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Desoxycorticosterone Acetate

Desoxycorticosterone Acetate (DOCA) is a synthetic mineralocorticoid hormone that plays a key role in the regulation of sodium, potassium, and water balance in the body.
It is commonly used in research to study the effects of excess mineralocorticoid activity on the cardiovascular system, kidney function, and other physiological processes.
PubCompare.ai, an AI-driven protocol comparison tool, can help optimize your DOCA research by identifying the most reproducible and effective methods from the literature, preprints, and patents.
This cutting-edge platform uses advanced AI comparisons to improve your research outcomes and drive scientific discovery in this important area of study.

Most cited protocols related to «Desoxycorticosterone Acetate»

Angiotensin II-induced Hypertension Modeling

Cited 18 times

C57BL/6, RAG-1^−/−, and AT1a^−/− mice were obtained from Jackson ImmunoResearch Laboratories. The p47^phox^−/− mice and their appropriate controls were obtained from Taconic. All experimental protocols were approved by the institutional Animal Care and Use Committee at Emory University. All mice were on a C57BL/6 background. 490 ng/min/kg angiotensin II was infused and blood pressure was measured both invasively and noninvasively, as previously described (69 (link)). Animals were maintained in a sterile environment and were regularly screened for infections. For adoptive transfer, mice were anesthetized with xylazine/ketamine and cells were injected via tail vein. Angiotensin II infusion and blood pressure monitoring was begun 3 wk after adoptive transfer. In some experiments, 8 mg/kg etanercept (AmGen) or a neutralizing IFNγ antibody (eBioscience; clone R4-6A2; 0.5 mg per injection per 30 g mouse) was administered i.p. 3 d before and every 3 d during angiotensin II infusion. In some mice, DOCA-salt hypertension was created as previously described, and studies were performed after 40 d from the induction of hypertension (14 (link)).

Guzik T.J., Hoch N.E., Brown K.A., McCann L.A., Rahman A., Dikalov S., Goronzy J., Weyand C, & Harrison D.G. (2007). Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction. The Journal of Experimental Medicine, 204(10), 2449-2460.

Publication 2007

Adoptive Transfer Angiotensin II Animals Antibodies, Neutralizing Blood Pressure Cells Clone Cells Desoxycorticosterone Acetate Etanercept High Blood Pressures Infection Institutional Animal Care and Use Committees Interferon Type II Ketamine Mus NCF1 protein, human Sterility, Reproductive Tail Veins Xylazine

Mouse Model of Intracranial Aneurysm Formation

Cited 15 times

Experiments were conducted in accordance with the guidelines approved by the University of California, San Francisco, Institutional Animal Care and Use Committee. Intracranial aneurysms were induced in 8–10 week-old male mice (C57BL/6J, Jackson Laboratory) using a previously described method with modifications.^{7 (link), 13 (link)} We combined induced systemic hypertension and a single injection of elastase into the cerebrospinal fluid at the right basal cistern. (Detailed methods are presented in the online supplements.)To induce systemic hypertension, we used deoxycorticosterone acetate-salt hypertension (DOCA-salt hypertension).^{14 (link)} Mice underwent nephrectomy followed by an implantation of DOCA pellet one week later; 1% sodium chloride drinking water was started on the same day as the DOCA pellet implantation.^{14 (link), 15 (link)} Mice received a single injection of elastase (25–35 milli-units) into the cerebrospinal fluid at the right basal cistern on the same day as DOCA pellet implantation.^{7 (link), 13 (link)} Aneurysms were defined as a localized outward bulging of the vascular wall, whose diameter was greater than the parent artery diameter.^{7 (link), 13 (link)}Two blinded observers performed daily neurological examination using a previously described method with modifications.^{16 (link)–19 (link)} Neurological symptoms were scored as followings; 0: normal function; 1: reduced eating or drinking activity demonstrated by a weight loss greater than two grams of body weight (approximately 10% weight loss) over 24 hours; 2: flexion of the torso and forelimbs upon lifting of the whole animal by the tail; 3: circling to one side with a normal posture at rest; 4: leaning to one side at rest; 5: no spontaneous activity. Mice were sacrificed when they developed neurological symptoms (score 1–5). All asymptomatic mice were sacrificed 28 days after aneurysm induction. The brain samples were perfused with phosphate-buffered saline, followed by a gelatin containing blue dye in order to visualize cerebral arteries, as well as to assess for aneurysm formation and subarachnoid hemorrhage.

