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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. 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). Agarwal, R. (2010). Regulation of circadian blood pressure: from mice to astronauts. Curr. Opin. Nephrol. Hypertens. 19, 51–58. doi: 10.1097/MNH.0b013e3283336ddb

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We also compared readings to the Oura Ring 3 and found they offered similar resting heart rate insights. Since ENaC dysfunction can be fatal, ENaC activity is tightly regulated. ENaC is primarily regulated by controlling its presence in the PM. ENaC is delivered to the PM through clathrin-mediated exocytosis and is removed from the PM through ubiquitylation. However, Na + transport is also regulated through proteolytic cleavage of ENaC ( Rossier and Stutts, 2009). Multiple proteases have been shown to increase activity of ENaC including serine, cysteine, furin, and alkaline proteases ( Chraibi et al., 1998; Hughey et al., 2004; Butterworth et al., 2012; Haerteis et al., 2012). Increase in activity of ENaC by proteolytic cleavage is achieved by releasing a 43-amino acid inhibitory domain of γ-subunit ( Zachar et al., 2015). For a more comprehensive review please refer to ( Kleyman and Eaton, 2020). Serum Glucocorticoid-Induced Kinase 1 AT and WZ: writing. CG, AT, and WZ: review and editing. WZ: supervision. All authors contributed to the article and approved the submitted version. Funding One of the keyways by which aldosterone regulates ENaC is through a serine/threonine serum glucocorticoid-induced kinase 1 (SGK1). SGK1 expression was increased 60min post-injection of physiological dose of aldosterone ( Chen et al., 1999; Bhargava et al., 2001). Although the levels of SGK1 rise in the presence of aldosterone, it must be phosphorylated at Thr256 and Ser422 by pyruvate dehydrogenase kinase 1 (PDK1) to be fully active ( Park et al., 1999). Phosphorylation of a third highly conserved residue (Ser397) also increased SGK1 activity ( Chen et al., 2009). mTORC2 was also identified as a kinase for SGK1 and is required for ENaC activation ( Lu et al., 2010). Huby, A. C., Antonova, G., Groenendyk, J., Gomez-Sanchez, C. E., Bollag, W. B., Filosa, J. A., et al. (2015). Adipocyte-derived hormone leptin is a direct regulator of aldosterone secretion, which promotes endothelial dysfunction and cardiac fibrosis. Circulation 132, 2134–2145. doi: 10.1161/CIRCULATIONAHA.115.018226Anderson, 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. HealthGo™ Blood Pressure Regulator Ring is a wearable blood pressure-reducing device that can be used anywhere and at any time. The ring activates the acupoints on your hands, which helps to lower blood pressure naturally and effectively! Let us hear Daniel's story on how she overcome high blood pressure with HealthGo™ Blood Pressure Regulator Ring! Chen, L., Wu, H., Pochynyuk, O. M., Reisenauer, M. R., Zhang, Z., Huang, L., et al. (2011). Af17 deficiency increases sodium excretion and decreases blood pressure. J. Am. Soc. Nephrol. 22, 1076–1086. doi: 10.1681/ASN.2010121270

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The adrenal cortex is divided into three functionally distinct regions: zona glomerulosa (production of mineralocorticoids), zona fasciculata (production of glucocorticoids), and zona reticularis (production of androgenic hormones; Vinson, 2016). Aldosterone biosynthesis occurs solely in the mitochondria of zona glomerulosa cells, which was demonstrated in the late 1980s where only isolated mitochondria of zona glomerulosa synthesized aldosterone ( Ohnishi et al., 1988). This division of the adrenal cortex is crucial as adrenal steroid hormones are derived from cholesterol, thus functional zonation is one way to control the production of steroid hormones. Bassett, M. H., Zhang, Y., Clyne, C., White, P. C., and Rainey, W. E. (2002). Differential regulation of aldosterone synthase and 11beta-hydroxylase transcription by steroidogenic factor-1. J. Mol. Endocrinol. 