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The Treatment of Hypertension with Nutrition, Nutritional Supplements, Lifestyle and Pharmacologic Therapies
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Increased dietary sodium intake is associated with hypertension, cerebrovascular accident (CVA), left ventricular hypertrophy (LVH), diastolic dysfunction (DD), CHD, MI, renal insufficiency, proteinuria, arterial stiffness, platelet dysfunction and increased sympathetic nervous system (SNS) activation. A reduction in dietary sodium intake lowers BP and the risk of all of these diseases [2–5,10–15,18,19,53–61]. Decreasing dietary sodium intake in hypertensive patients, especially in the salt-sensitive patients and those with an overactive renal epithelial sodium channel, lowers BP by 4–6/2–3 mmHg proportional to the amount of sodium restriction, reduces the intravascular volume, and may prevent or delay hypertension in high-risk patients [54].
Nonclassical Ion Channels in Depression
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
ASIC1a gene deletion or inhibition has been demonstrated to induce an anti-depressive effect41,42, while restoring ASIC1a expression in the amygdala reduced the anti-depressant-like behavior in ASIC1a−/− mice41, thus suggesting that ASIC1a antagonists may be a promising avenue for alleviating depressive symptoms. Pharmacologically, treatment with A-317567 and psalmotoxin (PcTx1), both potent ASIC1a inhibitors, also results in the induction of antidepressant effects41. Amiloride is a blocker of epithelial sodium channels. Studies in a rat model showed that amiloride decreased symptoms of chronic stress-induced anhedonia with elevation of serum adrenocorticotropic hormone and corticosterone. These findings suggest that inhibition of ASICs can affect the hypothalamic-pituitary-adrenal axis to relieve depressive-like behaviors43.
Nutraceuticals for Hypertension Control
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
Balázs Varga, Mariann Bombicz, Andrea Kurucz, Béla Juhász
All the aforementioned vascular events are further deteriorated if aldosterone is present (Fels, Oberleithner et al. 2010). The mechanism behind the aldosterone-sensitivity of endothelial cells may be related to epithelial sodium channels located on the surface of endothelial cells activated by aldosterone (Kusche-Vihrog, Callies et al. 2010). Through these channels, endothelial cells react to increased serum sodium by altering the viscosity of their plasma membrane and the submembranous actin network (Oberleithner, Kusche-Vihrog et al. 2010), which eventually results in reduction of physiological vasodilation and in increased stiffness (Kusche-Vihrog and Oberleithner 2012). Difference in salt-sensitivity or insensitivity, i.e. individual responses to sodium overload, may be attributable to expression or activity of such protein products of genes as epithelial sodium channels, among probable multiple others.
An overview of alogliptin + pioglitazone for the treatment of type 2 diabetes
Published in Expert Opinion on Pharmacotherapy, 2022
Brian Tomlinson, Paul Chan, Christopher Wai Kei Lam
Pioglitazone causes a dose-related increase in body weight which is partly due to fat deposition in subcutaneous fat stores while there is reduction in visceral fat and other sites of ectopic fat deposition [56]. It also increases total body fluid, which accounted for 75% of the weight gain in one study [117]. Despite the increase in total body sodium, blood pressure is usually reduced, and peripheral vasodilatation may contribute to the sodium retention [118]. The volume retention appears to be related to alteration of sodium handling by activation of PPAR-γ receptors in the endothelial cells lining the renal collecting duct [119]. Increased expression of epithelial sodium channels appears to be involved [120]. Fluid retention with pioglitazone is dose-related and is greater when used in combination with a sulfonylurea or insulin [121,122].
Serum uric acid and blood pressure among adolescents: data from the Nutrition and Health Survey in Taiwan (NAHSIT) 2010–2011
Published in Blood Pressure, 2021
Kuan-Hung Lin, Fu-Shun Yen, Harn-Shen Chen, Chii-Min Hwu, Chen-Chang Yang
Experimental and animal studies demonstrated a plausible physiological mechanism that links hyperuricaemia and hypertension through endothelial dysfunction resulting from blocking nitric oxide release [24] and activation of the renin–angiotensin system [25]. Gruskin conducted a small comparable study [26], which demonstrated that the hypertensive adolescents were found to have elevated levels of UA (mean, >6.5 mg/dL) and that plasma renin activity was higher in hypertensive adolescents with hyperuricaemia than in those with normouricaemia. A recent experimental study found that elevated UA induced hypertension through up-regulation of distal nephron epithelial sodium channel expression [27]. A growing body of evidence from cross-sectional and longitudinal studies in children and adolescents demonstrated that UA plays a causal role in elevated BP and in the development of early hypertension [6]. Two randomised, double-blinded, placebo-controlled trials had shown that either allopurinol, a xanthine oxidase inhibitor [10,11], or probenecid, a uricosuric agent [11], reduces BP through their urate-lowering effects.
The role of dietary salt and alcohol use reduction in the management of hypertension
Published in Expert Review of Cardiovascular Therapy, 2021
According to the theoretical description, hypertension could result from a rise in cardiac output or in total peripheral resistance, or both. The evidence has proposed that excessive sodium retention is a contributing factor in genetically predisposed (salt-sensitive) persons [46]. Sodium sensitivity is the responsiveness of BP to the variations in salt ingestion. The degree of BP variation after sudden variations in salt ingestion differs significantly from person to person [161,162]. The diminished kidney sodium excretion can cause the preliminary volume increase and afterward, it will lead to hypertension [163,164]. The way by which sodium reabsorption rise is not well known. The probable mechanism of action includes; the thick ascending limb Na-K-2Cl cotransporter, raised an action of the proximal tubular Na-H exchanger, the distal tubular Na-Cl cotransporter, and the collecting duct epithelial sodium channel [165–167]. The association between hypertension and the activity of the proximal Na-H exchanger has been supported by evidence [166]. The raised action of the epithelial sodium channel in the collecting tubule is blamed for hypertension [167]. The abnormality of a bidirectional sodium-calcium exchanger leads to enlarged calcium entrance into the smooth muscle of the blood vessel in reply to excessive sodium ingestion. The raised calcium entrance leads to vasoconstriction and hypertension as evidence by a study conducted on sodium-sensitive hypertensive rats and transgenic mice [168,169].