Makino H., Tada Y., Wada K., Liang E.I., Chang M., Mobashery S., Kanematsu Y., Kurihara C., Palova E., Kanematsu M., Kitazato K, & Hashimoto T. (2012). Pharmacological stabilization of intracranial aneurysms in mice— a feasibility study. Stroke; a journal of cerebral circulation, 43(9), 2450-2456.

Publication 2012

Aneurysm Animals Arteries Blood Vessel Body Weight Brain Cerebral Arteries Cerebrospinal Fluid Desoxycorticosterone Acetate Dietary Supplements Forelimb Gelatins High Blood Pressures Institutional Animal Care and Use Committees Intracranial Aneurysm Males Mus Nephrectomy Neurologic Examination Neurologic Symptoms Ovum Implantation Pancreatic Elastase Parent Phosphates Saline Solution Sodium Chloride Subarachnoid Hemorrhage Tail Torso

CXCR2 Blockade Attenuates Angiotensin II-Induced Hypertension

Cited 12 times

WT mice (C57BL/6J, male) and CXCR2 knockout mice (CXCR2^-/-, B6.129S2(C)-Cxcr2^tm1Mwm/J) were purchased from Jackson Laboratory (Sacramento, CA). Mice at 8 to 12 weeks of age were used in an angiotensin II-induced hypertension model by subcutaneous infusion of angiotensin II (Sigma-Aldrich, St. Louis, MO) at a dose of 490 ng/kg/min or saline using osmotic mini-pumps (Alzet MODEL 1007D; DURECT, Cupertino, CA) for 14/28 days as described previously.^{16 (link)} Deoxycorticosterone acetate (DOCA)-salt-induced hypertension was also created as previously described.^{17 (link)} The selective CXCR2 antagonist SB265610 (Axon, Groningen, The Netherlands) was administered intraperitoneally (2 mg/g/d) beginning 1 day before angiotensin II/DOCA infusion and continued during angiotensin II/DOCA-salt treatment. To determine whether SB265610 could reverse established hypertension, SB265610 treatment was initiated 2 weeks after either angiotensin II infusion (for 28 days) or DOCA-salt challenge (for 21 days). All investigations were approved by the Animal Care and Use Committee of Dalian Medical University and conformed to the US National Institutes of Health Guide for the Care and Use of Laboratory Animals.

Wang L., Zhao X.C., Cui W., Ma Y.Q., Ren H.L., Zhou X., Fassett J., Yang Y.Z., Chen Y., Xia Y.L., Du J, & Li H.H. (2016). Genetic and Pharmacologic Inhibition of the Chemokine Receptor CXCR2 Prevents Experimental Hypertension and Vascular Dysfunction. Circulation, 134(18), 1353-1368.

Publication 2016

Angiotensin II Animals Animals, Laboratory Axon Desoxycorticosterone Acetate High Blood Pressures Males Mice, House Mice, Knockout Osmosis Saline Solution SB 265610 Subcutaneous Infusions

