Kidney sodium regulation

Ingelfinger, ). R., Pratt, R. E., Ellison, K., and Dzau, V. J. (1986). Sodium regulation of antiotensmogen mRNA expression in rat kidney cortex and medulla, /. Clin, fnwt. 78, 1311-1315. 

Inability of the hypothalamus gland to synthesize antidiuretic hormone (ADH), which is required by the kidneys to regulate sodium. 

The sodium-to-water ratio in the body must be properly balanced or unfortunate effects may result. The hypothalamus area of the brain is fairly efficient at regulation of this ratio when sodium is high, thirst results when excess urination causes loss of water, the body also excretes sodium to help maintain the balance. People traveling long distances in desert or other dry climates may ingest salt (NaCl) as a way to retain water in their systems. The kidneys also play a role in sodium regulation. 

Hypertension is an increase of blood pressure to levels greater than normal that arises because of a mismatch between the volume of the vascular tree and the volume of blood. Blood volume depends on total body sodium content, which is a balance between sodium intake and output. Total body sodium is controlled by variable excretion of sodium by the kidneys. To regulate sodium balance, the primary variable that the kidney monitors is not total body sodium but rather systemic blood pressure. Renal regulation of blood pressure is via the release of the peptide hormone renin from specialized renal cells. Release of rerun ultimately leads to the production of angiotensin H. Angiotensin II increases total peripheral resistance and blood pressure and also leads to an increase in aldosterone. Aldosterone is a steroid... 

Sodium-Potassium-Dependent ATPase 552 Sodium Reabsorption in the Kidney 553 Regulation of Sodium Reabsorption 554 Aldosterone... 

In an attempt to conserve sodium, the kidney secretes renin increased plasma renin activity increases the release of aldosterone, which regulates the absorption of potassium and leads to kafluresis and hypokalemia. Hypokalemia is responsible in part for decreased glucose intolerance (82). Hyponatremia, postural hypotension, and pre-renal azotemia are considered of tittle consequence. Hypemricemia and hypercalcemia are not unusual, but are not considered harmful. However, hypokalemia, progressive decreased glucose tolerance, and increased semm cholesterol [57-88-5] levels are considered... 

Aldosterone, the most potent of the mineralocorticoids (Figure 25.43), is involved in the regulation of sodium and potassium balances in tissues. Aldosterone increases the kidney s capacity to absorb Na, Cl, and HgO from the glomerular filtrate in the kidney tubules. 

Sodium and water balance are primarily regulated by the kidney Reductions in nephron mass decrease glomerular filtration and subsequent reabsorption of sodium and water, leading to edema. 

Aldosterone A hormone produced in and secreted by the zona glomerulosa of the adrenal cortex. Aldosterone acts on the kidneys to reabsorb sodium and excrete potassium. It is also a part of the renin-angiotensin-aldosterone system, which regulates blood pressure and blood volume. 

The maintenance of plasma volume and plasma osmolarity occurs through regulation of the renal excretion of sodium, chloride, and water. Each of these substances is freely filtered from the glomerulus and reabsorbed from the tubule none is secreted. Because salt and water intake in the diet may vary widely, the renal excretion of these substances is also highly variable. In other words, the kidneys must be able to produce a wide range of urine concentrations and urine volumes. The most dilute urine produced by humans is 65 to 70 mOsm/1 and the most concentrated the urine can be is 1200 mOsm/1 (recall that the plasma osmolarity is 290 mOsm/1). The volume of urine produced per day depends largely upon fluid intake. As fluid intake increases, urine output increases to excrete the excess water. Conversely, as fluid intake decreases or as an individual becomes dehydrated, urine output decreases in order to conserve water. 

There are seven membrane forms of GC, designated GC-A to GC-G [33], Two forms, GC-A and GC-B (Mr = 120kDa), serve as receptors for atrial natriuretic peptide (ANP) and related peptides. ANP is a 28-amino-acid peptide isolated originally from cardiac atria as an important factor in the regulation of sodium excretion and blood pressure. GC-A binds ANP, as well as brain natriuretic peptide (BNP), and is located in vascular tissue and kidney. 

There is another system involved in blood pressure regulation the renin-angiotensin-aldosterone system (Fig. 2). The arterial blood pressure in the kidney influences intrarenal baroreceptors which together with the sodium load at the macula densa lead to renin liberation, angiotensin formation and aldosterone secretion, which by influencing the sodium balance changes the blood volume and influences the arterial blood pressure. 

Mineralocorticoids play a major role in regulating the balance of electrolytes and water, especially in the kidneys, where they facihtate reabsorption of sodium ions and water from urine. 

Pharmacokinetics Sodium bicarbonate in water dissociates to provide sodium and bicarbonate ions. Sodium is the principal cation of extracellular fluid. Bicarbonate is a normal constituent of body fluids and normal plasma level ranges from 24 to 31 mEq/L. Plasma concentration is regulated by the kidney. Bicarbonate anion is considered labile because, at a proper concentration of hydrogen ion, it may be converted to carbonic acid, then to its volatile form, carbon dioxide, excreted by lungs. Normally, a ratio of 1 20 (carbonic acid bicarbonate) is present in extracellular fluid. In a healthy adult with normal kidney function, almost all the glomerular filtered bicarbonate ion is reabsorbed less than 1% is excreted in urine. 

Mecfianism of Action A synthetic hormone that decreases osteoclast activity in bones, decreases tubular reabsorption of sodium and calcium in the kidneys, and increases absorption of calcium in the GI tract. Therapeutic Effect Regulates serum calcium concentrations. 

In terms of mineral content, potato is best known as an important source of dietary potassium, which plays a fundamental role in acid-base regulation and fluid balance and is required for optimal functioning of the heart, kidneys, muscles, nerves, and digestive systems. Health benefits of sufficient potassium intake include reduced risk of hypokalemia, osteoporosis, high blood pressure, stroke, inflammatory bowel disease (IBD), kidney stones, and asthma. A high intake of potassium and low intake of sodium have been hypothesized to reduce the risk of stroke (Larsson et al., 2008 Swain et al., 2008). However, most American women 31-50 years old consume no more than half of the recommended amoimt of potassium and men s intake is only moderately higher (lOM, 2004). 

Adrenocorticoid hormones are produced in the adrenal glands. They regulate a variety of metaholic processes. The most important mineralo-corticoid is aldosterone, an aldehyde as well as a ketone, which regulates the reahsorption of sodium and chloride ions in the kidney, and increases the loss of potassium ions. Aldosterone is secreted when hlood sodium ion levels are too low to cause the kidney to retain sodium ions. If sodium levels are elevated, aldosterone is not secreted, so some sodium will he lost in the urine and water. Aldosterone also controls swelling in the tissues. 

Knepper MA, Brooks HL Regulation of the sodium transporters NHE3, NKCC2, and NCC in the kidney. Curr Opin Nephrol Hypertens 2001 10 655. [PMID 11496061]... 

Urodilatin is synthesized in the distal tubules of the kidneys by alternative processing of the ANP precursor. It elicits potent natriuresis and diuresis, and thus functions as a paracrine regulator of sodium and water excretion. It also relaxes vascular smooth muscle. 

Dopamine has also natriuretic and diuretic effects in kidney. There has been evidence that abnormalities of the renal dopamine system can lead to salt- sensitive hypertension [48]. In rat kidney, deamination represents the major pathway in the metabolism of dopamine, but when MAO is inhibited, methylation appears to offer an alternative metabolic pathway [49]. Thus COMT inhibition may be important in the regulation of renal sodium excretion. 

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