Sodium, renal tubular reabsorption

Sodium bicarbonate increases renal tubular reabsorption of amphetamine, resulting in a prolonged amphetamine elimination half-life be aware of this combination. 

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. 

ANGIOTENSIN II RECEPTOR ANTAGONISTS LITHIUM Risk of lithium toxicity 1 excretion of lithium possibly due to 1 renal tubular reabsorption of sodium in proximal tubule Watch for lithium toxicity monitor lithium levels... 

Vaupshas H J, Levy M 1990 Distribution of saline following acute volume loading postural effects. Clinical and Investigative Medicine 13 165-177 Velanovich V 1989 Crystalloid versus colloid fluid resuscitation a meta-analysis of mortality. Surgery 105 65-71 Vukmir R B, Bircher N G, Radovsky A et al 1995 Sodium bicarbonate may improve outcome in dogs with brief or prolonged cardiac arrest. Critical Care Medicine 23 515-522 Walton R J 1979 Effect of intravenous sodium lactate on renal tubular reabsorption of phosphate in man. Clinical Science 57 125-127... 

Elevates osmotic pressure of glomerular filtrate, increases flow of water into interstitial fluid and plasma, inhibiting renal tubular reabsorption of sodium, chloride, producing diuresis. Enhances flow of water from eye into plasma, reducing intraocular pressure (IOP)... 

Clinical effects of lithium are slow in onset and may not be apparent before a week or two of daily treatment. Lithium is cleared exclusively by the kidney at a rate 20% of that of creatinine. Clearance is influenced by many factors, including renal function, serum sodium concentration, hydration state, pregnancy, and the presence of other drugs. High urinary levels of sodium inhibit renal tubular reabsorption of lithium, thus decreasing its plasma levels. By decreasing blood volume, thiazides may increase lithium plasma levels. Any drug that can cross the blood-brain barrier can cross the placental barrier The answer is (C). 

Jabbour SA, Goldstein BJ. Sodium glucose co-transporter 2 inhibitors blocking renal tubular reabsorption of glucose to improve glycaemic control in patients with diabetes. Int J Chn Pract 2008 62(8) 1279-84. 

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. 

Hesse, I.F.A. and Johns, E.J. (1984). The subtype of a-adrcnoceptor involved in the neural control of renal tubular sodium reabsorption in the rabbit. J. Physiol. 328, 527-538. 

Dietary salt restriction was one of the first successful therapeutic maneuvers for the reduction of blood pressure. During the past two decades, a variety of pharmacologic agents have been developed which promote diuresis by interfering with the tubular reabsorption of sodium. Although diuretic agents differ significantly in chemical structure and in their mechanism of action on the renal tubule, they all have in common the ability to decrease blood pressure. 

Kidney Methylxanthines exert mild diuretic action by inhibiting tubular reabsorption of sodium and water. In addition, it increases renal blood flow and glomerular filtration rate. 

Renal function is depressed by opioids. It is believed that in humans this is chiefly due to decreased renal plasma flow. In addition, opioids have been found to have an antidiuretic effect in humans. Mechanisms may involve both the CNS and peripheral sites. Opioids also enhance renal tubular sodium reabsorption. The role of opioid-induced changes in antidiuretic hormone (ADH) release is controversial. Ureteral and bladder tone are increased by therapeutic doses of the opioid analgesics. Increased sphincter tone may precipitate urinary retention, especially in postoperative patients. Occasionally, ureteral colic caused by a renal calculus is made worse by opioid-induced increase in ureteral tone. 

Elhawary AM, Pang CC, b I-Adrenergic receptors mediate renal tubular sodium and water reabsorption in the rat. Br J... 

The renal toxicity associated with aldesleukin is dose-related. It manifests as uremia, oliguria, fluid retention, and pronounced renal tubular sodium reabsorption (77). No evidence of tubular dysfunction has been found. There is reduced renal plasma flow associated with reduced renal prostaglandin synthesis and increased plasma renin activity, which may explain the mechanism (84). 

The mechanisms by which NSAIDs affect cardiovascular function are complex and controversial. They may include reduced blood flow, a reduction in the filtered load of sodium, an increase in tubular reabsorption of sodium, and a reduction in the synthesis of PGE-1, which may be associated with raised blood viscosity and increased peripheral vascular resistance. This is perhaps the primary mechanism, which is due to increased renal synthesis of endothelin-1. 

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