DOCA-salt Hypertension Model in Mice

Cited 7 times

Baseline BP was recorded by telemetry in uni-nephrectomized SA and NT cohorts for 3 days, then mice were randomly divided into 4 groups (n=12/group), either implanted subcutaneously with a DOCA-silicone (DOCA:silicone=1:3; DOCA: 1 mg/g body weight) or an empty silicone (sham surgery) sheet. Drinking water from DOCA implanted mice was replaced by 1% NaCl solution. BP was continuously recorded for 3 additional weeks. At the end of the protocol, the mice were sacrificed and the brains and plasma were collected for enzyme activity assays, peptide level measurements, immuno-precipitation and western blot analysis. In another set of experiments, uni-nephrectomized NT mice were divided into 4 groups (n=6/group) and infused intracerebroventricularly (icv) for 3 weeks, with either ADAM17 siRNA (0.1 nmoles/day) or artificial cerebrospinal fluid (aCSF) while receiving DOCA-salt or sham treatment. BP was recorded daily by radiotelemetry as described above. Another subset of NT mice was infused with Losartan (2 μg/hour icv)^{13 (link)} for 3 weeks while receiving DOCA-salt treatment. Spontaneous baroreceptor reflex sensitivity (SBRS), reflecting the baroreflex control of heart rate (HR), was calculated using the sequence method as described.^{7 (link), 8 (link)} Autonomic function was assessed, in conscious freely moving mice, before and 3 weeks after DOCA-salt treatment, using a pharmacological method involving ip injection of propranolol (β-blocker, 4 mg/kg), atropine (muscarinic receptor blocker, 1 mg/kg) and chlorisondamine (ganglionic blocker, 5 mg/kg).^{8 (link)} Each injection was separated by at least a 3-hour recovery period. Changes in HR (ΔHR) or mean arterial pressure (ΔMAP) were calculated following administration of these blockers. At the end of the protocol, mice were euthanized and the brains and plasma were collected and stored at −80°C until used in the various assays.

Xia H., Sriramula S., Chhabra K.H, & Lazartigues E. (2013). Brain ACE2 shedding contributes to the development of neurogenic hypertension. Circulation research, 113(9), 1087-1096.

Publication 2013

ADAM17 protein, human AT protocol Atropine Baroreflex Biological Assay Blepharofacioskeletal Syndrome Body Weight Brain Cerebrospinal Fluid Chlorisondamine Chronotropism, Cardiac Consciousness Desoxycorticosterone Acetate Enzyme Assays Ganglionic Blockers Hypersensitivity Immunoprecipitation Injections, Intraperitoneal Losartan Mice, House Muscarinic Acetylcholine Receptor Nervous System, Autonomic Operative Surgical Procedures Peptides Placebos Plasma Propranolol Rate, Heart RNA, Small Interfering Silicones Sodium Chloride Telemetry Western Blot

Mitochondrial Oxidative Stress and Hypertension

Cited 7 times

Hypertension was induced by angiotensin II (490 ng/kg/min) as described previously 25 (link) using either C57Bl/6 or mice transgenic for human SOD2 (tg^SOD2 mice). In addition, mice received a separate minipump for co-infusion of either TEMPOL, mitoTEMPO or vehicle as described in the figure legends. In other animals, mitoTEMPO treatment was started seven days after saline or angiotensin II minipump placement. Blood pressure was monitored using either the tail cuff method or telemetry as previously described 26 (link), 27 (link). Following 14 days of angiotensin II infusion the animals were sacrificed by CO₂ inhalation and aortas were extracted for the analysis of nitric oxide and O₂^∸ production, and endothelial functions. DOCA-salt induced hypertension was induced as described previously 28 (link) using C57Bl/6 mice. Ten days after surgery the mice were implanted with osmotic pumps containing saline or mitoTEMPO (0.7 mg/kg/day). Seventeen days after surgery the animals were sacrificed by CO₂ inhalation and segments of mouse aorta were used for analysis of vascular nitric oxide and O₂^∸ production. Endothelium-dependent vasodilatation was analyzed in isolated 3-mm aortic segments in organ chambers as we have previously described 27 (link).

Dikalova A.E., Bikineyeva A.T., Budzyn K., Nazarewicz R.R., McCann L., Lewis W., Harrison D.G, & Dikalov S.I. (2010). Therapeutic Targeting of Mitochondrial Superoxide in Hypertension. Circulation research, 107(1), 106-116.