28, 125–135. doi: 10.1677/jme.0.0280125 Diacylglycerol seems to be a key second messenger of ANG II signaling as its inhibition dampens ANG II response in normal human adrenal GC ( Natarajan et al., 1988a, b, 1990). DAG appears to control aldosterone synthesis through its downstream target protein kinase C (PKC), inhibition of which reduces aldosterone production upon ANG II stimulation ( Kapas et al., 1995; Wang, 2006). PKC likely promotes steroidogenesis by increasing the expression and/or activity of STAR. Phorbol 12-myristate 13-acetate (PMA) activates PKC pathway, leading to increased STAR phosphorylation and expression, and progesterone synthesis ( Manna et al., 2009). Protein kinase D (PKD) also promotes STAR expression since overexpression of constitutively active PKD mutant results in upregulated STAR mRNA expression ( Olala et al., 2014). Both PKC and PKD effects on STAR expression are dependent on CREB ( Manna et al., 2009; Olala et al., 2014). ANG II has also been shown to increase the local concentration of cholesterol by promoting the uptake of lipoprotein cholesterol ester, increasing local mitochondrial cholesterol concentration, and activating cholesterol ester hydrolase (CEH; Cherradi et al., 2001, 2003). PKC is considered as an important factor in these effects because PMA-activated PKC pathway mimics ANG II-induced production of aldosterone, high-density lipoprotein receptor scavenger receptor class B type I, and the low-density lipoprotein receptor in the human NCI-H295R adrenocortical cell line ( Pilon et al., 2003). PKC and Ca 2+ activate nonreceptor Src kinase resulting in transactivation of epidermal growth factor receptor (EGFR) and activation of p42/p44 mitogen-activating protein kinase (MAPK) pathway ( Hodges et al., 2007). ANG II stimulation activates p42/p44 MAPK in GC ( Cherradi et al., 2003). P42/p44 likely phosphorylates CEH thereby increasing the concentration of cholesterol available for aldosterone synthesis. This process may be crucial, as the phosphorylation of CEH and production of pregnenolone are reduced upon p42/p44 inhibition ( Cherradi et al., 2003). Guagliardo, N. A., Yao, J., Hu, C., Schertz, E. M., Tyson, D. A., Carey, R. M., et al. (2012). TASK-3 channel deletion in mice recapitulates low-renin essential hypertension. Hypertension 59, 999–1005. doi: 10.1161/HYPERTENSIONAHA.111.189662The nephron, the functional unit of the kidney, is the main target of aldosterone ( Figure 1). Aldosterone exerts its action on the aldosterone-sensitive distal nephron (ASDN) comprising the late distal convoluted tubule (DCT2), the connecting tubule (CNT), and the collecting duct distal segments of the nephron ( Bachmann et al., 1999; Reilly and Ellison, 2000). ASDN governs unidirectional Na + transport from the filtrate into the circulation and bi-directional K + transport ( Gumz et al., 2015; Roy et al., 2015). There are two cell types in these segments: principal cells (PC) and intercalated cells (IC). PC are involved in Na + and K + transport while IC predominantly regulate acid–base homeostasis ( Loffing and Kaissling, 2003; Roy et al., 2015). Aldosterone binds its mineralocorticoid receptor (MR; Shibata and Fujita, 2011). Almost all cells express MR, but whether they are affected by aldosterone depends on the presence of 11-β-hydroxysteroid dehydrogenase type-2 (11β-OHSD2), an enzyme that catalyzes 11-hydroxy-glucocorticoids to glucocorticoid metabolites ( Funder et al., 1988). Mineralocorticoids and glucocorticoids have a common chemical structure and have equal binding affinity for MR ( Arriza et al., 1987). To maintain the binding specificity in aldosterone-sensitive cells, 11β-OHSD2 catabolizes glucocorticoids rendering MR free to bind aldosterone. Both PC and IC express MR and 11β-OHSD2; however, PC has significantly higher levels of both proteins ( Naray-Fejes-Toth et al., 1994; Kyossev et al., 1996). Ligand-bound MR translocates to the nucleus, where it regulates expression of its target genes ( Naray-Fejes-Toth et al., 1994). Nevertheless, aldosterone also affects its target tissue through rapid non-genomic pathways ( Arima et al., 2003; Funder, 2005; Funder, 2006). News • Cardiovascular disease prevention An ultrasound sensor to measure pulse wave velocity and blood pressure The reports screen shows a couple of line summaries of all of your measurements. Tap on any one of these summaries to view the full report that you can then share with others. The reports look very professional and provide detailed, accurate data. 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.

