The Experts below are selected from a list of 60 Experts worldwide ranked by ideXlab platform
Jose Nascimento - One of the best experts on this subject based on the ideXlab platform.
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at1 and Aldosterone Receptors blockade prevents the chronic effect of nandrolone on the exercise induced cardioprotection in perfused rat heart subjected to ischemia and reperfusion
Cardiovascular Drugs and Therapy, 2014Co-Authors: Silvio Rodrigues Marquesneto, Emanuelle B Ferraz, Deivid C Rodrigues, Brian Njaine, Edson Rondinelli, Antonio Carlos Campos De Carvalho, Jose NascimentoAbstract:Purpose Myocardial tolerance to ischaemia/reperfusion (I/R) injury is improved by exercise training, but this cardioprotection is impaired by the chronic use of anabolic androgenic steroids (AAS). The present study evaluated whether blockade of angiotensin II receptor (AT1-R) with losartan and Aldosterone receptor (mineralocorticoid receptor, MR) with spironolactone could prevent the deleterious effect of AAS on the exercise-induced cardioprotection.
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the blockade of angiotensin at1 and Aldosterone Receptors protects rats from synthetic androgen induced cardiac autonomic dysfunction
Acta Physiologica, 2013Co-Authors: S Marques R Neto, A Da H Silva, Dos M Santos, E F Ferraz, Jose NascimentoAbstract:Aim This study aimed to evaluate the combined effects of exercise and antagonists of the angiotensin II and Aldosterone Receptors on cardiac autonomic regulation and ventricular repolarization in rats chronically treated with nandrolone decanoate (ND), a synthetic androgen. Methods Thirty male Wistar rats were divided into six groups: sedentary, trained, ND-treated, trained and ND-treated, trained and treated with both ND and spironolactone, and trained and treated with both ND and losartan. ND (10 mg kg−1 weekly) and the antagonists (20 mg kg−1 daily) of the angiotensin II AT1 (losartan) and Aldosterone (spironolactone) Receptors were administered for 8 weeks. Exercise training was performed using a treadmill five times each week for 8 weeks. Following this 8-week training and treatment period, electrocardiogram recordings were obtained to determine the time and frequency domains of heart rate variability (HRV) and corrected QT interval (QTc). Results Nandrolone decanoate treatment increased the QTc interval and reduced the parasympathetic indexes of HRV (RMSSD, pNN5 and high-frequency power) in sedentary and trained rats. The ratio between low- and high-frequency power (LF/HF) was higher in ND-treated groups. Both losartan and spironolactone treatments prevented the effects of ND on the QTc interval and the HRV parameters (RMSSD, pNN5, high-frequency power, and the LF/HF ratio). Conclusion Our results show that chronic treatment with a high dose of ND induces cardiac parasympathetic dysfunction and disturbances in ventricular repolarization in both sedentary and exercised rats. Furthermore, inhibiting the renin-angiotensin-Aldosterone system using losartan, or spironolactone, prevented these deleterious effects.
Ryo Katori - One of the best experts on this subject based on the ideXlab platform.
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characterization of renal Aldosterone Receptors in genetically hypertensive rats
American Journal of Physiology-renal Physiology, 1993Co-Authors: Masatsugu Horiuchi, Hisashi Nishiyama, Junkichi Hama, Toshihiko Takenaka, Hirokazu Kondo, Hirofumi Kino, Shuzo Nagata, Keiichi Sugimura, Ryo KatoriAbstract:To investigate the Aldosterone responsiveness of genetically hypertensive rats, we compared characteristics of renal cytosolic Aldosterone Receptors from the M strain of stroke-prone, spontaneously hypertensive rats (M-SHRSP) with normotensive Wistar-Kyoto rats (WKY). In M-SHRSP, blood pressure was elevated significantly at 6 wk of age, when their plasma Aldosterone concentrations were similar to those in WKY. Decreases in urine volume and sodium excretion were also observed in M-SHRSP. At 10 wk of age, M-SHRSP plasma Aldosterone concentrations became significantly higher than those in WKY. On the other hand, the concentration of renal cytosolic Aldosterone Receptors (type I, Aldosterone specific) had already increased at 6 wk of age in M-SHRSP, with no difference in affinity, and levels remained increased thereafter. There were no significant differences in molecular weights or ionic charges of either "activated" or "non-activated" Aldosterone-receptor complexes between M-SHRSP and WKY, indicating that the molecular properties were similar in both groups. These results suggest that the increased concentration of Aldosterone Receptors in the kidneys of M-SHRSP might increase their Aldosterone responsiveness and contribute to the development of high blood pressure in these animals.
