Synonym |
Atrial natriuretic peptide 2 |
Species |
Rat |
Protein Accession |
P11032 |
Purity |
Greater than 95% as determined by SDS-PAGE |
Endotoxin Level |
Less than 1 EU/µg |
Biological Activity |
Fully biologically active when compared to standard |
Expression System |
E. coli |
Fusion Tag |
None |
Predicted Molecular Mass |
3.3 kDa |
Formulation |
Lyophilized from a 0.2 µm filtered solution of 20mM PB, 150mM NaCl, pH 7.4 |
Reconstitution |
It is recommended to reconstitute the lyophilized Atrial natriuretic peptide 2 in sterile
18MΩ-cm H2O not less than 100µg/ml, which can then be further diluted to other aqueous
solutions. |
Storage & Stability |
Lyophilized Atriopeptin II although stable at room temperature for 3 weeks, should be stored
desiccated below -18°C. Upon reconstitution ANP Rat should be stored at 4°C between 2-7 days and
for future use below -18°C. Please prevent freeze-thaw cycles. |
FAQ
What is (Tyr0)-Atriopeptin II (rat), and how does it function in the body?
(Tyr0)-Atriopeptin II
(rat) is a synthetic peptide modeled after the naturally occurring atrial natriuretic peptide (ANP)
found in rats. It functions primarily by binding to specific receptors known as the natriuretic peptide
receptors, which are distributed throughout various tissues, especially in the cardiovascular and renal
systems. Once bound, the peptide stimulates the production of cyclic guanosine monophosphate (cGMP), a
secondary messenger that plays a critical role in various physiological processes. The increase in cGMP
levels results in vasodilation, which leads to a reduction in blood pressure. Additionally, this process
increases diuresis and natriuresis, which are the excretion of water and sodium through urine,
respectively. This helps regulate blood volume and potassium levels. Essentially, (Tyr0)-Atriopeptin II
(rat) mimics the dual actions of the natural ANP, influencing both vascular tone and volume homeostasis.
This peptide is of significant interest in the study of cardiovascular function and disease because of
its role in managing blood pressure and fluid balance. Moreover, it is noted for its potential
neuroprotective benefits, as ANP has been found to potentially reduce neuronal damage under certain
pathophysiological conditions. In the context of research, (Tyr0)-Atriopeptin II (rat) is used to
explore these mechanisms further and understand its benefits and applications in medical science. Given
its structure and function, it serves as a powerful tool for investigating cardiovascular physiology and
pathophysiology, along with its potential therapeutic implications.
What are the applications of
(Tyr0)-Atriopeptin II (rat) in scientific research?
(Tyr0)-Atriopeptin II (rat) has a wide range
of applications in scientific research, particularly in the study of cardiovascular and renal systems.
Its primary utility lies in understanding the mechanisms by which atrial natriuretic peptides regulate
blood pressure, blood volume, and sodium balance. Researchers utilize this peptide to study how it can
modulate the cardiovascular system's functions, including its potential to alleviate hypertension by
promoting vasodilation and increasing urine production to excrete excess fluid and sodium. This helps in
better understanding how these mechanisms can be harnessed to develop treatments for hypertension and
other cardiovascular disorders. In addition to cardiovascular applications, this peptide is valuable in
renal research to examine how it influences kidney function. Given its role in increasing diuresis and
natriuresis, (Tyr0)-Atriopeptin II (rat) helps scientists understand the pathways through which the body
maintains fluid and electrolyte balance. This is particularly important in conditions like chronic
kidney disease, where fluid retention and imbalanced electrolytes are common issues. The insights gained
from such studies could lead to new strategies that improve renal function and manage fluid overload.
Another area where this peptide finds application is in neuroscience research. There are ongoing studies
investigating its role in neuroprotection, as the atrial natriuretic peptide family is thought to
provide protective benefits to neurons under stress conditions, such as ischemia or trauma.
Understanding these effects could open avenues for new therapeutic targets for neurological disorders.
Overall, (Tyr0)-Atriopeptin II (rat) is a versatile research peptide that aids scientists in dissecting
complex biological pathways, potentially leading to innovative treatments for a variety of health
conditions that involve fluid balance and vascular function.
What are the known physiological
effects of (Tyr0)-Atriopeptin II (rat) in vivo studies?
