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  • 1
    Online Resource
    Online Resource
    New York, NY :Springer,
    Keywords: Drugs-Solubility-Testing. ; Electronic books.
    Description / Table of Contents: Proceedings of a workshop held in Baltimore, Maryland, September 4-6, 1996.
    Type of Medium: Online Resource
    Pages: 1 online resource (299 pages)
    Edition: 1st ed.
    ISBN: 9781468460360
    Series Statement: Advances in Experimental Medicine and Biology Series ; v.423
    Language: English
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  • 2
    Online Resource
    Online Resource
    San Rafael :Morgan & Claypool Life Science Publishers,
    Keywords: Potassium in the body. ; Potassium -- Metabolism -- Regulation. ; Electronic books.
    Description / Table of Contents: Several physiological mechanisms act to regulate renal potassium excretion and distribution. Together they comprise an integrated control system that may be envisioned as being made up of several interacting negative feedback control mechanisms, all affecting removal of potassium from the extracellular fluid by renal excretion or transfer across cell membranes into or out of the intracellular compartment. The intent of this presentation is to describe the mechanisms of potassium regulation, beginning in Chapter 1 with an overview of the system, Chapter 2 with mechanisms that determine movement of potassium between the extracellular and intracellular compartments, in Chapter 3 focusing on renal tubular transport systems, and in Chapter 4 presenting the mechanisms of control of aldosterone secretion. Greatest emphasis will be on describing the integrated functions of the components, in Chapter 5, as they operate together in a system to regulate extracellular potassium concentration in response to commonly encountered challenges. In addition, interactions between potassium regulation and commonly used medications will be considered in Chapter 6, and in Chapter 7 the causes and treatment of dysregulation of potassium will be discussed. Table of Contents: Preface / Introduction / Regulaton of Potassium Distribution / Potassium Transport in Segments of the Nephron / Regulation of Potassium Excretion / Control of Aldosterone Secretion / System Analysis of Potassium Regulation / Pharmacotherapeutics Interactions / Disorders of Potassium Control / References / Author Biography.
    Type of Medium: Online Resource
    Pages: 1 online resource (103 pages)
    Edition: 1st ed.
    ISBN: 9781615045013
    Series Statement: Colloquium Series on Integrated Systems Physiology: from Molecule to Function Series
    DDC: 615.7
    Language: English
    Note: Intro -- Preface -- Introduction -- Regulaton of Potassium Distribution -- 2.1 Effect of Sodium, Potassium ATPase Activity on Distribution -- 2.2 Hormonal Effects on Distribution -- 2.3 Aldosterone's Effect on Distribution -- 2.4 Factors Transiently Affecting Distribution -- Potassium Transport in Segments of the Nephron -- 3.1 Reabsorption in the Proximate Tubule -- 3.2 Reabsorption in the Loop of Henle -- 3.3 Secretion and Absorption in the Distal Nephron -- Regulation of Potassium Excretion -- 4.1 Effect of Tubular Flow Rate on Reabsorption -- 4.2 Hormonal Effects on Reabsorption -- 4.2.1 Angiotensin II -- 4.2.2 Vasopressin -- 4.2.3 Prostaglandin E2 -- Control of Aldosterone Secretion -- 5.1 Cellular Mechanisms of Aldosterone Secretion -- 5.2 Control of Renin Release -- 5.3 Long-term Control of Aldosterone -- System Analysis of Potassium Regulation -- 6.1 Tenets of the Hypothesis -- 6.1.1 The Mathematical Model -- 6.2 Comparison of Model Simulations with Experimental Data -- 6.3 Model Prediction -- 6.3.1 Clinically Relevant Model Predictions -- 6.4 Questions Raised by the Model -- 6.5 Summary -- Pharmacotherapeutics Interactions -- 7.1 Diuretics -- 7.2 Inhibitors of Angiotensin Formation or Receptor Binding -- 7.3 Mineralocorticoid Antagonists -- 7.4 Beta Adrenergic Receptor Antagonists -- 7.5 Insulin -- Disorders of Potassium Control -- 8.1  Hyperkalemia -- 8.2  Hypokalemia -- 8.2.1 Clinical Symptoms -- 8.3  Etiology of Potassium Depletion and Hypokalemia -- 8.3.1 Gastrointestinal Loss -- 8.3.2 Loss in Sweat -- 8.4  Diagnosis and Treatment -- 8.4.1 Dietary Modification -- 8.4.2 Potassium Supplements -- 8.4.3 Potassium Sparing Diuretics -- 8.5  Summary -- References -- Author Bibliography.