Publication 2010

Angiotensin II Animals Animals, Transgenic Aorta Blood Pressure Blood Vessel Desoxycorticosterone Acetate Endothelium High Blood Pressures Homo sapiens Inhalation Mice, Inbred C57BL Mice, Laboratory MitoTEMPO Osmosis Oxide, Nitric Saline Solution SOD2 protein, human Tail Telemetry tempol Vasodilation

Most recents protocols related to «Desoxycorticosterone Acetate»

Glucocorticoid Regulation in Rainbow Trout

Cited 1 time

Juvenile rainbow trout (15.47 g ± 0.88) were obtained from Pisciculture Rio Blanco (Pontificia Universidad Católica de Valparaiso, Valparaíso, Chile). Fish were held under a temperature of 14 ± 1 °C and photoperiod conditions of L/D 12:12. Juvenile fish were fed with Skretting pellets. Fish were sedated with benzocaine (25 mg/L) and intraperitoneally injected with metyrapone (Sigma-Aldrich, St. Louis, MO, USA) (1 mg/kg of fish) for one hour and then divided into different groups. Fish in the first and second groups were treated with vehicle solution (DMSO, PBS 1x) and 11-deoxycorticosterone acetate (DOC, USBiological, Salem, MA, USA), respectively, at physiological concentrations (1 mg/kg). Fish in the third and fourth groups were treated with mifepristone (RU486, Sigma-Aldrich) (1 mg/kg) and mifepristone (1 mg/kg) plus DOC (1 mg/kg), respectively. Finally, fish in the fifth and sixth groups were treated with eplerenone (Santa Cruz Biotechnology, Santa Cruz, CA, USA) (1 mg/kg) and eplerenone (1 mg/kg) plus DOC (1 mg/kg), respectively. Three hours after treatment, all rainbow trout (n = 24, four fish per group) were euthanized with benzocaine (Veterquimica, RM, San Bernardo, Chile) (300 mg/L). Heparinized obtained blood was centrifugated at 5000× g for 10 min and the plasma was stored at −80 °C. Myotomal skeletal muscle was isolated from the epaxial area, frozen in liquid nitrogen for 6 h, and then stored at −80 °C.

Zuloaga R., Aravena-Canales D., Aedo J.E., Osorio-Fuentealba C., Molina A, & Valdés J.A. (2023). Effect of 11-Deoxycorticosterone in the Transcriptomic Response to Stress in Rainbow Trout Skeletal Muscle. Genes, 14(2), 512.

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Publication 2023

Aftercare ARID1A protein, human Benzocaine BLOOD Desoxycorticosterone Acetate Eplerenone FILIP1L protein, human Fishes Freezing Metyrapone Mifepristone Myotomy Nitrogen Oncorhynchus mykiss Pellets, Drug physiology Plasma R-38486 Skeletal Muscles Sulfoxide, Dimethyl

Carotid Artery Telemetry in Prdm6 Mice

Eight-week-old male Prdm6^fl/+ SM22-Cr mice and the WT littermates were anesthetized and placed on a heating pad to maintain their temperature at 37.0–38.0°C. The tip of the radiotelemetric device TA11PA-C10 (Data Sciences Int.) was implanted into the common carotid artery toward the heart attached to a SI TA11PA-C10 transmitter placed in a pouch underneath the skin along the mouse’s flank. Mice were fed an 8% salt diet. The rationale for use of a high-salt diet was its higher success rate in causing hypertension in heterozygous loss of function mice in prior studies and the fact that other models such as Deoxycorticosterone acetate (DOCA) salt and angiotensin II (AngII) would have caused RAAS activation downstream from renin. The recordings of the heart rate and beat-by-beat arterial BP started 7 days after surgery for acclimation. Data were analyzed using the Dataquest ART version 2.1 (Data Sciences International).

Gunawardhana K.L., Hong L., Rugira T., Uebbing S., Kucharczak J., Mehta S., Karunamuni D.R., Cabera-Mendoza B., Gandotra N., Scharfe C., Polimanti R., Noonan J.P, & Mani A. (2023). A systems biology approach identifies the role of dysregulated PRDM6 in the development of hypertension. The Journal of Clinical Investigation, 133(4), e160036.