In vivo studies on (Tyr0)-Atriopeptin II
(rat) have highlighted several significant physiological effects, especially concerning cardiovascular
and renal functions. The peptide's most notable impact is its ability to lower blood pressure through
vasodilation. By binding to receptors on vascular smooth muscle cells, it increases levels of cGMP,
resulting in the relaxation of these muscles and the widening of blood vessels. This vasodilatory effect
helps decrease systemic vascular resistance, leading to a reduction in blood pressure. Another critical
effect observed in vivo is the regulation of fluid and electrolyte balance. (Tyr0)-Atriopeptin II (rat)
stimulates both diuresis and natriuresis, processes critical for maintaining fluid homeostasis. It
achieves this by increasing the glomerular filtration rate (GFR) in the kidneys, thereby promoting the
excretion of water and sodium. This not only aids in blood pressure control but also helps in reducing
blood volume, providing relief in conditions such as congestive heart failure where fluid overload is an
issue. The peptide's influence extends to cardiovascular remodeling as well. In vivo studies have
suggested that (Tyr0)-Atriopeptin II (rat) may help to prevent pathological cardiac hypertrophy, a
condition where the heart muscle thickens due to chronic high blood pressure or other stressors. It does
this by attenuating the signaling pathways that lead to such remodeling, thus preserving cardiac
function and preventing the development of heart failure. Beyond cardiovascular and renal systems, some
research hints at potential neuroprotective roles of (Tyr0)-Atriopeptin II (rat) in vivo. There is
evidence to suggest that it might mitigate neuron damage in conditions of oxidative stress or ischemia,
potentially providing a protective mechanism against certain neurological disorders. These physiological
effects make it a critical subject of study for understanding and potentially addressing a range of
health conditions.
How does (Tyr0)-Atriopeptin II (rat) interact with other signaling pathways
related to cardiovascular health?
(Tyr0)-Atriopeptin II (rat), through its action on natriuretic
peptide receptors, specifically interacts with signaling pathways that have significant implications for
cardiovascular health. Its primary interaction is with pathways mediated by cGMP, a secondary messenger
crucial for vascular tone regulation. Upon binding to its receptors, guanylyl cyclase activity is
prompted, amplifying cGMP production. cGMP serves as a pivotal player in several signaling pathways,
promoting vasodilation by activating protein kinase G, which subsequently reduces intracellular calcium
concentration, resulting in the relaxation of vascular smooth muscle cells. This pathway is critical for
maintaining vascular homeostasis and blood pressure control. Moreover, (Tyr0)-Atriopeptin II (rat)
affects endothelin-1 (ET-1) pathways. ET-1 is a potent vasoconstrictor, and the peptide can modulate its
release, promoting vasodilatory mechanisms over vasoconstriction. This modulation is significant for
maintaining balanced vascular tone and preventing excessive vasoconstriction that contributes to
hypertension. Additionally, the peptide indirectly influences the renin-angiotensin-aldosterone system
(RAAS), which is central to blood pressure and fluid balance regulation. By promoting natriuresis and
diuresis, (Tyr0)-Atriopeptin II (rat) effectively counteracts the fluid-retaining effects of
aldosterone, reducing circulating blood volume. This antagonistic action helps attenuate RAAS
overactivity, a common contributor to cardiovascular disease. The peptide’s interactions also extend to
inflammatory pathways. It has been suggested that elevated cGMP levels resulting from (Tyr0)-Atriopeptin
II administration may have anti-inflammatory actions within the cardiovascular system, although these
interactions are still under investigation. The interplay with these pathways highlights the peptide's
potential as a therapeutic agent that can target multiple mechanisms involved in cardiovascular
diseases. By influencing various pathways, (Tyr0)-Atriopeptin II (rat) helps maintain vascular tone,
regulate fluid balance, and potentially curb inflammatory responses, making it a multifaceted component
in cardiovascular health research.
What are the potential clinical implications of
(Tyr0)-Atriopeptin II (rat) based on current research findings?
Based on current research
findings, (Tyr0)-Atriopeptin II (rat) holds several potential clinical implications, primarily within
the realm of cardiovascular health. Its ability to induce vasodilation and manage blood pressure offers
therapeutic prospects in the treatment of hypertension. By promoting the relaxation of vascular smooth
muscles, it could be developed into a medication that lowers blood pressure effectively in patients with
essential hypertension, providing an alternative or adjunctive treatment option to existing
antihypertensive drugs. Additionally, its diuretic and natriuretic effects make it a candidate for
managing fluid overload conditions such as congestive heart failure (CHF). In CHF, excessive fluid
accumulation can lead to symptomatic edema and further stress on the heart. By facilitating the
excretion of excess sodium and water, (Tyr0)-Atriopeptin II (rat) could help alleviate these symptoms,
potentially improving quality of life and outcomes for patients with heart failure. Beyond
cardiovascular applications, there is emerging interest in the peptide’s potential neuroprotective
effects. Research into its role in mitigating neuronal damage suggests that it might be beneficial in
conditions such as stroke or traumatic brain injury, where neuroprotection is a critical therapeutic
target. This could lead to the development of novel treatments that help preserve brain function after
injury. There's also the possibility of the peptide being used in research or therapeutic contexts to
explore its anti-inflammatory capacities, as elevated cGMP levels have been associated with reduced
inflammatory responses. While these implications are promising, it is important to note that translating
these findings into clinical practice would require rigorous testing in human clinical trials to
establish safety and efficacy. Nonetheless, (Tyr0)-Atriopeptin II (rat) represents a fascinating area of
exploration that could yield novel treatments for various conditions affecting the cardiovascular and
nervous systems, highlighting the continuous need for innovative research strategies in these
fields.
