Synonym |
ANF |
Species |
Mouse, Rabbit |
Protein Accession |
P04133 |
Purity |
Greater than 98% as determined by SDS-PAGE |
Endotoxin Level |
Less than 1 EU/μg |
Biological Activity |
Measured by its ability to stimulate cGMP production in A7r5 rat aortic smooth muscle cells. The
ED50 for this effect is typically 0.5-2 ng/mL. |
Expression System |
E. coli |
Fusion Tag |
None |
Predicted Molecular Mass |
Approximately 3.3 kDa |
Formulation |
Lyophilized from a 0.2 μm filtered solution in Acetonitrile and TFA |
Reconstitution |
It is recommended to reconstitute the lyophilized Atrial Natriuretic Factor (1-28) in sterile 18
MΩ-cm H2O not less than 100 µg/mL, which can then be further diluted to other aqueous solutions.
|
Storage & Stability |
Store lyophilized protein at -20°C. Aliquot the product after reconstitution to avoid repeated
freezing/thawing cycles. Reconstituted protein can be stored at 4°C for a limited period of
time. |
FAQ
What is Atrial Natriuretic Factor (1-28) and what role does it play in mice and rabbits?
Atrial
Natriuretic Factor (ANF), also known as Atrial Natriuretic Peptide (ANP), is a critical peptide hormone
predominantly secreted by heart muscle cells. Specifically, the version (1-28) refers to the active
amino acid sequence that constitutes the peptide in various species, including mice and rabbits. In
these animals, just as in humans, ANF plays a pivotal role in cardiovascular homeostasis. It is
primarily involved in the reduction of blood volume, pressure, and sodium concentration by promoting
renal sodium excretion, which ultimately affects fluid balance and blood pressure regulation. ANF is
released in response to atrial distention, typically due to increased blood volume or
pressure.
In mice and rabbits, ANF engages with specific receptors such as the guanylyl
cyclase-coupled receptor NPRA, leading to the generation of the secondary messenger cGMP. This signaling
cascade is vital for numerous cellular processes including vasodilation, inhibition of renin and
aldosterone secretion, and modulation of renal sodium reabsorption. These effects together help the
organism maintain cardiovascular stability.
Furthermore, studies in mice and rabbits have shed
light on additional roles of ANF beyond the cardiovascular system. In mice, for example, ANF has been
associated with metabolic regulation, affecting lipid metabolism and insulin sensitivity. Similarly, in
rabbits, it has been found that ANF can modulate inflammation and immunity, indicating its broader
systemic impacts. These insights have expanded understanding of ANF’s physiological functions and its
potential therapeutic applications.
In a research context, studying ANF in these animals has
provided valuable insights into cardiovascular disorders, contributing to the development of therapeutic
strategies targeting heart failure, hypertension, and related conditions. Researchers have leveraged
genetic knockout and transgenic mouse models to investigate the precise role of ANF and its interactions
with other cardiovascular and metabolic pathways, leading to greater understanding not only in model
organisms but with potential implications for human health.
How does Atrial Natriuretic Factor
influence blood pressure regulation in mouse and rabbit models?
Atrial Natriuretic Factor plays a
crucial role in regulating blood pressure, a fundamental aspect of cardiovascular health. In mouse and
rabbit models, ANF exerts its blood pressure-lowering effects through several mechanisms. Upon release
from cardiac atria in response to increased blood volume or atrial stretch, ANF interacts with the
specific receptor NPRA (Natriuretic Peptide Receptor A) on target cells in various tissues including the
kidneys, blood vessels, and adrenal glands. The binding of ANF to NPRA activates guanylyl cyclase,
leading to an increase in intracellular cGMP levels, a secondary messenger that mediates vasorelaxation
and natriuresis.
In the renal system, ANF directly encourages the excretion of sodium and water
by increasing the glomerular filtration rate and inhibiting sodium reabsorption in the convoluted
tubules of the nephron. This natriuretic effect reduces blood volume, consequently lowering blood
pressure. The vasodilatory action of ANF also contributes significantly by directly relaxing the smooth
muscles of blood vessels, further decreasing vascular resistance and facilitating blood flow.