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Publication 2023

Acclimatization Angiotensin II Arteries Common Carotid Artery Desoxycorticosterone Acetate Diet Heart High Blood Pressures Loss of Heterozygosity Males Medical Devices Mice, Laboratory Rate, Heart Renin Skin Sodium Chloride, Dietary

Synthesis and Characterization of AS1411-Conjugated ACSSD

The synthetic routes of AS1411-containing ACSSD are shown in Figure 1. Briefly, CSSD was synthesized by our previous report with some modifications.16 (link) DOCA (2.0 g) and EDC (2.93 g) were placed into a flask and dissolved in 80 mL ethanol. Cystamine dihydrochloride (2.3 g) in distilled water was slowly dropped into the above solution. After 24 h stirring, the reacted solution was concentrated on a rotary evaporator in vacuo. The resulting solution was deposited at −20 ℃ and rinsed with ice-cold water. Then, DOCA conjugated cystamine (DOCA-Cys) was produced by drying under vacuum conditions. Next, 1.0 g CSA was dissolved in 20 mL of distilled water. EDC (0.165 g) and DOCA-Cys (0.19 g) in 20 mL ethanol were slowly introduced into the CSA solution. After 24 h reaction, the mixture was transferred into dialysis bags for dialysis as stated above. Further, the solution was freeze-dried for 72 h and CSSD was obtained. In the third step, for AS1411 conjugation, the carboxyl units of CSSD were activated. CSSD (50 mg) was dispersed in 5 mL distilled water and 8 mL dimethyl sulfoxide (DMSO). EDC (10.9 mg) was added. AS1411 (30 OD, oligonucleotide sequence: 5′-NH₂-GGTGGTGGTGGTTGTGGTGGTGGTGG-3′) was dissolved in the mixture of DMSO and distilled water and introduced into the above solution under stirring. After 24 h, the reaction solution was dialyzed against water and lyophilized.
Figure 1

Synthetic scheme of ACSSD conjugate.

The chemical structures of copolymers were analyzed by FTIR spectroscopy (Bruker Tensor II, Germany) and ¹H NMR spectroscopy (Bruker DMX 500 spectrometer, Germany). The conjugation ratio of DOCA groups in the conjugate was studied by an elemental analyzer (Vario Micro Cube, Elementar, Germany). The critical micelle concentration (CMC) value of the copolymer was analyzed by using a pyrene fluorescence probe. The fluorescent spectra were measured by a Hitachi F-7000 spectrophotometer.

Yu J., Xie X., Wang L., Liu W., Xu H., Lu X., Li X., Ren J, & Li W. (2023). Smart Chondroitin Sulfate Micelles for Effective Targeted Delivery of Doxorubicin Against Breast Cancer Metastasis. International Journal of Nanomedicine, 18, 663-677.

Publication 2023

1H NMR AS 1411 Cold Temperature Cystamine Cystamine Dihydrochloride Desoxycorticosterone Acetate Dialysis Ethanol Fluorescent Probes Freezing Ice Micelles Oligonucleotides pyrene Spectroscopy, Fourier Transform Infrared Spectroscopy, Nuclear Magnetic Resonance Spectrum Analysis Sulfoxide, Dimethyl Vacuum

DOCA-salt Hypertension Model in Mice

Experiments were conducted using adult (12–16 weeks old) wildtype (WT) male C57Bl/6NJ mice purchased from Jackson Laboratory and housed in a humidity- and temperature-controlled facility following a 12-h light/dark cycle. Mice were fed standard mouse chow and water ad libitum. All animal studies were approved by the East Carolina University Animal Care and Use Committee (AUP #W254) and were performed per the National Institutes of Health Guidelines for the Care and Use of Laboratory Animals. Mice underwent a DOCA-salt hypertension paradigm as described previously [1 (link)]. Mice were briefly anesthetized with isoflurane (2%) and oxygen flow 1 L/min and placed on a heating pad to maintain body temperature. The mice underwent a uninephrectomy in which the right kidney was removed by making an incision to the skin in the retroperitoneal region. Mice were divided randomly into 4 groups (n = 12/group) and were then implanted subcutaneously with a DOCA-silicone sheet (DOCA group, DOCA:silicone = 1:3, DOCA 1 mg/g body weight) or an empty silicone sheet (Sham group). Pre- and post-operative care included buprenorphine injection to relieve pain (0.05 mg/kg, sc). The DOCA group were switched to 1% NaCl in drinking water and the sham group received autoclaved tap water. After the duration of the protocol, mice received heavy anesthesia using 5% isoflurane and were euthanized by decapitation. The brains were collected and stored at −80 °C until further use.

