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Kidney Structure and Physiology
Published in Joseph D. Bronzino, Donald R. Peterson, Biomedical Engineering Fundamentals, 2019
Joel M. Henderson and Mostafa Belghasem
Aldosterone, a steroid hormone secreted by the adrenal cortex, acts on the distal convoluted tubules causing increased sodium reabsorption and potassium secretion. As a result of increased sodium reabsorption, concomitant water reabsorption also occurs, resulting in increased blood volume and elevated blood pressure. Aldosterone acts by the activation of the Na-K ATPase pump on the basolateral membrane of the distal convoluted tubular epithelium, and by increasing the luminal membrane permeability to sodium. Aldosterone is released from the adrenal cortex in response to decreased plasma sodium and increased plasma potassium concentrations, through a direct eect on the adrenal cortex.
Toxic Responses of the Kidney
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
The glomerular filtrate is delivered to the proximal convoluted tubule where nearly 90% of water, electrolytes, glucose, and amino acids are reabsorbed. Selective elimination (secretion) of waste products and certain organic compounds also occurs by the cells composing the straight portion of the proximal tubule (pars recta). As the filtrate passes through the tubule it remains isotonic with the blood. Even with 90% reabsorption accomplished within the proximal tubule, the filtrate still requires further concentration to prevent the elimination of a large quantity of dilute urine. This is accomplished by the proximal descending and distal ascending tubular limbs, the loop of Henle, and the collecting duct. The major purpose of the descending and ascending limbs of the proximal and distal tubules and loop of Henle is to create a hypertonic gradient within the surrounding tissue fluid which increases in osmotic strength as it nears the medullary papilla. In the ascending limb, sodium is actively transported out of the tubule (with passive diffusion of chlorine) and retention of water. As a result of this process, tissue fluid surrounding the tubule becomes increasingly hypertonic, while as the filtrate ascends the tubule, it becomes hypotonic to the surrounding environment. The cells which compose the walls of the descending limb allow the passage of water, which results in the filtrate remaining isosmotic with the surrounding tissue fluid. When the filtrate is delivered to the distal convoluted tubule, it is hypotonic to the surrounding tissue fluid. As the filtrate moves through the distal tubule, water and sodium are removed and hydrogen, potassium, and ammonia enter the tubule with the net production of an isotonic filtrate that reaches the collecting duct. When the filtrate enters the collecting duct, further concentration of urine results. As the collecting duct enters the medulla and passes through the osmotic gradient established by the loop of Henle and ascending and descending tubular limbs, water is removed and the filtrate is concentrated. Antidiuretic hormone (ADH), produced by the posterior lobe of the pituitary, exerts its effect on the cells composing the collecting duct. Decreased levels of antidiuretic hormone result in less water being removed from the distal tubule and collecting duct with the net production of dilute urine. Because of the anatomical structure and functional activity of the kidney briefly described above, nephrotoxins may act on a specific area within the kidney.
Environmental benign RP-HPLC method for the simultaneous estimation of anti-hypertensive drugs using analytical quality by design
Published in Green Chemistry Letters and Reviews, 2023
Naveenarani Dharuman, Karunanidhi Santhana Lakshmi, Manikandan Krishnan
Benidipine is a long-acting, dihydropyridine calcium channel blocker used as an anti-anginal and anti-hypertensive agent [6]. It is chemically (benidipine, (±)-(R*)−3- [(R*)−1-benzyl-3-piperidyl] methyl-1,4-dihydro-2,6-dimethyl- 4-(m-nitrophenyl)−3,5-pyridine dicarboxylate hydrochloride (Figure 1a). It inhibits L, T, and N-type calcium channels and has a strong vascular selectivity. The drug has anti-oxidant properties and an increase in nitric oxide production. In addition, it shows cardioprotective benefits in patients with ischemic heart disease. It also shows renal protective effects [7]. Chlorthalidone (Figure 1b) is a thiazide type diuretic used exclusively as antihypertensive. It is effective in BP reduction and improving cardiovascular outcomes [8]. The IUPAC name of chlorthalidone is benzenesulfonamide, 2-chloro-5-(2,3-dihydro-1-hydroxy-3-oxo-1H-isoindol-1-yl) [9]. It blocks the sodium-chloride cotransporter in the ascending loop of Henle's distal convoluted tubule [10]. The literature study reveals that few HPLC (High-performance liquid chromatography) techniques were reported for chlorthalidone [11–14], while for benidipine HPLC/UPLC (Ultra performance liquid chromatography) [15] and with the combination of BEN and CHD stability indicating HPLC [16] and RP-HPLC [17] technique has been discussed.
Pesticide-induced changes in cholinesterase activity and chronic kidney disease of unknown etiology among farmers in Nakhon Ratchasima, Thailand
Published in Human and Ecological Risk Assessment: An International Journal, 2021
Ekarat Sombatsawat, Dana Boyd Barr, Parinya Panuwet, Mark Gregory Robson, Wattasit Siriwong
Previous studies have provided strong evidence that pesticides can cause damage to many tissues and organs, including the kidneys (Jamal et al. 2016). Several studies have demonstrated the nephrotoxic effects of pesticides based on research in laboratory animals (El-Bini Dhouib et al. 2015; Kaya et al. 2018). According to previous research, accumulation of pesticides in kidney tubular cells could increase levels of reactive oxygen species which subsequently induced proximal tubule injury (Mølck and Friis 1997). Nephrotoxicity can be detected by a change in renal function as assessed by the glomerular filtration rate (GFR), serum creatinine (SCr), or urinary output (Barnett and Cummings 2018). Although knowledge of the pathogenesis of kidney injury from OP and carbamate poisoning is limited, the suggested mechanisms include BuChE activity in the renal distal convoluted tubule and an increase in oxidative stress (Mamoulakis et al. 2017; Tsarouhas et al. 2018). In cases of OP and carbamate poisoning, the progression from nephropathy to chronic renal insufficiency (Ghosh et al. 2018) and premature death (Ramirez-Rubio et al. 2013) is generally undetected, as renal damage occurs gradually.