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Search results for: Aldosterone 21-Acetate C23H30O6 CAS: 2827-21-6

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#33101347   2020/09/25 To Up

Amaranth as a Source of Antihypertensive Peptides.

Amaranth is an ancestral crop used by pre-Columbian cultures for 6000 to 8000 years. Its grains have a relevant chemical composition not only from a nutritional point of view but also due to the contribution of components with good techno-functional properties and important potential as bioactive compounds. Numerous studies have shown that amaranth storage proteins possess encrypted sequences that, once released, exhibit different physiological activities. One of the most studied is antihypertensive activity. This review summarizes the progress made over the last years (2008-2020) related to this topic. Studies related to inhibition of different enzymes of the Renin-Angiotensin-Aldosterone system, in particular Angiotensin Converting Enzyme (ACE) and Renin, as well as those referring to potential modulation mechanisms of tissue or local Renin-Angiotensin-Aldosterone system, are analyzed, including , , , and assays. Furthermore, the potential use of these bioactive peptides or products containing them, in the elaboration of functional food matrices is discussed. Finally, the most relevant conclusions and future requirements in research and development of food products are presented.
Agustina E Nardo, Santiago Suárez, Alejandra V Quiroga, María Cristina Añón

1342 related Products with: Amaranth as a Source of Antihypertensive Peptides.

100ul 100ul 100ul 100ul 100ul50ul100ug 100ul50ul1ml100ug 100ul

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#32852721   // To Up

Renin-Angiotensin-Aldosterone System Inhibitors and Risk of Death in Patients Hospitalised with COVID-19: A Retrospective Italian Cohort Study of 43,000 Patients.

The epidemic due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been spreading globally, raising increasing concerns. There are several controversial hypotheses on the potentially harmful or beneficial effects of antihypertensive drugs acting on the renin-angiotensin-aldosterone system (RAAS) in coronavirus disease 2019 (COVID-19). Furthermore, there is accumulating evidence, based on several observational studies, that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) do not increase the risk of contracting SARS-CoV-2 infection. On the other hand, conflicting findings regarding the role of ACEIs/ARBs as prognosis modifiers in COVID-19 hospitalised patients have been reported.
Gianluca Trifirò, Marco Massari, Roberto Da Cas, Francesca Menniti Ippolito, Janet Sultana, Salvatore Crisafulli, Paolo Giorgi Rossi, Massimiliano Marino, Manuel Zorzi, Emanuela Bovo, Olivia Leoni, Monica Ludergnani, Stefania Spila Alegiani,

2188 related Products with: Renin-Angiotensin-Aldosterone System Inhibitors and Risk of Death in Patients Hospitalised with COVID-19: A Retrospective Italian Cohort Study of 43,000 Patients.

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#32556536   2020/06/17 To Up

The physiological and molecular mechanisms to maintain water and salt homeostasis in response to high salt intake in Mongolian gerbils (Meriones unguiculatus).

Desert rodents are faced with many challenges such as high dietary salt in their natural habitats and they have evolved abilities to conserve water and tolerate salt. However, the physiological and molecular mechanisms involved in water and salt balances in desert rodents are unknown. We hypothesized that desert rodents regulated water and salt balances by altering the expression of AQP2 and α-ENaC in the kidney. Mongolian gerbils (Meriones unguiculatus), a desert species, were acclimated to drinking water with different salt contents: (0, control; 4% NaCl, moderate salt, MS; 8% NaCl, high salt, HS) for 4 weeks. The gerbils drinking salty water had lower body mass, food intake, water intake, metabolic water production and urine volume. The HS gerbils increased the expression of arginine vasopressin (AVP) in the hypothalamus, and also enhanced the expression of AQP2 and cAMP/PKA/CREB signaling pathway in the kidney. In addition, these gerbils reduced serum aldosterone levels and α-ENaC expression in the kidney. Creatinine clearance was lower in the HS group than that in the control group, but serum and urine creatinine levels did not change. These data indicate that desert rodents rely on AVP-dependent upregulation of AQP2 and aldosterone-dependent downregulation of α-ENaC in the kidney to promote water reabsorption and sodium excretion under high salt intake.
Zahra Nouri, Xue-Ying Zhang, De-Hua Wang

2768 related Products with: The physiological and molecular mechanisms to maintain water and salt homeostasis in response to high salt intake in Mongolian gerbils (Meriones unguiculatus).

1 G100 mg1mg 1 G 500 G96 wells (1 kit)96 wells

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#32469228   2020/05/29 To Up

Pharmacological suppression of endogenous glucocorticoid synthesis attenuated blood pressure and heart rate response to acute restraint in Wistar rats.

