Aldosterone Receptors - Explore the Science & Experts | ideXlab

Scan Science and Technology

Contact Leading Edge Experts & Companies

Aldosterone Receptors

The Experts below are selected from a list of 60 Experts worldwide ranked by ideXlab platform

Jose Nascimento – 1st expert on this subject based on the ideXlab platform

  • 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, 2014
    Co-Authors: Silvio Rodrigues Marquesneto, Emanuelle B Ferraz, Deivid C Rodrigues, Brian Njaine, Edson Rondinelli, Antonio Carlos Campos De Carvalho, Jose Nascimento

    Abstract:

    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.

  • the blockade of angiotensin at1 and Aldosterone Receptors protects rats from synthetic androgen induced cardiac autonomic dysfunction
    Acta Physiologica, 2013
    Co-Authors: S Marques R Neto, A Da H Silva, Dos M Santos, E F Ferraz, Jose Nascimento

    Abstract:

    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 – 2nd expert on this subject based on the ideXlab platform

  • characterization of renal Aldosterone Receptors in genetically hypertensive rats
    American Journal of Physiology-renal Physiology, 1993
    Co-Authors: Masatsugu Horiuchi, Hisashi Nishiyama, Junkichi Hama, Toshihiko Takenaka, Hirokazu Kondo, Hirofumi Kino, Shuzo Nagata, Keiichi Sugimura, Ryo Katori

    Abstract:

    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 – 3rd expert on this subject based on the ideXlab platform

  • novel Aldosterone Receptors specificity conferring mechanism at the level of the cell membrane
    Steroids, 1994
    Co-Authors: Martin Wehling

    Abstract:

    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.