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Hypokalemia Hypokalemia describes the condition in which your body lacks adequate potassium. Several factors can contribute.

Excessive diarrhea or vomiting, or diuretics that cause your body to excrete large amounts of urine, may deplete your body of potassium. Certain conditions in which your intestines are unable to digest and absorb nutrients might reduce your intake of potassium. Eating disorders such as bulimia or anorexia might also cause hypokalemia.

Read more: Hypertension Minerals work to regulate muscular contractions, including the heart muscle. Through an interaction between potassium, sodium and calcium, your specialized cells depolarize and are able to perform their jobs. For your heart, that job is pumping blood. When your potassium levels are too low, this interaction is in jeopardy; it manifests itself as an increase in blood pressure. In a study published in the "Journal of the American Medical Association" in December 1997, the relationship between potassium and blood pressure is explored. This study suggests that low dietary potassium contributes to hypertension, and that adding dietary potassium is sometimes enough to control high blood pressure. Acid-Base Balance All dietary minerals work in cooperation to maintain homeostasis in your body. Homeostasis includes a slightly higher than neutral pH of your blood. Without an adequate supply of potassium, you risk suffering from alkalosis. Alkalosis occurs when your body fluids are too basic, or alkaline. More specifically, alkalosis caused by low potassium is referred to as hypokalemic alkalosis. When your body is not in homeostasis, it cannot function properly. Alkalosis can cause tremors, confusion, uncontrollable muscle spasm, nausea and vomiting. Kidney Stones If you get too little potassium in your diet, the likelihood of developing kidney stones increases. Urinary calcium is the main cause of kidney stones. Potassium balances out the amount of calcium in your urinary tract. Without adequate potassium, an increase in urinary calcium occurs. More urinary calcium can mean painful kidney stones.

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Potassium homeostasis
Potassium, the most abundant intracellular cation, is essential for the life of the organism. Potassium is obtained through the diet, and common potassium-rich foods include meats, beans, fruits, and potatoes. Gastrointestinal absorption is complete, resulting in daily excess intake of approximately 1 mEq/kg/d (60-100 mEq). Ninety percent of this excess is excreted through the kidneys, and 10% is excreted through the gut. Potassium homeostasis is maintained predominantly through the regulation of renal excretion. The most important site of regulation is the collecting duct, where aldosterone receptors are present.

Excretion is increased by (1) aldosterone, (2) high sodium delivery to the collecting duct (eg, diuretics), (3) high urine flow (eg, osmotic diuresis), (4) high serum potassium level, and (5) delivery of negatively charged ions to the collecting duct (eg, bicarbonate). Excretion is decreased by (1) absence or relative deficiency of aldosterone, (2) low sodium delivery to the collecting duct, (3) low urine flow, (4) low serum potassium level, and (5) renal failure. Kidneys adapt to acute and chronic alterations in potassium intake. When potassium intake is chronically high, potassium excretion likewise is increased. In the absence of potassium intake, obligatory renal losses are 10-15 mEq/d. Thus, chronic losses occur in the absence of any ingested potassium. The kidney maintains a central role in the maintenance of potassium homeostasis, even in the setting of chronic renal failure. Renal adaptive mechanisms allow the kidneys to maintain potassium homeostasis until the glomerular filtration rate drops to less than 15-20 mL/min. Additionally, in the presence of renal failure, the proportion of potassium excreted through the gut increases. The colon is the major site of gut regulation of potassium excretion. Therefore, potassium levels can remain relatively normal under stable conditions, even with advanced renal insufficiency. However, as renal function worsens, the kidneys may not be capable of handling an acute potassium load.

Serum potassium level

Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a very poor indicator of total body stores. Because potassium moves easily across cell membranes, serum potassium levels reflect movement of potassium between intracellular and extracellular fluid compartments, as well as total body potassium homeostasis. Mechanisms for sensing extracellular potassium concentration are not well understood. Evidence suggests that adrenal glomerulosa cells and pancreatic beta cells may play a role in potassium sensing, resulting in alterations in aldosterone and insulin secretion.[1, 2] As both of these hormonal systems play important roles in potassium homeostasis, these new findings are no surprise; however, the molecular mechanisms by which these potassium channels signal changes in hormone secretion and activity have still not been determined. Muscle contains the bulk of body potassium, and the notion that muscle could play a prominent role in the regulation of serum potassium concentration through alterations in sodium pump activity has been promoted for a number of years. Insulin stimulated by potassium ingestion increases the activity of the sodium pump in muscle cells, resulting in an increased uptake of potassium. Studies in a model of potassium deprivation demonstrate that acutely, skeletal muscle develops resistance to insulin-stimulated potassium uptake even in the absence of changes in muscle cell sodium pump expression. However, long term potassium deprivation results in a decrease in muscle cell sodium-pump expression, resulting in decreased muscle uptake of potassium.[3, 4, 5] Thus, there appears to be a well-developed system for sensing potassium by the pancreas and adrenal glands, resulting in rapid adjustments in immediate potassium disposal and for longterm potassium homeostasis. High potassium states stimulate cellular uptake via insulinmediated stimulation of sodium-pump activity in muscle and stimulate potassium secretion by the kidney via aldosterone-mediated enhancement of distal renal expression of secretory potassium channels (ROMK). Low potassium states result in insulin resistance, impairing potassium uptake into muscle cells, and cause decreased aldosterone release, lessening renal potassium excretion.