Glucocorticoids (GCS) are known to modulate cardiovascular response during stress conditions. The present study was aimed to test the hypothesis that permissive and/or stimulating effect of GCs is essential for the maintenance of peripheral vascular resistance and for the adequate response of cardiovascular system to stressor exposure. The effects of acute pharmacological adrenalectomy (PhADX) on humoral and cardiovascular parameters were studied in adult Wistar rats under the basal conditions and during the acute restraint stress. Acute PhADX was performed by the administration of metyrapone and aminoglutethimide (100 mg/kg s.c. of each drug) resulting in a suppression of endogenous glucocorticoid synthesis. Blood pressure (BP), heart rate (HR) and core body temperature were measured using radiotelemetry. BP responses to administration of vasoactive agents were determined in pentobarbital-anesthetized animals. PhADX considerably attenuated stress-induced increase of BP, HR and core body temperature. PhADX did not abolish BP and HR lowering effects of ganglionic blocker pentolinium indicating preserved sympathetic function in PhADX rats. BP response to exogenous norepinephrine administration was attenuated in PhADX rats, suggesting reduced sensitivity of cardiovascular system. Suppression of corticosterone synthesis by PhADX increased basal plasma levels of ACTH, aldosterone and plasma renin activity in unstressed animals but there was no further increase of these hormones following stressor exposure. In conclusion, PhADX attenuated stress-induced rise of blood pressure, heart rate and core body temperature indicating an important permissive and/or stimulating role of glucocorticoids in the maintenance of the adequate response of cardiovascular system and thermoregulation to several stimuli including acute exposure to stressor.
M Bencze, A Vavřínová, J Zicha, M Behuliak

2673 related Products with: Pharmacological suppression of endogenous glucocorticoid synthesis attenuated blood pressure and heart rate response to acute restraint in Wistar rats.

100 UG100 mg5096T1 kit1 mg50 µg1096T

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#31527789   2019/09/17 To Up

Sympathectomy-induced blood pressure reduction in adult normotensive and hypertensive rats is counteracted by enhanced cardiovascular sensitivity to vasoconstrictors.

The effect of chemical sympathectomy on cardiovascular parameters and the compensatory role of adrenal hormones, the renin-angiotensin system, and cardiovascular sensitivity to vasoconstrictors were studied in spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. Sympathectomy was induced in 20-week-old rats by daily intraperitoneal guanethidine administration (30 mg/kg b.w.) for 2 weeks. Basal blood pressure (BP), heart rate (HR), and restraint stress-induced cardiovascular changes were measured by radiotelemetry. The BP response to catecholamines was determined in rats with implanted catheters. Sympathectomy decreased BP only transiently, and after 14-day guanethidine treatment, BP returned to basal values in both strains. Sympathectomy permanently lowered HR, improved baroreflex sensitivity, and decreased the low-frequency domain of systolic blood pressure variability (a marker of vascular sympathetic activity). Guanethidine also attenuated the BP and HR responses to restraint stress. On the other hand, the BP response to catecholamines was augmented in sympathectomized rats, and this was not due to the de novo synthesis of vascular adrenergic receptors. Sympathectomy caused adrenal enlargement, enhanced the expression of adrenal catecholamine biosynthetic enzymes, and elevated plasma adrenaline levels in both strains, especially in WKY rats. Guanethidine also increased the plasma levels of aldosterone and corticosterone in WKY rats only. In conclusion, sympathectomy produced a transient decrease in BP, a chronic decrease in HR and improvement in baroreflex sensitivity. The effect of sympathectomy on BP was counteracted by increased vascular sensitivity to catecholamines in WKY rats and SHRs and/or by the enhanced secretion of adrenal hormones, which was more pronounced in WKY rats.
Anna Vavřínová, Michal Behuliak, Michal Bencze, Martin Vodička, Peter Ergang, Ivana Vaněčková, Josef Zicha

2820 related Products with: Sympathectomy-induced blood pressure reduction in adult normotensive and hypertensive rats is counteracted by enhanced cardiovascular sensitivity to vasoconstrictors.

50 ul50 ul100 ul100 ul100ug Lyophilized100ug Lyophilized100ug Lyophilized96 tests100ug Lyophilized100ug Lyophilized100ug Lyophilized100 μg

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#30542083   2018/12/12 To Up

Association of ACE2 genetic polymorphisms with hypertension-related target organ damages in south Xinjiang.

