Impaired Renin Responsiveness With Secondary Hypoaldosteronism

Gossain, Ved V.; Ferrara, Edward V.; Werk, Emile E.; Srivastava, Laxmi S.; Privitera, Philip J.; Hanenson, Irwin B.

doi:10.1001/archinte.1973.03650120085016

Cited by 11 publications

(1 citation statement)

References 32 publications

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“…Support for this hypothesis was provided by Tuck et al (99), who found a diminished plasma renin response to isoproterenol in fi ve hyperkalemic diabetic patients with "hyporeninemic hypoaldosteronism" and evidence of autonomic and/or peripheral neuropathy. In contrast, several studies describe normal plasma and/or urinary catecholamines in patients with selective hypoaldosteronism (123)(124)(125)(126), and deChatel et al (98) found no relation between decreased plasma epinephrine levels and defects in the renin-aldosterone axis in 59 diabetics. In summary, it seems unlikely that decreased sympathetic nervous system activity and/or low circulating plasma epinephrine levels can explain the hyporeninemia in most diabetic subjects.…”

Section: Impaired Renin-aldosterone Axismentioning

confidence: 98%

Clinical Disorders of Hyperkalemia

DeFronzo¹,

BIa²,

Smith³

1982

Annu. Rev. Med.

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Potassium DistributionTotal body potassium in a healthy adult is approximately 50 meqlkg body weight or about 3500 meq for a 70-kg man (1, 2). Most of this is located within cells (Figure 1), primarily muscle, at a concentration of about 150 meq/L. Only 2% of total body potassium is located in the extracellular fl uid, normally at concentrations of 3.5 -5.0 meq/L. The maintenance of this high intracellular to extracellular K concentration depends upon the Na-K ATPase pump (3, 4) as well as other fac tors, including H+ balance, plasma tonicity, and plasma insulin, epinephrine, and aldosterone concentrations (5). The large difference in potassium concentration across the cell mem brane is critical for normal cell fu nction since it is the primary determinant of the resting membrane potential. Small changes in the intracellular/ex tracellular K ratio can severely disturb neuromuscular fu nction, particu larly of the heart. A gain (or loss) fr om the extracellular space of an amount of potassium equal to only I % of the total body K content (35 meq) can cause a 50% increase (or decrease) in plasma K concentration. Such a change would have pronounced effects on neuromuscular func ti on. Like wise, redistribution of a similar amount of potassium fr om the intracellular to extracellular (or vice versa) fluid compartmen t without net gain or loss of K fr om the body, would similarly affect neuromuscular excitability. Thus, it is important that both the total amount of potassium within the body and the distribution of potassium between intracellular and extracellu lar fl uid compartments be closely regulated.In healthy man, potassium enters only via the gastrointestinal tract. Approximately 100 meq of K is ingested per day and essentially all of this is absorbed fr om the stomach and upper gastrointestinal tract. Approxi-521 0066-4219/8 2/040 1-0521 $02.00 Annu. Rev. Med. 1982.33:521-554. Downloaded from www.annualreviews.org Access provided by Haifa University on 01/05/15. For personal use only.Quick links to online content Further ANNUAL REVIEWS

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