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Urinary sodium

NHCOCH3. White crystals, m.p. 18l-l83"C. Soluble sulphacetamide is the sodium salt which is soluble in water. Il is prepared by acetylating sulphanilamide and hydrolysing one acetyl group. Being more soluble than most of the sulphonamides it is used in treating infections of the urinary tract and of the conjunctiva. [Pg.376]

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]

Nickel carbonyl should be used in totally enclosed systems or under good local exhaust. Plants and laboratories where nickel carbonyl is used should make use of air-monitoring devices, alarms should be present in case of accidental leakage, and appropriate personal respiratory protective devices should be readily available for emergency uses. Monitoring of urinary nickel levels is useful to help determine the severity of exposure and identify appropriate treatment measures. Some large-scale users of nickel carbonyl maintain a supply of sodium diethyldithiocarbamate, or Antabuse, a therapeutic agent, on hand for use in case of overexposure. [Pg.14]

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]

Methybcanthine Diuretics. The mild diuretic effect of drinking coffee, from caffeine, and tea, mainly from theophylline, has been recogni2ed for along time. But the methylxanthines (Table 5) are of very limited efficacy when used as diuretics. The excretion of sodium and chloride ions are increased, but the potassium excretion is normal. Methylxanthines do not alter the urinary pH. Even though the methylxanthines have been demonstrated to have minor direct effects in the renal tubules, it is beUeved that they exert their diuretic effects through increased renal blood flow and GER (71). [Pg.210]

In an unusual variant on the Chichibabin reaction, treatment of 3-hydroxypyridine with sodium amide at 200° affords 2,6-di-aminopyridine (21). Coupling of the product with benzenediazo-nium chloride gives phenazopyridine (22). This drug is used as an analgesic for the urinary tract in conjunction with antibacterial agents for treatment of urinary infections. [Pg.255]

Diuretics promote the urinary excretion of sodium and water by inhibiting the absorption of filtered fluid across the renal tubular epithelium. The ensuing reduction in Na reabsorption reduces the Na content of the body, the critical determinant of extracellular and plasma fluid volumes. Thus, the use of diuretics is primarily indicated in the treatment of edematous diseases and of arterial hypertension. [Pg.429]

Several diseases involving dysregulation of MR function have been described although most of them are not causatively linked to the receptor itself. Pseudohypoaldosteronism for example is a syndrome of mineralocorticoid resistance characterized by urinary salt loss and dehydration. However, only very rarely mutations in the MR gene have been found in these patients so far. In most cases, this syndrome appears to be linked to defects in the subunits of the amiloride-sensitive sodium channel ENaC, a major target of mineralocorticoid action in the kidney. [Pg.546]

This electrolyte plays a vital role in the acid-base balance of the body. Bicarbonate may be given IV as sodium bicarbonate (NaHC03) in the treatment of metabolic acidosis, a state of imbalance that may be seen in diseases or situations such as severe shock, diabetic acidosis, severe diarrhea, extracorporeal circulation of blood, severe renal disease, and cardiac arrest. Oral sodium bicarbonate is used as a gastric and urinary alkalinizer. It may be used as a single drug or may be found as one of the ingredients in some antacid preparations. It is also useful in treating severe diarrhea accompanied by bicarbonate loss. [Pg.638]

Diuretics have been the mainstay for HF symptom management for many years. 0 Diuretics are used for relief of acute symptoms of congestion and maintenance of euvolemia. These agents interfere with sodium retention by increasing urinary sodium and free water excretion. No prospective data exist on I the effects of diuretics on patient outcomes.14 Therefore, the... [Pg.43]

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]

Color, yellow character, hazy glucose (-) ketones (-) specific gravity 1.020 pH 5.0 (+) protein coarse granular casts, 5 to 10/low-powered field white blood cell (WBC) count, 5 to 10/high-powered field red blood cell (RBC) count, 2 to 5/high-powered field no bacteria nitrite (-) blood small osmolality 325 mOsm urinary sodium 77 mEq/L (77 mmol/L) creatinine 63 mg/dL (5569 pmol/L)... [Pg.365]

The kidney is unable to adjust to abrupt changes in sodium intake in patients with severe CKD. Therefore, patients should be advised to refrain from adding salt to their diet, but should not restrict sodium intake. Changes in sodium intake should occur slowly over a period of several days to allow adequate time for the kidney to adjust urinary sodium content. Sodium restriction produces a negative sodium balance, which causes fluid excretion to restore sodium balance. The resulting volume contraction can decrease perfusion of the kidney and hasten the decline in GFR. Saline-containing intravenous (IV) solutions should be used cautiously in patients with CKD because the salt load may precipitate volume overload. [Pg.381]

ACE-I, angiotensin-converting enzyme inhibitor ADH, antidiuretic hormone (or vasopressin) ARB, angiotensin II receptor blocker, MESNA, sodium 2-mercaptoethanesulfonate TCA, tricyclic antidepressant Ul, urinary incontinence SUI, stress urinary incontinence UUI, urge urinary incontinence. [Pg.806]

Monitor the patient for resolution of hematuria after each successive therapeutic intervention. Frequency of monitoring is based on the severity of hemorrhaging. Monitor urinary output and serum chemistries (including sodium, potassium, chloride, blood urea nitrogen, and serum creatinine) daily for renal dysfunction. Check the CBC at least daily to monitor hemoglobin and platelet count. [Pg.1482]

Massey, L. K., Wise, K. J., The effect of dietary caffeine on urinary excretion of calcium, magnesium, sodium and potassium in healthy young females, Nutrition Research, 4, 43, 1984. [Pg.358]

The metabolic fate of chlordan was studied in rabbits by analysis of the relative chlorine content of chlordan added to normal rabbit s urine and of the chlorine content of the urinary excretory product. The method of analysis was similar to the one previously used (, 4) In addition, hydrolysis of chlordan and of the urinary excretory products was carried out by adding solid sodium hydroxide to saturation to a 10-ml. solution of these substances in hot absolute ethyl alcohol. The mixture was refluxed for 3 hours in a round-bottomed flask immersed in boiling water and the amount of inorganic chlorine determined. Hydrolysis was similarly carried out with solutions of the respective substances in aqueous sodium hydroxide. [Pg.229]

A negative correlation was found between PbB and systolic pressure in Belgian men in the Cadmibel study (a cross-sectional population study of the health effects of environmental exposure to cadmium) (Staessen et al. 1991). In this study, blood pressure and urinary cation (positive ions found in the urine, such as sodium, potassium, and calcium) concentration data were obtained from 963 men and 1,019 women multiple stepwise regression analyses were conducted adjusting for age, body mass index, pulse... [Pg.55]

Kawano Y., Kawasaki T., Kawazoe N. et al. (1990). Circadian variations of urinary dopamine, norepinephrine, epinephrine and sodium in normotensive and hypertensive subjects. Nephron 55(3), 277-82. [Pg.214]

The answer is a. (Hardman, pp 16-20.) Sodium bicarbonate is excreted principally in the urine and alkalinizes it. Increasing urinary pH interferes with the passive renal tubular reabsorption of organic acids (such as aspirin and phenobarbital) by increasing the ionic form of the drug in the tubular filtrate. This would increase their excretion. Excretion of organic bases (such as amphetamine, cocaine, phencyclidine, and morphine) would be enhanced by acidifying the urine. [Pg.275]


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Urinary Sodium, Potassium, and Chloride

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