Martin Wehling - One of the best experts on this subject based on the ideXlab platform.
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novel Aldosterone Receptors specificity conferring mechanism at the level of the cell membrane
Steroids, 1994Co-Authors: Martin WehlingAbstract:Abstract Functional studies in extra-renal, nonepithelial cells such as smooth muscle cells and more recently circulating human lymphocytes have provided increasing evidence that Aldosterone produces not only classical genomic effects, but also rapid non-genomic effects on transmembrane electrolyte movements. These involve activation of the sodium/proton-exchanger of the cell membrane at very low, physiological concentrations of Aldosterone with an acute onset within 1–2 minutes. A second messenger cascade involved is the inositol-1,4,5,-trisphosphate/calcium pathway which responds over the same rapid time course. Such changes clearly cannot be explained by genomic mechanisms, which are responsible for later effects than the membrane-related rapid responses. In addition to its rapid time course the unique characteristics of this new pathway for steroid action include a 10000-fold selectivity for Aldosterone over cortisol and the ineffectiveness of spironolactones, classical mineralocorticoid antagonists, as antagonists of the response. Subsequently binding sites have been demonstrated in the plasma membrane of human lymphocytes which show pharmacological (Aldosterone specificity) and kinetic (high turnover) properties idetical with those of the rapid Aldosterone effects in the same cells. SDS-PAGE analysis of the receptor protein has shown a molecular weight of ∼50 kd. The present paper reviews the data supporting a new, two-step model for non-genomic and genomic Aldosterone effects. It also suggests a novel specificity-conferring mechanism for mineralocorticoid action at the membrane level.
Decio Armanini - One of the best experts on this subject based on the ideXlab platform.
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choice of diuretic therapy and reconsideration for Aldosterone Receptors blockers
Hypertension, 2010Co-Authors: Decio Armanini, Cristina FioreAbstract:To the Editor: In an interesting editorial, Kaplan1 has focused recently on the choice of thiazide diuretics and concluded that chlorthalidone, alone or in addition to other antihypertensive drugs, may replace hydrochlorothiazide (HCTZ). The author also states that HCTZ and chlorthalidone, even at low doses (12.5 to 25.0 mg), can lower serum potassium and that an addition of small doses of spironolactone or eplerenone could provide maximal antihypertensive efficacy and prevent hypokalemia, particularly in resistant patients. A very important issue dealing with all diuretics is the volume depletion and activation of the renin-angiotensin-Aldosterone system. Diuretics, with the exception of Aldosterone receptor blockers, do not directly affect …
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transient pseudo hypoaldosteronism following resection of the ileum normal level of lymphocytic Aldosterone Receptors outside the acute phase
Journal of Endocrinological Investigation, 1999Co-Authors: Mariechristine Vantyghem, Decio Armanini, C Hober, A Evrard, A Ghulam, D Lescut, A Racadot, J P Triboulet, J LefebvreAbstract:Pseudo-hypoaldosteronism (PHA) is due to mineralocorticoid resistance and manifests as hyponatremia and hyperkalemia with increased plasma Aldosterone levels. It may be familial or secondary to abnormal renal sodium handling. We report the case of a 54-year-old woman with multifocal cancer of the colon, who developed PHA after subtotal colectomy, ileal resection and jejunostomy. She was treated with 6 g of salt daily to prevent dehydration, which she stopped herself because of reduced fecal losses. One month later she was admitted with signs of acute adrenal failure, i.e. fatigue, severe nausea, blood pressure of 80/60 mmHg, extracellular dehydration, hyponatremia (118 mmol/l); hyperkalemia (7.6 mmol/l), increased blood urea nitrogen (BUN) (200 mg/dl) and creatininemia (2.5 mg/dl), and decreased plasma bicarbonates level (HCO3-: 16 mmol/l; N: 27- 30). However, the plasma cortisol was high (66 μg/100 ml at 10:00 h; N: 8-15) and the ACTH was normal (13 pg/ml, N: 10-60); there was a marked increase in plasma renin activity (>37 ng/ml/h; N supine 2000 pg/ml; N supine <150) and plasma AVP (20 