A side effect of some diuretics is low potassium. Yes, some diuretics — also called water pills — decrease potassium in the blood. Diuretics are commonly used to treat high blood pressure hypertension. They lower blood pressure by helping your body eliminate sodium and water through your urine.
However, some diuretics can also cause you to eliminate more potassium in your urine. This can lead to low potassium levels in your blood hypokalemia.
Not all diuretics cause this problem. Nephrocalcinosis, nephrolithiasis, hypomagnesemia, and hyperuricemia can potentially complicate treatment with some diuretic agents. Reported idiosyncratic reactions to diuretics include interstitial nephritis, noncardiogenic pulmonary edema, pancreatitis, and myalgias. Conclusions: Potential side effects of a diuretic can often be anticipated from its mode of action on the kidney.
These complications may be mitigated with careful monitoring, dosage adjustment, and replacement of electrolyte losses. Other side effects are idiosyncratic and cannot be prevented. Abstract Background: Diuretics are widely used and generally safe, but like any therapeutic agents, they may cause side effects. Publication types Review. This altered handling of sodium and water leads to both diuresis increased water loss and natriuresis increased sodium loss. By acting on the thick ascending limb, which handles a significant fraction of sodium reabsorption, loop diuretics are very powerful diuretics.
These drugs also induce renal synthesis of prostaglandins, which contributes to their renal action including the increase in renal blood flow and redistribution of renal cortical blood flow. Thiazide diuretics , which are the most commonly used diuretic, inhibit the sodium-chloride transporter in the distal tubule.
Nevertheless, they are sufficiently powerful to satisfy many therapeutic needs requiring a diuretic. Their mechanism depends on renal prostaglandin production. Because loop and thiazide diuretics increase sodium delivery to the distal segment of the distal tubule, this increases potassium loss potentially causing hypokalemia because the increase in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine.
The increased hydrogen ion loss can lead to metabolic alkalosis. Part of the loss of potassium and hydrogen ion by loop and thiazide diuretics results from activation of the renin-angiotensin-aldosterone system that occurs because of reduced blood volume and arterial pressure. Increased aldosterone stimulates sodium reabsorption and increases potassium and hydrogen ion excretion into the urine. There is a third class of diuretic that is referred to as potassium-sparing diuretics.
Unlike loop and thiazide diuretics, some of these drugs do not act directly on sodium transport. Some drugs in this class antagonize the actions of aldosterone aldosterone receptor antagonists at the distal segment of the distal tubule. This causes more sodium and water to pass into the collecting duct and be excreted in the urine. The reason for this is that by inhibiting aldosterone-sensitive sodium reabsorption, less potassium and hydrogen ion are exchanged for sodium by this transporter and therefore less potassium and hydrogen are lost to the urine.
Other potassium-sparing diuretics directly inhibit sodium channels associated with the aldosterone-sensitive sodium pump, and therefore have similar effects on potassium and hydrogen ion as the aldosterone antagonists. Because this class of diuretic has relatively weak effects on overall sodium balance, they are often used in conjunction with thiazide or loop diuretics to help prevent hypokalemia.
Carbonic anhydrase inhibitors inhibit the transport of bicarbonate out of the proximal convoluted tubule into the interstitium, which leads to less sodium reabsorption at this site and therefore greater sodium, bicarbonate and water loss in the urine. These are the weakest of the diuretics and seldom used in cardiovascular disease. Their main use is in the treatment of glaucoma. Through their effects on sodium and water balance, diuretics decrease blood volume and venous pressure.
This decreases cardiac filling preload and, by the Frank-Starling mechanism , decreases ventricular stroke volume and cardiac output , which leads to a fall in arterial pressure. The decrease in venous pressure reduces capillary hydrostatic pressure , which decreases capillary fluid filtration and promotes capillary fluid reabsorption, thereby reducing edema if present. There is some evidence that loop diuretics cause venodilation, which can contribute to the lowering of venous pressure.
Long-term use of diuretics results in a fall in systemic vascular resistance by unknown mechanisms that helps to sustain the reduction in arterial pressure. Antihypertensive therapy with diuretics is particularly effective when coupled with reduced dietary sodium intake. The efficacy of these drugs is derived from their ability to reduce blood volume, cardiac output, and with long-term therapy, systemic vascular resistance.
Thiazide diuretics, particularly chlorthalidone, are considered "first-line therapy" for stage 1 hypertension.
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