In
addition to its direct effects, ANF influences blood pressure by modulating hormone secretion. It
decreases the secretion of renin, subsequently reducing the production of angiotensin II, a potent
vasoconstrictor, and lowers aldosterone levels, decreasing sodium and water retention. This hormonal
interplay underscores ANF’s comprehensive approach to blood pressure regulation, involving multiple
physiological systems.
Studying these mechanisms in mouse and rabbit models has provided
substantial insight into ANF’s cardioprotective functions and potential as a therapeutic target. These
models are used to explore genetic variations influencing ANF activity and the resultant phenotypic
effects on blood pressure regulation, offering potential pathways for intervention in hypertension and
related cardiovascular diseases.
What are the differences in the action of Atrial Natriuretic
Factor between mice and rabbits?
The action of Atrial Natriuretic Factor across different
species, including mice and rabbits, is generally conserved, focusing on vasodilation and natriuresis.
However, there are specific differences in how each species responds to ANF that can be attributed to
variations in physiology, receptor expression, and hormonal environment.
One key difference lies
in the cardiovascular physiology of mice and rabbits. Mice, being smaller animals, have a higher heart
rate and blood volume relative to body size compared to rabbits. This difference influences ANF’s
systemic effects, particularly in how effectively it can modulate heart rate along with blood pressure.
In mice, ANF has been observed to have a more pronounced effect on heart rate modulation than in
rabbits, reflecting physiological adaptations.
The expression patterns of ANF receptors also show
variance between mice and rabbits, affecting the peptide's pharmacokinetics and hemodynamic outcomes.
Mice have been reported to exhibit higher receptor density in certain tissues which could influence the
local efficacy of ANF. Moreover, the downstream signaling pathways activated by ANF can differ slightly
in their magnitude and duration between these species, possibly affecting the overall hormonal response
profile.
Furthermore, the hormonal regulatory systems interacting with ANF vary in specificity
and feedback loops. For instance, while both species experience reduced renin and aldosterone levels due
to ANF, the magnitude and duration of these hormonal changes can differ, affecting blood pressure
regulation and renal function outcomes in distinct ways. Rabbits might have a more pronounced feedback
mechanism regulating atrial stretch and hormone secretion, thereby tweaking their systemic adaptation to
ANF signaling in contrast to mice.
These differences highlight why species-specific models are
essential in research, enabling a nuanced understanding of ANF’s roles and implications in
cardiovascular physiology. By studying both species, researchers can validate findings, draw
comparisons, and refine therapeutic approaches, ensuring robust and translatable pharmacological
insights into human health applications.
Can Atrial Natriuretic Factor influence metabolic
processes in research models involving mice and rabbits?
Yes, Atrial Natriuretic Factor is
intricately involved in several metabolic processes, particularly demonstrated in research models
involving mice and rabbits. Traditionally recognized for its cardiovascular effects, ANF has also shown
significant influence on metabolism, including lipid and glucose regulation.
In mice, extensive
research has revealed that ANF can modulate lipid metabolism by promoting lipolysis in adipose tissues.
ANF’s ability to bind to specific receptors expressed in brown fat cells stimulates cGMP production,
which activates protein kinase G (PKG) and lipases necessary for breaking down triglycerides into free
fatty acids. This process is crucial in energy expenditure and weight regulation. As a result, animal
models have illuminated the potential benefits of ANF in preventing obesity and related metabolic
disorders. Moreover, its impact on enhancing fatty acid oxidation underscores its role in improving
insulin sensitivity and glucose utilization, which could be beneficial in diabetes management.
In
rabbit models, studies have corroborated the metabolic effects of ANF, highlighting its capacity to
influence energy homeostasis. Furthermore, ANF has been found to exert anti-inflammatory effects in
these animals, which are pivotal in metabolic health. Given the role inflammation plays in the
progression of metabolic syndrome and insulin resistance, ANF’s immunomodulatory functions add another
layer to its physiological impacts.
These findings underscore ANF’s utility in understanding the
interplay between cardiovascular health and metabolism in research. By utilizing both mouse and rabbit
models, scientists can explore the underlying molecular mechanisms, genetic factors, and potential
therapeutic interventions that could leverage ANF’s diverse roles. The comparative approach also ensures
more comprehensive insights, ensuring that the benefits of ANF modulation are fully understood and can
be harnessed in clinical settings, particularly for managing metabolic and cardiovascular
disorders.