pmol/l; N: 0.5-2.5). The plasma ANH level was 38 pmol/l (N supine: 5-25). A urinary steroidogram resulted in highly elevated tetrahydrocortisol (THF: 13.3 mg/24h; N: 1.4±0.8) with no increase in tetrahydrocortisone (THE: 3.16 mg/24h; N: 2.7±2.0) excretion, and with low THE/THF (0.24; N: 1.87±0.36) and α THF/THF (0.35; N: 0.92±0.42) ratios. The number of mineralocorticoid Receptors in mononuclear leukocytes was in the lower normal range for age, while the number of glucocorticoid Receptors was reduced. Small-bowel resection in ileostomized patients causes excessive fecal sodium losses and results in chronic sodium depletion with contraction of the plasma volume and severe secondary hyperaldosteronism. Nevertheless, this hyperaldosteronism may be associated with hyponatremia and hyperkalemia suggesting PHA related to the major importance of the colon for the absorption of sodium. In conclusion, this case report emphasizes 1) the possibility of a syndrome of acquired PHA with severe hyperkalemia after resection of the ileum and colon responding to oral salt supplementation; 2) the major increase in AVP and the small increase in ANH; 3) the strong increase in urinary THF with low THE/THF and α THF/THF ratios; 4) the normal number of lymphocytic mineralocorticoid Receptors outside the acute episode.
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transient pseudohypoaldosteronism in obstructive renal disease with transient reduction of lymphocytic Aldosterone Receptors results in two affected infants
Hormone Research in Paediatrics, 1993Co-Authors: U Kuhnle, Graziella Guariso, M Sonega, Gk Hinkel, W Hubl, Decio ArmaniniAbstract:We report two patients with transient pseudohypoaldosteronism due to obstructive renal disease. Both patients presented with a salt-losing episode simulating adrenal insufficiency. In one patient, transient reduction of Aldosterone Receptors could be documented, while in the second patient the clinical and biochemical parameters were consistent with transient pseudohypoaldosteronism. Aldosterone Receptors were normal in both patients when studied after the surgical correction of the obstruction.
H. Oberleithner - One of the best experts on this subject based on the ideXlab platform.
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Aldosterone receptor sites on plasma membrane of human vascular endothelium detected by a mechanical nanosensor
Pflügers Archiv - European Journal of Physiology, 2008Co-Authors: L. Wildling, P. Hinterdorfer, K. Kusche-vihrog, Y. Treffner, H. OberleithnerAbstract:The mineralocorticoid hormone Aldosterone acts on target cells of kidney, colon, and the cardiovascular system through genomic and nongenomic pathways. Although the classical intracellular mineralocorticoid receptor plays a key role in mediating both pathways, it is unclear whether there are specific Aldosterone Receptors located on the cell surface. To search for such sites in vascular endothelium, we used an atomic force microscope (AFM) which measures unbinding forces based on single molecular recognition between an Aldosterone-loaded AFM tip and the cell membrane. Aldosterone was tethered covalently via linker molecules to an AFM tip. Human endothelial cells (EA.hy926) were grown in culture and studied in buffer at 37°C. Using the Aldosterone-functionalized AFM tip as a mechanical nanoscale indenter, unbinding forces could be measured at randomly chosen sites of the plasma membrane. Sites with strong interactions between AFM tip and cell surface could be identified exhibiting unbinding forces of about 65 pN. The binding probability between the Aldosterone-loaded tip and the cell surface at selected membrane sites was 53 ± 7.2%. Addition of an excess supply of Aldosterone to the bath solution blocked the binding of the Aldosterone-loaded tip to the cell surface. The binding probability was reduced to 8.0 ± 1.8% when an excess supply of Aldosterone was added to the bath. However, it was not influenced by the addition of spironolactone or dexamethasone. We conclude that Aldosterone receptor sites exist on the cell surface of vascular endothelial cells distinct from the classical mineralocorticoid Receptors and insensitive to glucocorticoids. Binding of Aldosterone to these Receptors initiates an intracellular signaling cascade that precedes the classical genomic response and most likely participates in the control of vascular resistance.