How does (Tyr0)-Atriopeptin II (rat) compare to other atrial natriuretic peptides in
terms of efficacy and applications?
(Tyr0)-Atriopeptin II (rat) shares many functional
similarities with other atrial natriuretic peptides (ANPs), but it also has distinct features and
applications that make it a unique research tool. When compared to other natriuretic peptides, such as
B-type natriuretic peptide (BNP) and C-type natriuretic peptide (CNP), (Tyr0)-Atriopeptin II (rat)
mainly differs in its origin, receptor affinity, and resulting physiological effects. Unlike BNP and
CNP, which are primarily associated with the ventricular myocardium and vascular endothelium
respectively, atriopeptin peptides like (Tyr0)-Atriopeptin II originate from the cardiac atria. This
difference in origin influences their role and effectiveness in various cardiovascular processes. In
terms of receptor interaction, (Tyr0)-Atriopeptin II (rat) primarily binds to the natriuretic peptide
receptor A (NPR-A), similar to ANP, leading to guanylyl cyclase activation and subsequent cGMP
production. This action is crucial in maintaining vascular homeostasis and regulating blood pressure.
Meanwhile, BNP also targets NPR-A, but CNP primarily binds to natriuretic peptide receptor B (NPR-B),
which suggests variations in efficacy and application due to receptor specificity. Thus,
(Tyr0)-Atriopeptin II is particularly effective in research focused on conditions directly influenced by
NPR-A pathways, including vasodilation and natriuretic responses. The applications of (Tyr0)-Atriopeptin
II (rat) in research also diverge based on its specific physiological effects. While all natriuretic
peptides are involved in cardiovascular health, (Tyr0)-Atriopeptin II’s effects on diuresis and sodium
excretion are predominantly studied in the context of hypertension and fluid overload conditions,
whereas BNP levels are often used as a biomarker for heart failure diagnosis. CNP, being less involved
in fluid balance, is primarily researched for its effects on bone growth and vascular development.
Overall, the efficacy and applications of (Tyr0)-Atriopeptin II (rat) are tailored to its receptor
affinity and physiological effects, making it an indispensable tool in research areas focused on
cardiovascular and renal functions, with distinct advantages in studying processes regulated
specifically by NPR-A.
Are there any side effects or potential risks associated with the use of
(Tyr0)-Atriopeptin II (rat) in research settings?
In research settings, (Tyr0)-Atriopeptin II
(rat) is primarily used in controlled experimental conditions, which typically minimizes the potential
for adverse side effects. However, understanding its physiological impact remains critical for ensuring
experimental integrity and addressing any unintended effects that may arise. Generally, the peptide’s
primary actions involve lowering blood pressure and altering fluid and electrolyte balance. Thus, one
potential risk in research settings, particularly in in vivo studies, is hypotension, as its
vasodilatory effects could lead to excessively low blood pressure if not monitored adequately.
Similarly, its diuretic and natriuretic effects may cause dehydration and electrolyte imbalances, such
as hyponatremia or hypokalemia, especially in experiments where fluid intake is not carefully
controlled. These imbalances could impact other physiological processes within animal models,
influencing the overall experimental outcomes. Researchers must also consider the route of
administration and dosage, as improper dosing or administration methods could introduce variability and
affect results. High concentrations or inappropriate delivery can lead to overstimulation of the
natriuretic pathways, accentuating the aforementioned side effects. Despite these considerations, the
localized and controlled use of (Tyr0)-Atriopeptin II (rat) in laboratory studies generally ensures its
safety, with risks being manageable through appropriate experimental design and control measures.
Furthermore, as with any synthetic compound, there is a potential for immune responses, although this is
less common with peptides like (Tyr0)-Atriopeptin II when used in homologous species such as rat models.
Nevertheless, it is crucial for researchers to remain vigilant of any unexpected physiological responses
that could suggest an immunogenic reaction or other side effects. In summary, while (Tyr0)-Atriopeptin
II (rat) is largely safe for use in research settings, understanding and mitigating potential side
effects, such as hypotension and electrolyte imbalances, through careful planning and monitoring is
essential for optimizing experimental outcomes and ensuring the welfare of animal models.