Theobald D, & Sriramula S. (2023). Kinin B1 Receptor Mediates Bidirectional Interaction between Neuroinflammation and Oxidative Stress. Antioxidants, 12(1), 150.

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Publication 2023

Adult Anesthesia Animals Animals, Laboratory Body Temperature Body Weight Brain Buprenorphine Decapitation Desoxycorticosterone Acetate High Blood Pressures Humidity Isoflurane Kidney Males Mice, House Mice, Inbred C57BL Oxygen Pain Postoperative Care Retroperitoneal Space Silicones Skin Sodium Chloride

Quantifying Superoxide Levels via DHE

Levels of reactive oxygen species (ROS) were identified by dihydroethidium (DHE), which is relatively specific for the measurement of superoxide. DHE will exhibit a blue fluorescence until it is oxidized and interacts with the cell’s DNA to produce a bright fluorescent red staining of the nucleus. Freshly cut brains from DOCA and Sham mice were incubated with 10 μM DHE (Invitrogen) in a light protected humidified chamber at 37 °C for 15 min. Primary neurons that were cultured and treated in 12-well plates on poly-L-lysine glass coverslips were given 10 μM DHE and incubated in a light protected humidified chamber at 37 °C for 15 min. Fluorescent images of the DOCA/Sham brains and the primary neurons were obtained with a fluorescent microscope (Echo Revolve). Mean fluorescence intensity of the image was measured using ImageJ software (NIH) for quantification. To supplement this, production of ROS was also measured by spectrofluorometry using DHE probes. The neurons were cultured in 48-well plates and were briefly treated for their respective group. Following this, 10 μM DHE was added for 15 min. The plate was read via spectrofluorometer (Tecan Infinite m200) and fluorescence was detected at an excitation wavelength of 488 nm and emission wavelength of 610 nm. Data are expressed as total fluorescence (relative fluorescent units, RFU).

Theobald D, & Sriramula S. (2023). Kinin B1 Receptor Mediates Bidirectional Interaction between Neuroinflammation and Oxidative Stress. Antioxidants, 12(1), 150.

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Publication 2023

Brain Cells Desoxycorticosterone Acetate Dietary Supplements dihydroethidium ECHO protocol Fluorescence Light Lysine M-200 Mice, Laboratory Microscopy Neurons Poly A Reactive Oxygen Species Red Nucleus Spectrometry, Fluorescence Superoxides

Top products related to «Desoxycorticosterone Acetate»

Doca pellet by Innovative Research

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Dimethyl sulfoxide (dmso) by Merck Group

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DMSO is a versatile organic solvent commonly used in laboratory settings. It has a high boiling point, low viscosity, and the ability to dissolve a wide range of polar and non-polar compounds. DMSO's core function is as a solvent, allowing for the effective dissolution and handling of various chemical substances during research and experimentation.

Tail cuff method by Kent Scientific

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The Tail-cuff method is a non-invasive technique used to measure blood pressure in small laboratory animals, such as mice and rats. The method involves placing a cuff around the animal's tail and using an automated detection system to measure systolic and diastolic blood pressure.

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Clarity western cl substrate by Bio-Rad

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Ta11pa c10 by Data Sciences International

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What are some common usages and applications of Desoxycorticosterone Acetate (DOCA)?

Desoxycorticosterone Acetate (DOCA) is a synthetic mineralocorticoid hormone commonly used in research to study the effects of excess mineralocorticoid activity on various physiological processes. It is frequently utilized to investigate the regulation of sodium, potassium, and water balance in the body, as well as its impacts on the cardiovascular system and kidney function. DOCA is an important tool for researchers working to understand the underlying mechanisms of conditions like hypertension, water-electrolyte imbalances, and other disorders related to mineralocorticoid excess.

What are some key differences between DOCA and other mineralocorticoid compounds?