Several factors regulate the distribution of potassium between the intracellular and extracellular space, as follows: Glycoregulatory hormones: (1) Insulin enhances potassium entry into cells, and (2) glucagon impairs potassium entry into cells. y Adrenergic stimuli: (1) Beta-adrenergic stimuli enhance potassium entry into cells, and (2) alpha-adrenergic stimuli impair potassium entry into cells. y pH: (1) Alkalosis enhances potassium entry into cells, and (2) acidosis impairs potassium entry into cells. An acute increase in osmolality causes potassium to exit from cells. An acute cell/tissue breakdown releases potassium into extracellular space.

Aldosterone is the principal mineralocorticoid in man. Its functions include regulation of extracellular volume and potassium homeostasis through its effects on the renal distal convoluted tubule. Extra-renal actions of aldosterone on cardiovascular tissues, the colon and salivary glands are also well established. Excess production of aldosterone, due to either primary or secondary disorders, is prevalent in the general population, and is an important cause of morbidity and mortality. This chapter reviews the physiology of aldosterone action, as well as the clinical features, biochemical diagnosis, and treatment of hyperaldosteronism.


Aldosterone Regulation
Aldosterone is synthesized in the zona glomerulosa of the adrenal gland. Its production is restricted to this layer of the adrenal cortex because of zonal-specific expression of aldosterone synthase (CYP11B2). Aldosterone secretion is under the control of three primary factors: angiotensin II, potassium, and adrenocorticotropic hormone (ACTH). The renin-angiotensin system (RAS) is a principal regulator of aldosterone secretion. Renin, an enzyme produced in the juxtaglomerular apparatus of the kidney, catalyzes the conversion of angiotensinogen (an inactive precursor peptide) to angiotensin I. Angiotensin I undergoes further enzymatic conversion by angiotensin-converting enzyme (ACE) to produce angiotensin II. Angiotensin II acts via the angiotensin receptor to stimulate the release of aldosterone by increasing the transcription of aldosterone synthase. The RAS serves to regulate

two critical functions in the human body: sodium homeostasis and arterial pressure (1). Through complex negative feedback loops (Figure 1), activity of the RAS can be suppressed or enhanced by sodium balance, intravascular volume, and other factors. For example, renin (and consequently aldosterone) production is stimulated by low tubular sodium or low renal perfusion; conversely, renin is suppressed by high sodium content or high perfusion pressure. Angiotensin II and other components of the RAS are also expressed locally in the zona glomerulosa and regulate aldosterone production in a paracrine fashion. Aldosterone secretion is also directly stimulated by potassium (Figure 1), which increases transcription of aldosterone synthase in the zona glomerulosa. ACTH is another aldosterone secretagogue, although the effect is modest and transient. Prolonged ACTH infusion over 24 hours leads to a return of aldosterone levels to baseline (2). Other factors that regulate aldosterone include dopamine, atrial natriuretic peptide (ANP) and heparin, which all inhibit its production (2).

Figure 1. Renin-angiotensin-aldosterone and potassiumaldosterone negative-feedback loops. Aldosterone production is determined by input from each loop. (Adapted and redrawn from Williams GH, Dluhy RG. Disease of the adrenal cortex. In: Fauci AD, Braunwald E, Isselbacher KJ, et al, eds. Harrison's Principles of Internal Medicine. 15th ed. New York: McGraw-Hill, 2001)

Aldosterone Action
The primary functions of aldosterone are to regulate extracellular volume and potassium balance. These effects are mediated through the effects of aldosterone on the distal nephron. Aldosterone binds to the type I mineralocorticoid receptor in the cytosol of distal cortical collecting principal cells. Translocation of the hormonereceptor complex to the nucleus leads to modification of target gene expression, and subsequently increased number of open sodium channels on apical cell

membranes. The resulting increase in reabsorption of sodium generates a negative electrical gradient in the tubular lumen, which promotes potassium and hydrogen ion excretion to maintain electrical neutrality (2, 3).

