Taiy Chemical
Atrial Natriuretic Factor (1-28) (mouse, Rabbit,
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.
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