Essential hypertension (EH) is a principal contributing factor in worldwide cardiovascular disease mortality. Although interventions that minimize environmental risk factors for EH are associated with reduced cardiovascular disease, such approaches are limited for individuals with high genetic EH risk. In this study, we investigated possible associations between ACE2 polymorphisms and hypertension-related target organ damages in south Xinjiang, China. Four hundred and two hypertensive patients were enrolled as study participants in an EH group, and 233 normotensive individuals were enrolled as control subjects. Participants were recruited from the south Xinjiang region. Fourteen ACE2 polymorphisms were genotyped by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Risk genotypes of rs2074192 (TT+CT, OR = 1.72, 95% CI: 1.17-2.53), rs2106809 (TT, OR = 1.71, 95% CI: 1.13-2.58), rs4240157 (CC+CT, OR = 1.99, 95% CI: 1.17-3.41), rs4646155 (TT+CT, OR = 1.94, 95% CI: 1.06-3.54), rs4646188 (TT+CT, OR = 3.25, 95% CI: 1.95-5.41), rs4830542 (CC+CT, OR = 1.88, 95% CI: 1.10-3.23), and rs879922 (CC+CG, OR = 4.86, 95% CI: 2.74-8.64) were associated with EH. Hypertensive patients carrying the control genotype of rs2074192 (CC, OR = 2.37, 95% CI: 1.28-4.39) were associated with CAS ≥50%, while those carrying a high-EH-risk genotype of rs4240157 (OR = 2.62, 95% CI: 1.24-5.54), rs4646155 (OR = 2.44, 95% CI: 1.16-5.10), or rs4830542 (CC+CT, OR = 2.20, 95% CI: 1.03-4.69) were associated with atrial fibrillation (AF), larger left atrial diameter, and higher levels of renin-angiotensin-aldosterone system (RAAS) activation (renin and angiotensin I/II). In conclusion, the ACE2 variant rs2074192 was associated with EH and EH with CAS ≥50%, while 3 ACE2 variants (rs4240157, rs4646155, and rs4830542) were associated with EH- and hypertension-related AF and left atrial remodeling in south Xinjiang, China.
Yi Luo, Cheng Liu, Tianwang Guan, Yanfang Li, Yanxian Lai, Fang Li, Haiyan Zhao, Tutiguli Maimaiti, Abudurexiti Zeyaweiding

1105 related Products with: Association of ACE2 genetic polymorphisms with hypertension-related target organ damages in south Xinjiang.

1mg0.1ml2 Pieces/Box

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#29972645   2018/07/16 To Up

Treatment of sleep apnea with a combination of a carbonic anhydrase inhibitor and an aldosterone antagonist: a patent evaluation of CA2958110 and IN6616DEN2012.

Sleep apnoea syndrome (SAS), is a sleep disorder and characterized by very shallow breath or repetitive cessation of breathing during sleep (sleep apnoea). At present, no pharmacological agents have proved to be successful against SAS, and the syndrome is only treated by surgical interventions or devices such as intraoral mandibular advancement and Continuous Positive Air Pressure (CPAP) techniques. Areas covered: two patents published in 2016 describing a new pharmacological application of inhibitors of the metalloenzyme Carbonic Anhydrases (CAs, EC 4.2.1.1) and an aldosterone antagonist agents and their therapeutic application was analysed. Expert opinion: The present patents address an important healthcare problem by proposing a new pharmacological approach and may represent a valid alternative for the treatment of sleep apnea. One of the interesting points raised by these patents is the advantage of using a minor quantity of pharmacological agents in combination than active agent alone and consequently, a significant reduction of the side effects.
Andrea Angeli, Claudiu T Supuran

1601 related Products with: Treatment of sleep apnea with a combination of a carbonic anhydrase inhibitor and an aldosterone antagonist: a patent evaluation of CA2958110 and IN6616DEN2012.

5mg100ul1,000 tests50 ug 100ug1 mg25 mg1000 tests 5 G2.5 mg100ug

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#29717226   2018/05/01 To Up

Aldosterone Impairs Mitochondrial Function in Human Cardiac Fibroblasts via A-Kinase Anchor Protein 12.

Aldosterone (Aldo) contributes to mitochondrial dysfunction and cardiac oxidative stress. Using a proteomic approach, A-kinase anchor protein (AKAP)-12 has been identified as a down-regulated protein by Aldo in human cardiac fibroblasts. We aim to characterize whether AKAP-12 down-regulation could be a deleterious mechanism which induces mitochondrial dysfunction and oxidative stress in cardiac cells. Aldo down-regulated AKAP-12 via its mineralocorticoid receptor, increased oxidative stress and induced mitochondrial dysfunction characterized by decreased mitochondrial-DNA and Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) expressions in human cardiac fibroblasts. CRISPR/Cas9-mediated knock-down of AKAP-12 produced similar deleterious effects in human cardiac fibroblasts. CRISPR/Cas9-mediated activation of AKAP-12 blunted Aldo effects on mitochondrial dysfunction and oxidative stress in human cardiac fibroblasts. In Aldo-salt-treated rats, cardiac AKAP-12, mitochondrial-DNA and PGC-1α expressions were decreased and paralleled increased oxidative stress. In myocardial biopsies from patients with aortic stenosis (AS, n = 26), AKAP-12, mitochondrial-DNA and PGC-1α expressions were decreased as compared to Controls (n = 13). Circulating Aldo levels inversely correlated with cardiac AKAP-12. PGC-1α positively associated with AKAP-12 and with mitochondrial-DNA. Aldo decreased AKAP-12 expression, impairing mitochondrial biogenesis and increasing cardiac oxidative stress. AKAP-12 down-regulation triggered by Aldo may represent an important event in the development of mitochondrial dysfunction and cardiac oxidative stress.
Jaime Ibarrola, Rafael Sadaba, Ernesto Martinez-Martinez, Amaia Garcia-Peña, Vanessa Arrieta, Virginia Alvarez, Amaya Fernández-Celis, Alicia Gainza, Victoria Cachofeiro, Enrique Santamaria, Joaquin Fernandez-Irigoyen, Frederic Jaisser, Natalia Lopez-Andres

