276°
Posted 20 hours ago

Healthgo Blood Pressure Regulator Ring,Healthgo Blood Glucose Control Ring,Adjustable Blood Pressure Regulator Ring,Healthgo Ring (8SET)

£9.9£99Clearance
ZTS2023's avatar
Shared by
ZTS2023
Joined in 2023
82
63

About this deal

Canessa, C. M., Schild, L., Buell, G., Thorens, B., Gautschi, I., Horisberger, J. D., et al. (1994). Amiloride-sensitive epithelial Na+ channel is made of three homologous subunits. Nature 367, 463–467. Disruption in K + transport in GC is implicated in multiple aldosterone-related diseases. The deletion of TASK 1 and 3 causes primary hyperaldosteronism (PH) and low-renin essential hypertension, respectively, due to constant depolarization of GC membrane in mice ( Davies et al., 2008; Guagliardo et al., 2012). Mutations in another K + channel, a homotetrameric inward rectifier potassium channel (KCNJ5), are associated with (APA) and PH ( Ishihara et al., 2009; Choi et al., 2011; Monticone et al., 2012; Mulatero et al., 2012; Williams et al., 2015). These mutations increase aldosterone production due to altered channel selectivity leading to depolarization of the membrane ( Scholl et al., 2012; Oki et al., 2012b). In fact, ANG II-mediated regulation of aldosterone synthesis can occur by downregulating the expression of KCNJ5 ( Kanazirska et al., 1992). Overexpression of KCNJ5 blunts ANG II stimulatory effects on membrane potential, intracellular Ca 2+, and expression of STAR and ADS ( Oki et al., 2012a). Adrenocorticotropic Hormone Kanazirska, M. V., Vassilev, P. M., Quinn, S. J., Tillotson, D. L., and Williams, G. H. (1992). Single K+ channels in adrenal zona glomerulosa cells. II. Inhibition by angiotensin II. Am. J. Phys. 263, E760–E765. While it is clear that ACTH induces aldosterone synthesis, this effect seems to be transient. At first ACTH increases aldosterone synthesis of GC cells; however, after continuous induction by ACTH, GC phenotype changes to that of zona fasciculata leading to a decrease in aldosterone synthesis ( Crivello and Gill, 1983). In vivo findings are consistent with these results. Since ACTH is released in a pulsatile fashion in humans, Seely et al. (1989) investigated the effect of pulsatile and prolonged infusion of ACTH on aldosterone levels ( Seely et al., 1989). Pulsatile infusion resulted in an increase and maintenance of aldosterone, while prolonged infusion led to sharp increase followed by a continuous decrease in aldosterone levels ( Seely et al., 1989). These effects cannot be explained by sodium, potassium, angiotensin-II, or cortisol as their levels were the same in both groups, thus the mechanisms that govern these effects remain unknown. GC ADS mRNA levels were significantly increased and then dramatically decreased at 3 and 24h after ACTH treatment in rats, respectively ( Holland and Carr, 1993). Chronic infusion of ACTH for 2–3weeks resulted in disappearance of GC and consequently a decrease in aldosterone production ( Mitani et al., 1996). Similar transient effects of ACTH on aldosterone levels are seen in human male subjects ( Fuchs-Hammoser et al., 1980).

Blood Pressure Regulator Ring, Adjustable HealthGo Healthgo Blood Pressure Regulator Ring, Adjustable HealthGo

Although the accepted notion is that aldosterone is produced solely by adrenal glands, some studies have shown that the heart can synthesize aldosterone in response to stress. RT-PCR analyses showed expression of CYP11A1 and CYP21, the genes encoding steroidogenic enzymes involved in aldosterone synthesis, in adult human tissues (atria, ventricles, aorta apex, and intraventricular septum), and expression of CYP11B2 in the aorta and fetal heart ( Kayes-Wandover and White, 2000). Genetically hypertensive adrenalectomized and angiotensin II-treated rats had increased activity of ADS and produced aldosterone ( Takeda et al., 2000). Interestingly, expression of CYP11B2 was detectable by RT-PCR in failing human hearts, but not in normal hearts ( Young et al., 2001). Bose et al. (2021) most recently reported a novel mitochondrial complex consisting of ADS, mitochondrial translocase receptor (Tom22), and STAR. This complex is responsible for the production of aldosterone in rat hearts upon stress. However, the ability of the heart to produce aldosterone is still controversial. More studies are needed to elucidate the mechanisms responsible for cardiac aldosterone synthesis. Angiotensin IILe, T., and Schimmer, B. P. (2001). The regulation of MAPKs in Y1 mouse adrenocortical tumor cells. Endocrinology 142, 4282–4287. doi: 10.1210/endo.142.10.8441 Fuchs-Hammoser, R., Schweiger, M., and Oelkers, W. (1980). The effect of chronic low-dose infusion of ACTH (1-24) on renin, renin-substrate, aldosterone and other corticosteroids in sodium replete and deplete man. Acta Endocrinol. 95, 198–206. Debonneville, C., Flores, S. Y., Kamynina, E., Plant, P. J., Tauxe, C., Thomas, M. A., et al. (2001). Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression. EMBO J. 20, 7052–7059. doi: 10.1093/emboj/20.24.7052

