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== Regulation of potassium level == | == Regulation of potassium level == | ||
The potassium level is mainly regulated by the renin-angiotensin-aldosterone system in the kidneys. Increasing levels of potassium stimulates RAAS and therefore aldosterone production, which in turn stimulates the [[Na+/K+-ATPase]] in the distal tubules and collecting duct. This causes K+ and H+ loss. | The potassium level is mainly regulated by the renin-angiotensin-aldosterone system in the kidneys. Increasing levels of potassium stimulates RAAS and therefore aldosterone production, which in turn stimulates the [[Na+/K+-ATPase]] in the distal tubules and collecting duct. This causes K+ and H+ loss. This system is very effective and therefore prevents hyperkalaemia from developing, as long as the kidneys are functioning. | ||
The daily intake of potassium in the diet is approximately 40 – 120 mmol K+. This extra potassium reaches the extracellular space and not the cells in normal cases. 90% of excreted potassium is excreted by the kidneys, the remaining through the <abbr>GI</abbr> tract. | The daily intake of potassium in the diet is approximately 40 – 120 mmol K+. This extra potassium reaches the extracellular space and not the cells in normal cases. 90% of excreted potassium is excreted by the kidneys, the remaining through the <abbr>GI</abbr> tract. | ||
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==== Insulin ==== | ==== Insulin ==== | ||
Insulin enhances Na+/K+ ATPase activity, causing K+ to enter the cells. | Insulin enhances Na+/K+ ATPase activity, causing K+ to enter the cells. We use the fact that insulin causes intracellular movement of H+ in the management of [[hyperkalaemia]]. | ||
==== Others ==== | ==== Others ==== |