balance in the body. It is derived from
the larger precursor protein known as prohormone form (126 amino acids) cleaved to produce the 28-amino
acid active form. ANP is primarily produced by cardiac muscle cells in the heart's atria in response to
increased blood volume and atrial pressure. It plays a critical role in maintaining cardiovascular
homeostasis through its vasodilatory, natriuretic, and diuretic effects.
When released into the
bloodstream, ANP exerts its effects primarily through its interaction with specific receptors on the
surface of target cells, known as natriuretic peptide receptors (NPRs). These receptors are found in a
variety of tissues, including the kidneys, blood vessels, and adrenal glands. Upon binding to its
receptor, ANP activates a secondary messenger pathway, leading to an increase in cyclic guanosine
monophosphate (cGMP) levels. This cascade triggers a series of responses that collectively contribute to
its physiological actions.
In the kidneys, ANP promotes natriuresis, the process of excreting
sodium in the urine, by enhancing the glomerular filtration rate and inhibiting reabsorption of sodium
in the renal tubules. The result is an increase in urine production (diuresis), leading to a decrease in
blood volume and blood pressure. Furthermore, ANP inhibits the renin-angiotensin-aldosterone system
(RAAS), which is responsible for regulating sodium and fluid balance, thereby exerting a vasodilatory
effect on the vascular system.
Additionally, ANP has significant cardioprotective properties, as
it helps to reduce cardiac preload and afterload, improving cardiac output and function. By lowering
systemic vascular resistance, ANP decreases the workload on the heart, which is especially beneficial in
conditions such as heart failure and hypertension. ANP also exhibits inhibitory effects on the
sympathetic nervous system, which contributes to cardiovascular homeostasis.
Through its
multifaceted actions, ANP plays a crucial role in regulating blood pressure, volume homeostasis, and
cardiovascular health. Its effects are essential for preventing fluid overload, which can lead to
conditions such as hypertension and heart failure. Understanding the mechanisms and effects of ANP can
provide valuable insights into novel therapeutic approaches for treating cardiovascular
disorders.
What are the clinical applications of Thr-Ala-Pro-Arg-Atrial Natriuretic Factor
(1-28)?
Thr-Ala-Pro-Arg-Atrial Natriuretic Factor (1-28) has several promising clinical
applications due to its unique physiological properties and mechanisms of action. One of the primary
areas of therapeutic interest is its role in managing cardiovascular diseases, such as hypertension and
heart failure. By leveraging its potent natriuretic, diuretic, and vasodilatory effects, researchers are
investigating how ANP or its analogs could be utilized to alleviate symptoms and improve outcomes in
these conditions.
In patients with heart failure, where the heart struggles to pump blood
efficiently, ANP can serve as a beneficial therapeutic agent. Its ability to induce diuresis and
natriuresis helps reduce excess fluid retention, which is commonly observed in heart failure patients.
By decreasing blood volume and venous return to the heart, ANP alleviates cardiac preload, easing the
burden on the heart and improving cardiac output. Additionally, ANP’s vasodilatory properties reduce
systemic vascular resistance, thereby decreasing afterload and enhancing overall cardiac function. As a
result, ANP has the potential to provide symptomatic relief in heart failure patients and improve their
quality of life.
Hypertension, a condition characterized by persistently high blood pressure, is
another area where ANP may have therapeutic utility. By promoting sodium excretion and exerting
vasodilatory effects, ANP can help lower blood pressure levels, providing a novel approach to managing
hypertension. Researchers are exploring the use of ANP analogs or medications that mimic its actions to
develop new antihypertensive therapies for patients who may not respond well to traditional
treatments.
Beyond its role in cardiovascular health, ANP also holds potential in the management
of acute kidney injury (AKI) and other renal conditions. In AKI, the kidneys suddenly become unable to
filter waste products from the blood, leading to a dangerous accumulation of toxins. ANP’s natriuretic
effects can enhance renal perfusion and improve the glomerular filtration rate, aiding in the
preservation of kidney function during acute episodes.
Furthermore, ANP’s influence on the
renin-angiotensin-aldosterone system (RAAS) makes it a candidate for regulating fluid balance in
conditions where RAAS activity is dysregulated. By inhibiting the RAAS, ANP offers the potential to
mitigate fluid overload, thereby benefiting patients with conditions such as cirrhosis or nephrotic
syndrome, where edema is a significant concern.