Healthgo Blood Pressure Regulator Ring, Adjustable HealthGo

Bose, H. S., Sato, S., Aisenberg, J., Shalev, S. A., Matsuo, N., and Miller, W. L. (2000). Mutations in the steroidogenic acute regulatory protein (StAR) in six patients with congenital lipoid adrenal hyperplasia. J. Clin. Endocrinol. Metab. 85, 3636–3639. doi: 10.1210/jc.85.10.3636 Kyossev, Z., Walker, P. D., and Reeves, W. B. (1996). Immunolocalization of NAD-dependent 11 beta-hydroxysteroid dehydrogenase in human kidney and colon. Kidney Int. 49, 271–281. Chen, L., Zhang, X., and Zhang, W. (2015). Regulation of alphaENaC transcription. Vitam. Horm. 98, 101–135. doi: 10.1016/bs.vh.2014.12.004Anderson, J. V., Struthers, A. D., Payne, N. N., Slater, J. D., and Bloom, S. R. (1986). Atrial natriuretic peptide inhibits the aldosterone response to angiotensin II in man. Clin. Sci. 70, 507–512. Garty, H., and Palmer, L. G. (1997). Epithelial sodium channels: function, structure, and regulation. Physiol. Rev. 77, 359–396. Ishimura, K., and Fujita, H. (1997). Light and electron microscopic immunohistochemistry of the localization of adrenal steroidogenic enzymes. Microsc. Res. Tech. 36, 445–453. Horvath, A., Szabadkai, G., Varnai, P., Aranyi, T., Wollheim, C. B., Spat, A., et al. (1998). Voltage dependent calcium channels in adrenal glomerulosa cells and in insulin producing cells. Cell Calcium 23, 33–42. Anantharam, A., and Palmer, L. G. (2007). Determination of epithelial Na + channel subunit stoichiometry from single-channel conductances. J. Gen. Physiol. 130, 55–70. doi: 10.1085/jgp.200609716

ring patent reveals medical grade SpO2 and blood Fitbit smart ring patent reveals medical grade SpO2 and blood

Cugini, P., Scavo, D., Cornelissen, G., Lee, J. Y., Meucci, T., and Halberg, F. (1981). Circadian rhythms of plasma renin, aldosterone and cortisol on habitual and low dietary sodium intake. Horm. Res. 15, 7–27. There's no actionable insights here at all, it's really about presenting the data to you and letting you interpret or share and export the data to a medical professional if you wish. Jo, Y., King, S. R., Khan, S. A., and Stocco, D. M. (2005). Involvement of protein kinase C and cyclic adenosine 3',5'-monophosphate-dependent kinase in steroidogenic acute regulatory protein expression and steroid biosynthesis in Leydig cells. Biol. Reprod. 73, 244–255. doi: 10.1095/biolreprod.104.037721In addition to controls of proteolytic cleavage and subcellular localization, ENaC is also regulated at the transcriptional level via the disruptor of telomeric silencing 1 (Dot1), a histone H3 K79 methyltransferase. Dot1 can mono, di or tri- methylate H3 K79 leading to a wide range of epigenetic control of gene expression. Dot1 is implicated in complex cellular processes, such as cell cycle regulation, cell proliferation, DNA replication, apoptosis, telomeric silencing, and blood pressure control. Dot1 has at least five isoforms (a–e) created by alternative splicing, out of which Dot1a is the most prominent in mouse kidneys ( Nguyen and Zhang, 2011). Deletion of Dot1 specifically in the connecting tubules and collecting ducts facilitated development of kidney fibrosis and reduced kidney function under three experimental settings (streptozotocin-induced diabetes, during normal aging, and after unilateral ureteral obstruction) in mice ( Zhang et al., 2020). The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Publisher’s Note