2877 related Products with: Aldosterone Impairs Mitochondrial Function in Human Cardiac Fibroblasts via A-Kinase Anchor Protein 12.

100ug Lyophilized2ug100ug Lyophilized96T100 100 μg10 5ug100 μg2ug100 ug/vial100ug Lyophilized

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#28939891   2017/09/22 To Up

Differential Proteomics Identifies Reticulocalbin-3 as a Novel Negative Mediator of Collagen Production in Human Cardiac Fibroblasts.

Cardiac fibrosis is characterized by an excessive accumulation of extracellular matrix components, including collagens. Galectin-3 (Gal-3) and Cardiotrophin-1 (CT-1) are two profibrotic molecules that mediate Aldosterone (Aldo)-induced cardiac fibrosis. However the underlying mechanisms are not well defined. Our aim is to characterize changes in the proteome of human cardiac fibroblasts treated with Aldo, Gal-3 or CT-1 to identify new common proteins that might be new therapeutic targets in cardiac fibrosis. Using a quantitative proteomic approach in human cardiac fibroblasts, our results show that Aldo, Gal-3 and CT-1 modified the expression of 30, 17 and 89 proteins respectively, being common the reticulocalbin (RCN) family members. RCN-3 down-regulation triggered by Aldo, Gal-3 and CT-1 was verified. Treatment with recombinant RCN-3 decreased collagens expression in human cardiac fibroblasts through Akt phosphorylation. Interestingly, CRISPR/Cas9-mediated activation of RCN-3 decreased collagen production in human cardiac fibroblasts. In addition, recombinant RCN-3 blocked the profibrotic effects of Aldo, Gal-3 and CT-1. Interestingly, RCN-3 blunted the increase in collagens expression induced by other profibrotic stimuli, angiotensin II, in human cardiac fibroblasts. Our results suggest that RCN-3 emerges as a new potential negative regulator of collagen production and could represent a therapeutic target in the context of cardiac fibrosis.
Ernesto Martínez-Martínez, Jaime Ibarrola, Amaya Fernández-Celis, Enrique Santamaria, Joaquín Fernández-Irigoyen, Patrick Rossignol, Frederic Jaisser, Natalia López-Andrés

2970 related Products with: Differential Proteomics Identifies Reticulocalbin-3 as a Novel Negative Mediator of Collagen Production in Human Cardiac Fibroblasts.

100 μg96 samples

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#28722461   // To Up

[Disorders of water and electrolyte metabolism and changes in acid-base balance in patients with ascitic liver cirrhosis].

In patients with advanced cirrhosis with ascites disorders of water and electrolyte metabolism are often present and they are associated with changes in acid-base balance. These changes can be very complicated, their diagnosis and treatment difficult. Dilutional hyponatremia is the most common disorder. Hyponatremia in these patients is associated with increased morbidity and mortality before and after liver transplantation. Other common disorders include hyperchloremic acidosis, hypokalemia, metabolic alkalosis, lactic acidosis, respiratory alkalosis. If renal impairment occurs (for example hepatorenal syndrome), metabolic acidosis and retention of acid metabolites may develop. The pathogenesis of these conditions applies primarily hemodynamic changes. Activation of renin-angiotensin-aldosterone system and non-osmotic stimulation of antidiuretic hormone trigger serious changes in water and natrium-chloride metabolism. This activation is clinically expressed like oedema, ascites, hydrothorax, low to zero natrium concentration in urine and increased urinary osmolality, which is higher than serum osmolality. In practice, the evaluation can be significantly modified by the ongoing diuretic therapy. Closer monitoring of water and electrolyte metabolism together with acid-base balance in patients with ascitic liver cirrhosis is important, not only in terms of diagnosis but especially in terms of therapy.
Halima Gottfriedová, Miroslava Horáčková, Milena Čáslavská, Julius Špičák, Otto Schück

1169 related Products with: [Disorders of water and electrolyte metabolism and changes in acid-base balance in patients with ascitic liver cirrhosis].

100ug Lyophilized100ug Lyophilized 100 G96 tests

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