Taiy Chemical
(Tyr0)-Atriopeptin II (rat)
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.
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