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Cherradi, N., Pardo, B., Greenberg, A. S., Kraemer, F. B., and Capponi, A. M. (2003). Angiotensin II activates cholesterol ester hydrolase in bovine adrenal glomerulosa cells through phosphorylation mediated by p42/p44 mitogen-activated protein kinase. Endocrinology 144, 4905–4915. doi: 10.1210/en.2003-0325Cugini, 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. Arteaga, M. F., Wang, L., Ravid, T., Hochstrasser, M., and Canessa, C. M. (2006). An amphipathic helix targets serum and glucocorticoid-induced kinase 1 to the endoplasmic reticulum-associated ubiquitin-conjugation machinery. Proc. Natl. Acad. Sci. U. S. A. 103, 11178–11183. doi: 10.1073/pnas.0604816103 Gumz, M. L., Rabinowitz, L., and Wingo, C. S. (2015). An integrated view of potassium homeostasis. N. Engl. J. Med. 373, 1787–1788. doi: 10.1056/NEJMc1509656

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Any wearable needs to be wearable – something that's easy and pleasant to wear. Sadly, that wasn't the case with the Circul+. WNK4 is a serine/threonine kinase, mutations of which have been identified as a potential cause for PHA II ( Wilson et al., 2001; Lopez-Cayuqueo et al., 2018). The underlying mechanism behind this disease may be explained by a negative regulation of ENaC through WNK4 ( Figure 4). Both in vivo and in vitro studies have shown a significant reduction of ENaC surface expression upon interacting with WNK4 ( Ring et al., 2007a). ENaC-WNK4 interaction requires an intact COOH terminus of β and ϒ subunits but not the PY motif, differing from ENaC-Nedd4-2 interaction requiring the PY motif. In the presence of aldosterone, SGK1 phosphorylates WNK4 and abrogates its negative regulation of ENaC ( Ring et al., 2007a, b; Yu et al., 2013). The clinical relevance of ENaC-WNK4 interaction is illustrated by PHA II-associated R1185C mutation of WNK4, which decreases WNK4’s inhibitory effect on ENaC by enhancing SGK1-mediated phosphorylation of WNK4 at S1217 ( Na et al., 2013). Aldosterone also increases the expression of kidney-specific WNK1 (kinase-deficient variant), which consequently increases transepithelial Na + transport in cortical collecting duct cells potentially through regulation of ENaC ( Naray-Fejes-Toth et al., 2004). WNK1 appears to increase ENaC surface expression by activating SGK1 through a non-catalytic mechanism ( Xu et al., 2005a, b). This appears to be dependent on phosphatidylinositol 3-kinase, as its inhibition abrogates this effect ( Xu et al., 2005b). Both WNK4 and WNK1 are implicated in PHA II ( Wilson et al., 2001). Two other genes, KLHL3 and CUL3, encoding kelch-like 3 (Kelch) and cullin 3 (cul3) proteins, respectively, may explain the mechanism by which WNK4 and WNK1 cause PHA II. Cul3 is an integral member of cul3-RING ubiquitin ligase, an E3 ubiquitin ligase. It forms a scaffold for the RING finger protein and ubiquitin conjugating enzyme E2 ( Genschik et al., 2013). Kelch is an adaptor protein that connects cul3-RING ubiquitin ligase to its targets ( Ji and Prive, 2013). Mutations in KLHL3 and CUL3 have been implicated in PHA II and appear to cause hypertension and electrolyte disbalance ( Boyden et al., 2012; Louis-Dit-Picard et al., 2012). One mechanism by which these mutations cause PHA II is through Wnk1 and Wnk4, as both of these proteins are targets of Cul3-RING ubiquitin ligase ( Ohta et al., 2013; Shibata et al., 2013b). PHA II causing mutations in KLHL3 decreases Wnk4 binding to Cul3-RING ubiquitin ligase, decreasing WNK4 degradation and increasing its levels resulting in hypertension ( Mori et al., 2013; Wakabayashi et al., 2013; Wu and Peng, 2013; Susa et al., 2014). Ehrhart-Bornstein, M., Lamounier-Zepter, V., Schraven, A., Langenbach, J., Willenberg, H. S., Barthel, A., et al. (2003). Human adipocytes secrete mineralocorticoid-releasing factors. Proc. Natl. Acad. Sci. U. S. A. 100, 14211–14216. doi: 10.1073/pnas.2336140100Heitzmann, D., Derand, R., Jungbauer, S., Bandulik, S., Sterner, C., Schweda, F., et al. (2008). Invalidation of TASK1 potassium channels disrupts adrenal gland zonation and mineralocorticoid homeostasis. EMBO J. 27, 179–187. doi: 10.1038/sj.emboj.7601934