Blood Pressure Regulator Ring – Redetailed HealthGo™ Blood Pressure Regulator Ring – Redetailed

Obesity is a well-known cause of hypertension and is characterized by high aldosterone levels ( Goodfriend et al., 1998; Kurukulasuriya et al., 2011). One possibility is that adipocytes affect aldosterone production since they are active endocrine tissues ( Ronti et al., 2006). Indeed, Ehrhart-Bornstein et al. (2003) showed that isolated adipocyte secretory products could dramatically increase aldosterone production independent of ANG II in adrenocortical cells (NCI-H295R; Ehrhart-Bornstein et al., 2003). 2,13-epoxy-9-keto-10 (trans)-octadecenoic acid (EKODE) has also been shown to increase aldosterone production in a GC line. EKODE is produced by the oxidation of linoleic acid by hepatocytes. Incubation of adrenal cells with EKODE increased aldosterone production independently of ANG II. Interestingly, adult humans have a positive correlation with blood EKODE and aldosterone levels ( Goodfriend et al., 2004). However, EKODE is unlikely the molecule responsible for the effect seen by Ehrhart-Bornstein et al. (2003), as adipocyte secretory products were not oxidized by hepatocytes. A subsequent study showed that adipocyte-derived factors from SHR/cp rats (model of metabolic syndrome with hypertension) stimulate aldosterone production by increasing ADS expression and STAR activation despite ANG II receptor inhibition. Adipocyte-derived factors from normal rats failed to replicate these results ( Nagase et al., 2006). These effects might be mediated by leptin, which is a protein hormone secreted by adipocytes and is abnormally high in obese individuals ( Martinez-Rumayor et al., 2008; Huby et al., 2015). These in vitro studies have been validated and extended by in vivo investigations. For example, leptin infusion increased expression of ADS and serum aldosterone in a dose-dependent manner in mice with no effect on ANG II, K +, and corticosterone levels ( Belin de Chantemele et al., 2011; Huby et al., 2015). Huby et al. (2015) concluded that “leptin is a new regulatory factor of aldosterone secretion that acts directly in the adrenal cortex to promote ADS expression and aldosterone production” ( Huby et al., 2015). The leptin stimulatory effect on ADS and aldosterone was not abolished upon administration of ANG II or β adrenergic receptor inhibitors in mice, further supporting the notion of leptin as a novel effector of aldosterone production ( Huby et al., 2015). Leptin achieves these effects possibly through CaMK II, as leptin increased intracellular Ca 2+ concentration and elevated expression calmodulin and CaMK II ( Huby et al., 2015). Agreeably administration of leptin receptor antagonism abrogated leptin-mediated aldosterone secretion and lowered blood pressure in mice ( Huby et al., 2016). These studies carry crucial importance as hypertension in the obese population is a devastating health issue ( Kurukulasuriya et al., 2011). Davies, L. A., Hu, C., Guagliardo, N. A., Sen, N., Chen, X., Talley, E. M., et al. (2008). TASK channel deletion in mice causes primary hyperaldosteronism. Proc. Natl. Acad. Sci. U. S. A. 105, 2203–2208. doi: 10.1073/pnas.0712000105

References

I am diabetic and my blood pressure went down as well as my blood sugar just for wearing this ring. I work in a toxic environmentthat is very stressful and wearing the HealthGo has helped me relax and be calmer! It has also reduced my stress level." You're not going to get nudges to keep moving or be able to expand on data beyond simple step counts. The step counting doesn't appear to be saved in the app either, so you'll get to see what you've done for the day before it refreshes for the next day. It uses the fingers to press key points called ‘Acu Points’ on the skin surface rhythmically, to stimulate the body’s natural self-curative abilities. When these acupressure points for high BP are pressed, they release muscular tension and promote the circulation of blood to aid healing. Arriza, J. L., Weinberger, C., Cerelli, G., Glaser, T. M., Handelin, B. L., Housman, D. E., et al. (1987). Cloning of human mineralocorticoid receptor complementary DNA: structural and functional kinship with the glucocorticoid receptor. Science 237, 268–275.

Asda Great Deal

Free UK shipping. 15 day free returns.
Community Updates
*So you can easily identify outgoing links on our site, we've marked them with an "*" symbol. Links on our site are monetised, but this never affects which deals get posted. Find more info in our FAQs and About Us page.
New Comment