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 8 (1981), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. To determine if increases in plasma sodium concentration P[Na] have any sustained effects of the renin-aldosterone system, P[Na] was increased in a group of six dogs over a period of 6 days by increasing sodium intake from 10 to 200 mmol per day while a fixed 700 ml per day water intake was maintained along with a continuous i.v. infusion of antidiuretic hormone (ADH) at a rate of 2.4 units per day.2. P[Na] rose from 137.3 ± 2.0 to 153.6 ± 6.5 mmol/1 during the high intake period. Plasma potassium concentration, 22Na space, and mean arterial pressure all remained near control levels in response to Na loading.3. Plasma renin activity (PRA) averaged 1.0 ± 0.1 ngAI/ml per hour on the final low Na day and fell transiently to 0.6 ± 0.2 ngAI/ml per hour on the first day of sodium loading. For the duration of the study it remained at the control level. Plasma aldosterone concentration fell from the low Na level of 15.4 ± 2.4 ng/100 ml to 10.5 ± 1.5 ng/100 ml on the final day of high Na intake.4. We conclude that increases in P[Na] in the absence of concomitant changes in P[K], 22Na space and MAP do not have a sustained effect on control of renin release but may exert a negative effect on aldosterone secretion.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 8 (1981), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of maximally antidiuretic, subpressor antidiuretic hormone (ADH) administration on the renin-aldosterone system were studied in dogs during 4 days of continuous intravenous infusion of ADH at a rate of 0.067 mU/kg per min. Water intake was limited to 700 ml/day to avoid changes in fluid volume status.2. At the conclusion of the four-day study, plasma sodium concentration had fallen from 140.3 ± 0.8 to 137.2 ± 2.0 mmol/l, plasma potassium concentration, 22Na space, and mean arterial pressure remained within the control ranges.3. Neither plasma renin activity nor plasma aldosterone concentration showed any tendency to change in response to the ADH infusion.4. The results indicate that physiologic levels of ADH have no prolonged, direct effect on the renin-aldosterone system.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 2 (1975), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Many forms of human and experimental hypertension begin with compromised renal function. Essential hypertension may be another such case.2. The kidneys of subjects with essential hypertension excrete normal amounts of salt and water at higher-than-normal renal perfusing pressures. Other overt signs of renal dysfunction are few; renal disease is excluded by definition. However, renal blood flow and glomerular filtration rate are usually less than normal in essential hypertension.3. Renal afferent resistance can be calculated from arterial pressure, renal blood flow, and an estimate of glomerular capillary pressure. These calculations indicate that afferent resistance is increased to two or more times normal in essential hypertension.4. It is not clear whether afferent constriction causes hypertension or results from it. The ability of high pressure to produce vascular damage points to the latter. But, most essential hypertensives show low-to-normal plasma renin levels and a marked afferent dilation after saline loading. These observations do not suggest nephrosclerosis: they are consistent with a causal role for afferent constriction.5. We can speculate that, in essential hypertension, there is a defect in one of the mechanisms that sets afferent resistance. Afferent constriction could result from extrinsic influences (neural or humoral) or something totally within the kidney, such as abnormal handling of information from the macula densa.6. The effect of afferent constriction on salt-and-water excretion would theoretically be offset by elevated arterial pressure so that the actual salt-and-water excretion would be normal, but only so long as the arterial pressure remained elevated.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The Kaposi's sarcoma–associated herpesvirus (KSHV) latency-associated nuclear antigen (LANA) is expressed in all KSHV-associated tumors, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL). We found that β-catenin is overexpressed in both PEL cells and KS tissue. ...
    Type of Medium: Electronic Resource
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