Sodium excretion

Long-lasting vasoconstriction is produced by the ETs in almost all arteries and veins and several studies have shown that ET-1 causes a reduction in renal blood flow and urinary sodium excretion. ET-1 has been reported to be a potent mitogen in fibroblasts and aortic smooth muscle cells and to cause contraction of rat stomach strips, rat colon and guinea pig ileum. In the central nervous system, ETs have been shown to modulate neurotransmitter release. [Pg.544]

ACE inhibitors lower the elevated blood pressure in humans with a concomitant decrease in total peripheral resistance. Cardiac output is increased or unchanged heart rate is unchanged urinary sodium excretion is unchanged and potassium excretion is decreased. ACE inhibitors promote reduction of left ventricular hypertrophy. [Pg.140]

In normal human subjects, ANP infusion for one hour causes increased absolute and fractional sodium excretion, urine flow, GFR, and water clearance (53—55). As shown in many in vitro and in vivo animal studies, ANP achieves this by direct effect on the sodium reabsorption in the inner medullary collecting duct, ie, by reducing vasopressin-dependent free-water and sodium reabsorption leading to diuresis and by indirect effect through increased hemodynamic force upon the kidney. ANP inhibits the release of renin and aldosterone resulting in the decreased plasma renin activity and aldosterone concentration (56,57). [Pg.208]

Kuznetsova T, Staessen JA, Thijs L et al (2004) European Project On Genes in Hypertension (EPOGH) Investigators. Left ventricular mass in relation to genetic variation in angiotensin II receptors, renin system genes, and sodium excretion. Circulation 110 2644-2650... [Pg.954]

Urodilatin is a peptide similar to atrial natriuretic peptide, which is produced in the distal tubule of the kidney and promotes sodium excretion and diuresis by acting on receptors localized on the luminal site of the collecting duct of the nephron. [Pg.1268]

All patients with ascites require counseling on dietary sodium restriction. Salt intake should be limited to less than 800 mg sodium (2 g sodium chloride) per day. More stringent restriction may cause faster mobilization of ascitic fluid, but adherence to such strict limits is very difficult. Patients usually respond well to sodium restriction accompanied by diuretic therapy.14,22,31,32 The goal of therapy is to achieve urinary sodium excretion of at least 78 mEq (78 mmol) per day.22 While a 24-hour urine collection provides this information, a spot urine sodium/ potassium ratio greater than 1.0 provides the same information and is much less cumbersome to perform. [Pg.330]

Assess dietary sodium intake by patient food recall or by spot urine sodium/potassium ratio for appropriate sodium excretion. [Pg.335]

Loop diuretics such as furosemide enhance sodium excretion... [Pg.364]

Prolonged administration of loop diuretics can lead to a second type of diuretic resistance. Enhanced delivery of sodium to the distal tubule can result in hypertrophy of distal convoluted cells.17 Subsequently, increased sodium chloride absorption occurs in the distal tubule which diminishes the effect of the loop diuretic on sodium excretion. Addition of a distal convoluted tubule diuretic, such as metolazone or hydrochlorothiazide, to a loop diuretic can result in a synergistic increase in urine output. There are no data to support the efficacy of one distal convoluted tubule diuretic over another. The common practice of administering the distal convoluted tubule diuretic 30 to 60 minutes prior to the loop diuretic has not been studied, although this practice may first inhibit sodium reabsorption at the distal convoluted tubule before it is inundated with sodium from the loop of Henle. [Pg.366]

As nephron mass continues to decline, the sodium load overwhelms the remaining nephrons and total sodium excretion is decreased, despite the increase in sodium excretion by... [Pg.380]

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). [Pg.99]

Decrease blood calcium Increase blood calcium decrease blood phosphate activation of vitamin D 3 "Fight-or-flight" response reinforces effects of the sympathetic nervous system Reabsorption of sodium excretion of potassium... [Pg.123]

Atrial natriuretic peptide (ANP) is produced by specialized myocytes in the atria of the heart. Secretion is stimulated by increased filling and stretch of the atria in response to plasma volume expansion. The effects of ANP include vasodilation, diuresis (increased urine production), and increased sodium excretion. Taken together, these effects decrease blood volume and blood pressure toward normal. [Pg.213]

Explain how the control of sodium excretion regulates plasma volume... [Pg.307]

Describe the mechanisms by which sodium excretion is controlled... [Pg.307]

Sodium balance is achieved when salt intake is equal to salt output. The intake of salt in the average American diet (10 to 15 g/day) far exceeds what is required physiologically. Only about 0.5 g/day of salt is lost in sweat and feces. The remaining ingested salt must be excreted in the urine. The amount of sodium excreted by the renal system is determined by ... [Pg.336]