While DOCA is a synthetic mineralocorticoid, there are important distinctions between it and naturally occurring mineralocorticoids like aldosterone. Unlike aldosterone, DOCA does not undergo the same metabolic pathways and has a longer half-life in the body. This makes DOCA a useful research tool to study the specific effects of mineralocorticoid receptor activation, without the confounding factors of other hormonal systems. Additionally, DOCA can be administered through various routes, such as subcutaneous implants or drinking water, allowing for more controlled and consistent dosing compared to naturally fluctuating levels of endogenous mineralocorticoids.

How can PubCompare.ai help optimize Desoxycorticosterone Acetate research?

PubCompare.ai is an AI-driven protocol comparison tool that can be extremely helpful in optimizing Desoxycorticosterone Acetate (DOCA) research. The platform allows researchers to more efficiently screen the literature and leverage AI to pinpoint critical insights. By using PubCompare.ai, you can identify the most effective and reproducible protocols related to DOCA for your specific research goals. The platform's advanced AI analysis can highlight key differences in protocol effectiveness, enabling you to choose the best option to ensure accuracy and reliability in your DOCA-related studies. This can lead to improved research outcomes and accelerate scientific discovery in this important area of study.

Are there any common challenges or considerations when working with Desoxycorticosterone Acetate?

One key consideration when using Desoxycorticosterone Acetate (DOCA) is the potential for off-target effects due to its potent mineralocorticoid activity. Researchers must carefully monitor for unintended physiological changes, such as hypertension, electrolyte imbalances, or fluid retention, and adjust dosing or administration routes accordingly. Additionally, DOCA can have varying degrees of bioavailability and potency depending on the formulation and delivery method used. It is important to consult the literature and, if possible, leverage a tool like PubCompare.ai to identify the most reproducible and effective DOCA protocols to minimize these challanges.

How does PubCompare.ai help researchers choose the best DOCA protocols for their studies?

PubCompare.ai's AI-driven analysis can be invaluable in helping researchers identify the most effective and reproducible Desoxycorticosterone Acetate (DOCA) protocols for their specific research goals. The platform's advanced comparisons can highlight key differences between protocol methodologies, dosing regimens, and outcome measures - allowing you to make informed decisions on the best approach. By leveraging PubCompare.ai, you can save time, reduce the risk of failed experiments, and improve the overall quality and translatability of your DOCA-related research. This cutting-edge tool empowers you to choose the most optimized protocols and drive scientific discovery in this important area of study.

More about "Desoxycorticosterone Acetate"

Desoxycorticosterone Acetate (DOCA) is a synthetic mineralocorticoid hormone that plays a crucial role in regulating sodium, potassium, and water balance within the body.
This versatile compound is extensively utilized in research to study the effects of excessive mineralocorticoid activity on the cardiovascular system, kidney function, and other physiological processes.
To optimize your DOCA research, PubCompare.ai, an AI-driven protocol comparison tool, can be a valuable asset.
This cutting-edge platform employs advanced AI comparisons to help you identify the most reproducible and effective methods from the literature, preprints, and patents.
By leveraging this tool, you can improve your research outcomes and drive scientific discovery in this important area of study.
DOCA is often administered in the form of DOCA pellets, which can be implanted subcutaneously to induce a state of mineralocorticoid excess.
The tail-cuff method is a common technique used to monitor blood pressure changes in DOCA-treated animals.
Additionally, DMSO (Dimethyl Sulfoxide) is sometimes used as a solvent for DOCA in various experiments.
Key subtopics related to DOCA research include the use of ChemiDoc XRS for Western blot analysis, N,N-dimethylformamide as a solvent, Clarity Western Cl substrate for enhanced chemiluminescence, and various antibodies like TA11PA-C10 and BP-98A for detecting DOCA-related proteins.
The renin-angiotensin system, with Angiotensin II (Ang II) playing a significant role, is another important aspect to consider in DOCA-related studies.
PVDF (Polyvinylidene Fluoride) membranes are often utilized for Western blotting in DOCA research, providing a reliable platform for protein detection and analysis.
By incorporating these relevant terms and techniques, you can optimize your DOCA research and unlock new insights into the complex mechanisms governing fluid and electrolyte homeostasis.