Other Aldosterone Effects

Emerging evidence suggests that aldosterone has additional effects beyond regulation of sodium-potassium balance and arterial pressure, and that aldosterone excess leads to cardiovascular and renal toxicity and contributes to increased morbidity and mortality. Importantly, these adverse actions of aldosterone occur only in the sodium replete state when levels are inappropriately elevated, and appear to be at least in part independent of elevated blood pressure (4-7). Animals treated with excessive doses of aldosterone develop cardiovascular injury (6, 8). Patients with primary aldosteronism (PA), when compared with matched essential hypertensives, have increased left ventricular wall and carotid intima media thickness, as well as impaired diastolic and endothelial function (9-12). PA is also associated with higher incidence of myocardial infarction and stroke than essential hypertension with similar degree of blood pressure elevation (13, 14). Furthermore, small studies have shown improvement in endothelial function in hyperaldosteronism treated surgically or with mineralocorticoid receptor antagonists (11). The excess cardiovascular events associated with hyperaldosteronism also appear to be reversed after treatment (15). Excessive aldosterone production may also result in renal injury through mechanisms independent of blood pressure. Patients with PA have higher urinary albumin excretion and decreased intrarenal vascular resistance than controls matched for blood pressure elevation; these findings were reversed by medical or surgical treatment (16). Finally, there is some evidence to support an association between aldosterone and the metabolic syndrome: primary aldosteronism has been associated with hyperglycemia and insulin resistance in some (17) but not all (18) studies.

What is is potassium?
Small chemicals in the body known as electrolytes are crucial for cells to function. Potassium is one of the main electrolytes, and is concentrated within the cells of the body. Only 2% of the body's total potassium is available in the serum (the fluid part of the bloodstream that is not red or white blood cells or platelets). Small changes in the serum levels of potassium can affect body function. One of the important functions of potassium is maintenance of the cell electrical potential. The serum bathes the cells, and if the serum potassium level falls, cells with high electrical activity (for example, muscles and nerves) are particularly affected.

Normal potassium levels measured in the serum range from 3.5 to 5.0 mEq/liter. Normal daily intake of potassium is 70-100 mEq (270 to 390 mg/dl), and requires the kidneys to remove that same amount each day. If more is removed, the body's total potassium store will be decreased, and the result is hypokalemia (hypo=low + kal=potassium +emia= in the blood) occurs. Potassium enters the body through dietary intake. Examples of potassium rich foods include:
y y y y

Fresh fruits: bananas, cantaloupe, oranges, strawberries, kiwi, avocados, apricots Fresh vegetables: greens, mushrooms, peas, beets, tomatoes Meats: beef, fish, turkey, Juices: Orange, prune, apricot, grapefruit

What are the causes of low potassium?

Hypokalemia is not commonly caused by poor dietary intake. Excessive loss is the most common reason that potassium levels are low. Loss of potassium may occur from both the gastrointestinal (GI) tract and from the kidney. Potassium loss from the intestines may be caused by:
y y y

Vomiting Diarrhea Ileostomy: In some patients who have had bowel surgery and an ileotomy formed, significant potassium loss can occur.

y y

Villous adenoma (a type of colon polyp that can cause the colon to leak potassium) Laxative use

Causes of potassium loss from the kidney:

y y

Diuretic medications (water pills) like hydrochlorothiazide (HCTZ) orfurosemide (Lasix) Elevated corticosteroid levels, either from medication like prednisone or from Cushing's Syndrome

Elevated levels of aldosterone, a hormone that can increase with renal artery stenosis or adrenal tumors

y y

Renal tubular acidosis Low body magnesium levels

Low potassium levels may result from side effects of some medications:
y y y

Aminoglycosides like gentamicin (Garamycin) or tobramycin (Nebcin) Amphotericin B Prednisone

What Are the Symptoms of Low Potassium? Potassium affects the way neuromuscular cells discharge energy (depolarize) and then regenerate (repolarize) that energy to be able to fire again. When potassium levels are low, the cells cannot repolarize and are unable to fire repeatedly, as is needed for the function of muscles and nerves. It is understandable then that the effects of low potassium include: y muscle weakness,
y y

muscle aches, and muscle cramps.

Since the heart is also a muscle, there can be some changes in the electrocardiogram (EKG or ECG) that are associated with hypokalemia. Palpitations (irregular heartbeats) may be experienced by the patient. In severe cases, hypokalemia can lead to dangerous disturbances in heart rhythm (arrhythmias).

Potassium (K+) creates most of the osmotic pressure in intracellular fluid (ICF), and is the most abundant cation in ICF. It is essential for electrical activity of neurons and muscle cells. The primary substance regulating potassium concentration is aldosterone, which stimulates the distal tubule of the nephron unit to excrete potassium. Imbalances cause hypo- or hyperkalemia.

Hypokalemia is a consequence of vomiting, diarrhea, or kidney disease causing fatigue, confusion, and possible cardiac failure.

Hyperkalemia is a consequence of Addison's disease causing weakness, abnormal sensations, and cardiac arrhythmias with possible arrest

Potassium is essential for many body functions, including muscle and nerve activity. The electrochemical gradient of potassium between the intracellular and extracellular space is essential for nerve function; in particular, potassium is needed to repolarize the cell membrane to a resting state after an action potential has passed. Decreased potassium levels

in the extracellular space will cause hyperpolarization of the resting membrane potential. This hyperpolarization is caused by the effect of the altered potassium gradient on resting membrane potentialas defined by the Goldman equation. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential. In certain conditions, this will make cells less excitable. However, in the heart, it causes myocytes to become hyperexcitable. Lower membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential more likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the IKrpotassium current[13] and delays ventricular repolarization. This delayed repolarization may promote reentrant arrhythmias.