Taken together, the homeostatic responses elicited by the initial decrease in plasma volume serve to decrease sodium filtration, increase sodium reabsorption, and, consequently, decrease sodium excretion in the urine. This conservation of sodium leads to conservation of water and an expansion of plasma volume toward normal. [Pg.338]

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. [Pg.368]

Abnormalities in either the renal or tissue autoregulatory processes for sodium excretion, plasma volume, and arteriolar constriction ... [Pg.124]

Hypertension is more common and more severe in African Americans than in those of other races. Differences in electrolyte homeostasis, glomerular filtration rate, sodium excretion and transport mechanisms, plasma renin activity, and BP response to plasma volume expansion have been noted. [Pg.140]

Loop diuretics, particularly when administered by continuous infusion, increase urine volume and renal sodium excretion. Although thiazide... [Pg.877]

Edema develops when excess sodium is retained either as a primary defect in renal sodium excretion or as a response to a decrease in the effective circulating volume despite an already expanded or normal ECF volume. [Pg.897]

Many animal species excrete more calcium if fed an acid or acidforming compounds. In the calf, Steenbock and coworkers (13) observed hypercalciuria and acidic urine after feeding hydrochloric acid to the calf. Stehle (14) pointed out that calcium represented the main long-term fixed base to be lost in the urine of the dog loaded with excessive amounts of hydrochloric acid. Walzer and Browder (15) demonstrated that when infused with a sulfate containing solution, the dog excreted several fold more acid and calcium than saline-infused controls the increased calcium loss returned to normal upon removal of the sulfate. Marone, et al. (16) demonstrated increased excretion of calcium in the acidotic dog. Correction of the acidosis reduced the excessive fractional calcium excretion rate, but did not alter sodium excretion. [Pg.77]

Physiologists had postulated for a long time about the existence of a sodium excreting hormone to prevent Na overload and consequent deleterious effects of high blood pressure on the heart and vascular system. At least two such natriuretic factors have been described atrial or A-type and brain or B-type natriuretic factors. Structurally, the natriuretic factors are peptides with a cysteine-cysteine disulfide bridge creating a characteristic loop , this is illustrated by Figure 8.8. [Pg.273]

Vered Y, Grosskopf I, Palevitch D, Harsat A, Charach G, Weintraub MS, Graff F. (1997). The influence of Vida faba (broad bean) seedlings on urinaiy sodium excretion. Planta Med. 63(3) 237-40. [Pg.491]

Wang et al. injected a Texas-red-labelled phosphorothioated AS-ODN into the dopamine lA receptor in the rat renal interstitium. Fluorescence was detected after 24 h in both tubular epithelium and intra-renal vasculature. Treatment resulted in a 35% decrease in the dopamine lA receptor protein, causing a reduction in urinary sodium excretion and urine output [131],... [Pg.148]

Hydrocortisone exhibits anti-shock, anti-allergy, and anti-inflammatory action. It raises sugar content in the blood, increases potassium secretion, and lowers sodium excretion from the body. It exhibits anti-metaboUc action and reduces histamine synthesis in the body. [Pg.353]

Note Doses greater than 25 mg/day are likely to potentiate potassium excretion but provide no further benefit in sodium excretion or blood pressure reduction. [Pg.675]

Fig. 13. Relationship between furosemide excretion rate and sodium excretion rate in control subjects and patients with heart failure. The heavy line with large circles and shaded area represent mean and SEM in the controls. The drug is much less potent and efficacious in all but one of the patients compared to the controls. (From Brater C, Chennavasin P, Sdwell R. Furosemide in patients with heart failure Shift in dose-response curves. Clin Pharmacol Ther 1980 28 182-6, with permission from MOSBY Inc.)...

As a response to an increased sodium excretion and a low kidney perfusion specialized cells located at... [Pg.316]

Diuretics, typically spironolactone, form the main therapy, combined with restricted salt intake. Sodium restriction is usually unnecessary where fluid retention is mild, and if marked limitation (less than 40 mmol per day intake) is imposed, may lead to impaired nutrition and is poorly accepted. Diuretic treatment often requires reinforcement with loop diuretics. Treatment can be maintained if urinary sodium excretion is at least 30 mmol per day. Removal of ascites through diuresis requires fluid transfer through the intravascular fluid compartment. If diuresis is too intense the intravascular fluid volume is reduced and hypotension causes hepatorenal failure to follow. The aim should be, through monitoring weight loss, to restrict fluid removal to 0.5 kg per day. In this way the risks of hyponatraemia, renal and hepatic impairment should be reduced. [Pg.631]

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