Ongoing research continues to uncover new
clinical applications for ANP, and as our understanding of its bioactivity expands, it is likely that
its therapeutic potential will be harnessed in innovative ways to address unmet medical
needs.
Are there any significant side effects associated with the use of Thr-Ala-Pro-Arg-Atrial
Natriuretic Factor (1-28)?
Despite its therapeutic potential, the use of Thr-Ala-Pro-Arg-Atrial
Natriuretic Factor (1-28) must be approached with caution, as there can be certain side effects
associated with its administration. Most side effects stem from its potent natriuretic, diuretic, and
vasodilatory actions, leading to imbalances in electrolyte levels and blood pressure. Understanding
these side effects is crucial for the safe and effective use of ANP in clinical settings.
One of
the most significant potential side effects of ANP administration is hypotension, or abnormally low
blood pressure. Given its strong vasodilatory properties, ANP can lead to a significant reduction in
blood pressure, which may manifest as dizziness, lightheadedness, or fainting, particularly if ANP is
administered in higher doses or at a rapid rate. Monitoring of blood pressure during treatment with ANP
is essential to avoid excessive hypotension, especially in patients who may already have low baseline
blood pressure or those who are concurrently taking other antihypertensive medications.
Another
possible side effect is electrolyte imbalance, particularly hyponatremia, which is a low sodium level in
the blood. Since ANP promotes natriuresis — the excretion of sodium in the urine — excessive or
prolonged use can lead to sodium depletion, potentially causing hyponatremia. Symptoms of hyponatremia
may include headache, confusion, seizures, or muscle weakness. It becomes crucial to monitor serum
electrolyte levels closely during therapy with ANP to prevent or address such imbalances
promptly.
In some cases, the diuretic effect of ANP can lead to dehydration, especially in
patients who experience an excessive loss of fluids. Signs of dehydration include dry mouth, reduced
urine output, and increased heart rate. The risk of dehydration necessitates adequate fluid management
and monitoring during treatment, ensuring that patients maintain proper hydration
levels.
Moreover, ANP’s effects on the renal and cardiovascular systems may interact with certain
pre-existing conditions, and therefore, care must be exercised in patients with chronic kidney disease
or advanced heart disorders. Some individuals may experience renal impairment if ANP is used
inappropriately, making close monitoring of kidney function parameters paramount in susceptible
populations.
While the side effects of ANP are generally manageable, the potential for adverse
reactions underscores the importance of individualized treatment plans and vigilant monitoring during
therapy. The benefits of ANP must be carefully weighed against its risks, ensuring that its
administration is justified and beneficial for the patient’s specific clinical scenario. Through careful
management and supervision by medical professionals, the potential adverse effects of ANP can be
minimized, optimizing its therapeutic applications in patients who can potentially benefit from its
unique biological actions.
Can Thr-Ala-Pro-Arg-Atrial Natriuretic Factor (1-28) interact with
other medications or treatments?
Thr-Ala-Pro-Arg-Atrial Natriuretic Factor (1-28) possesses
significant physiological actions that can influence its interactions with other medications and
treatments. When considering the implementation of ANP therapy, it is critical to assess potential drug
interactions that could alter its efficacy and safety profile. Understanding these interactions allows
for more effective management and optimization of therapeutic outcomes.
ANP’s effects on the
cardiovascular system, renal function, and fluid-electrolyte balance can complicate interactions with
several cardiovascular medications. One of the notable interactions is with antihypertensive medications
such as ACE inhibitors, angiotensin receptor blockers (ARBs), and beta-blockers. Patients taking these
drugs may experience an amplified reduction in blood pressure when ANP is administered concurrently due
to its potent vasodilatory effects. Careful monitoring is required to prevent symptomatic hypotension,
and dosage adjustments of either ANP or the antihypertensive agents may be necessary to maintain
hemodynamic stability.
Additionally, ANP’s influence on renal sodium and water excretion can
interact with diuretics, which are commonly used to manage hypertension and heart failure. The
combination of ANP with other diuretics may result in excessive fluid and electrolyte loss, increasing
the risk of dehydration or electrolyte imbalances like hyponatremia or hypokalemia. Regular assessment
of fluid and electrolyte status is vital, and healthcare providers may need to modify dosages to
mitigate potential adverse effects.