What therapeutic potential does Atrial Natriuretic Factor hold based on studies in
mouse and rabbit models?
Atrial Natriuretic Factor holds significant therapeutic potential, as
evidenced by numerous studies in mouse and rabbit models. The peptide's primary therapeutic promise lies
in its cardiovascular benefits, with profound implications for treating hypertension, heart failure, and
related conditions. ANF’s ability to promote vasodilation and reduce blood pressure through natriuresis
has long been recognized, making it a compelling target for pharmacological interventions aimed at
managing hypertension.
In heart failure, where fluid overload and elevated cardiac pressures are
common, ANF’s diuretic effects provide symptomatic relief and counteract detrimental myocardial stretch.
Studies in mouse models with genetically modified ANF pathways have highlighted its utility in
attenuating cardiac remodeling and improving cardiac output, offering valuable insights into therapeutic
strategies aimed at enhancing endogenous ANF activity or mimicking its effects through synthetic
analogs.
Beyond cardiovascular applications, ANF has shown promise in metabolic and renal health.
Mouse and rabbit models have elucidated ANF’s role in lipid metabolism and glucose regulation,
suggesting potential avenues for addressing insulin resistance and obesity-related diseases. ANF’s
ability to promote lipolysis and enhance insulin sensitivity can help mitigate the effects of metabolic
syndrome and type 2 diabetes, expanding its therapeutic scope beyond traditional cardiovascular
applications.
Furthermore, ANF’s anti-inflammatory properties, as observed in both mice and
rabbits, suggest potential in treating inflammatory conditions. Chronic inflammation is at the core of
various pathologies, including atherosclerosis and metabolic dysfunctions, where ANF’s regulatory
effects could offer significant benefits.
The promising data derived from animal models
necessitate further translation into human studies, but these findings underscore ANF’s multifaceted
therapeutic potential. Ongoing research aims to optimize delivery mechanisms, target stability, and
ensure safety, with the ultimate goal of harnessing ANF’s full spectrum of benefits for clinical
application, indicating a bright future for this naturally occurring peptide in therapeutics.
How
does research on Atrial Natriuretic Factor in mice and rabbits contribute to human health
insights?
Research on Atrial Natriuretic Factor in mice and rabbits contributes extensively to
our understanding of human health through the elucidation of underlying pathways and identification of
potential therapeutic targets. These animals serve as invaluable models to study the multifaceted roles
of ANF, given the physiological and genetic resemblances they share with humans. The translational value
of such research lies in its application to human cardiovascular diseases, metabolic disorders, and
broader systemic conditions.
In cardiovascular research, mouse and rabbit models have been
seminal in unraveling ANF’s mechanisms in blood pressure regulation and heart function. By investigating
the peptide's effects on vasodilation, sodium excretion, and hormonal modulation, researchers have
expanded the understanding of hypertension and heart failure pathophysiology. These insights inform the
development of new therapeutic agents aimed at enhancing ANF’s beneficial effects or mimicking its
actions in disease models, which can later be applied to human treatments, thus offering strategies to
ameliorate symptoms and improve patient outcomes.
The metabolic implications of ANF in these
animal models also resonate with human health, particularly concerning obesity, diabetes, and metabolic
syndrome. The observed improvement in lipid metabolism and insulin sensitivity in response to ANF
provides a foundation for exploring innovative metabolic therapies. These findings also highlight the
intersection of cardiovascular and metabolic disorders, which is critical in developing comprehensive
treatment plans that address multiple facets of patient health.
Additionally, the immunological
impacts of ANF identified in animal research further enrich the understanding of inflammatory processes
in humans. Given that chronic inflammation is a shared pathway across various human diseases, insights
gained from mice and rabbits can pave the way for novel anti-inflammatory interventions with broad
applicability.
By shedding light on these diverse biological processes, animal research on ANF
not only clarifies its physiological roles but also propels translational research aimed at improving
human health outcomes, demonstrating a continuous bridge from bench-side discoveries to bedside
applications.