Considering ANP’s role in inhibiting the
renin-angiotensin-aldosterone system (RAAS), interactions with drugs affecting the RAAS, such as
mineralocorticoid receptor antagonists like spironolactone, are possible. Concurrent use of these drugs
could lead to additive effects on the suppression of aldosterone secretion, increasing the likelihood of
hyperkalemia, a condition characterized by elevated potassium levels in the blood.
Moreover, ANP
might interact with medications that have effects on renal function or blood glucose levels. In patients
receiving medications that can impair renal function, such as nonsteroidal anti-inflammatory drugs
(NSAIDs), the nephroprotective balance that ANP helps maintain could be disrupted. Likewise, in diabetic
patients, adjustments in insulin or oral hypoglycemic agents might be advisable, as fluctuations in body
water and electrolyte balance could alter glucose homeostasis.
These potential interactions
highlight the necessity of a comprehensive review of a patient's medication regimen before initiating
ANP therapy. Healthcare providers should remain vigilant for signs of drug interactions, adjusting
treatment protocols as needed to optimize therapeutic benefits while minimizing risk. Integration of ANP
therapy should be done in a collaborative manner, ensuring that all members of the healthcare team are
informed and actively involved in monitoring the patient’s response to treatment, and making necessary
adjustments to optimize safety and effectiveness. Such careful management allows for the safe and
beneficial application of ANP in clinical practice, maximizing its therapeutic potential across various
medical contexts.
How is Thr-Ala-Pro-Arg-Atrial Natriuretic Factor (1-28) administered, and what
are some important considerations during its administration?
Thr-Ala-Pro-Arg-Atrial Natriuretic
Factor (1-28) is typically administered intravenously due to its peptide nature, which makes oral
delivery ineffective. Intravenous administration allows for precise control over the dosage and duration
of the treatment, ensuring rapid bioavailability and enabling careful monitoring of its physiological
effects. However, due to its potent effects on blood pressure, volume homeostasis, and electrolyte
balance, several important considerations must be addressed during its administration to ensure patient
safety and therapeutic efficacy.
One key aspect of ANP administration is the individualized
dosing regimen, which should be tailored to the patient’s specific clinical condition and therapeutic
needs. The dosage and rate of infusion may vary depending on factors such as the severity of the
condition being treated, the patient's overall health status, and their response to initial dosing.
Titrating the dosage carefully is essential to achieve the desired therapeutic effect while minimizing
the risk of adverse events such as hypotension or electrolyte imbalances.
During ANP
administration, continuous monitoring of vital signs, particularly blood pressure and heart rate, is
crucial. Since ANP can induce rapid hemodynamic changes, monitoring helps detect and respond promptly to
any abnormal alterations in blood pressure or symptoms of hypotension. In some patients, especially
those with pre-existing cardiovascular conditions or those on concurrent antihypertensive therapy,
additional vigilance is warranted to prevent potential complications from excessive decreases in blood
pressure.
Furthermore, regular assessment of renal function and serum electrolyte levels is
paramount during ANP therapy. Given ANP’s natriuretic effect, there is a risk of developing electrolyte
imbalances, such as hyponatremia or hypokalemia, particularly if ANP is used in combination with other
diuretics. Monitoring renal parameters ensures that any signs of renal impairment or significant shifts
in electrolyte balance are detected early, allowing for timely intervention to correct imbalances and
avoid severe complications.
Attention should also be paid to the duration of ANP therapy, as
prolonged use could exacerbate side effects like electrolyte disturbances. Short-term ANP administration
is often preferred, as it allows clinicians to address acute clinical situations without prolonged
systemic exposure. The decision regarding the duration of therapy should be based on the patient’s
response and the resolution of clinical symptoms.
Additionally, proper storage and handling of
ANP are vital to maintain its stability and efficacy. Being a peptide hormone, ANP is susceptible to
degradation if not stored under appropriate conditions, such as refrigeration and protection from light.
Adhering to manufacturer guidelines for preparation and storage ensures the integrity of the
product.
Overall, the administration of ANP demands comprehensive patient assessment,
individualized treatment planning, and meticulous monitoring to maximize its therapeutic potential while
minimizing risks. With careful attention to these considerations, ANP can be effectively and safely
integrated into the management of specific clinical conditions, providing valuable therapeutic benefits.