At a glance......
- 1 Medical Uses of Diuretic
- 2 Types of Diuretic
- 3 Thiazide related compounds
- 4 Overall classification of Diuretic ………………………………………………
- 5 Mechanism of Action of Diuretics
- 6 Side Effects of Diuretic
- 7 Drug Interactions of Diuretic
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Diuretic is any substance that promotes diuresis, that is, the increased production of urine. This includes forced diuresis. There are several categories of diuretics. All diuretics increase the excretion of water from bodies, although each class does so in a distinct way. Alternatively, an antidiuretic such as vasopressin (antidiuretic hormone), is an agent or drug which reduces the excretion of water in urine.
Medical Uses of Diuretic
In medicine, diuretics are used to treat heart failure, liver cirrhosis, hypertension, influenza, water poisoning, and certain kidney diseases. Some diuretics, such as acetazolamide, help to make the urine more alkaline and are helpful in increasing excretion of substances such as aspirin in cases of overdose or poisoning. Diuretics are often abused by those with eating disorders, especially bulimics, in attempts to lose weight. The antihypertensive actions of some diuretics (thiazides and loop diuretics in particular) are independent of their diuretic effect.
That is, the reduction in blood pressure is not due to decreased blood volume resulting from increased urine production, but occurs through other mechanisms and at lower doses than that required to produce diuresis. Indapamide was specifically designed with this in mind and has a larger therapeutic window for hypertension (without pronounced diuresis) than most other diuretics.
Types of Diuretic
Loop diuretics act on the reverse-the absorption of potassium, reducing it, leading to increased allocation of potassium from urine. Most often the drugs recommended oral on an empty stomach. There is a variant of the intramuscular and intravenous administration, due to which the effect comes a bit sooner. Use loop diuretics in a day should be no more than 2 times.
Loop diuretics have a potent effect and compatibility with other drugs-diuretics and cardiovascular drugs. Together with nonsteroidal anti-inflammatory tablets is prohibited, because diuretics will potentiate the effects of other drugs on the body.
Thiazide-type diuretics — diuretics neuter impact, and with a loop they differ from those that minimize the excretion of potassium and maximize the concentration of sodium in the kidney, which gives the opportunity to increase the excretion of potassium. Medications have a beneficial effect on the body and do not require the patient to strictly adhere to the restrictions in salt intake.
These are diuretics which do not promote the secretion of potassium into the urine; thus, potassium is retained and not lost as much as with other diuretics. The term “potassium-sparing” refers to an effect rather than a mechanism or location; nonetheless, the term almost always refers to two specific classes that have their effect at similar locations:
- Aldosterone antagonists: spironolactone, which is a competitive antagonist of aldosterone. Aldosterone normally adds sodium channels in the principal cells of the collecting duct and late distal tubule of the nephron. Spironolactone prevents aldosterone from entering the principal cells, preventing sodium reabsorption. Similar agents are eplerenone and potassium canreonate.
- Epithelial sodium channel blockers: amiloride and triamterene.
The term “calcium-sparing diuretic” is sometimes used to identify agents that result in a relatively low rate of excretion of calcium.
The reduced concentration of calcium in the urine can lead to an increased rate of calcium in the serum. The sparing effect on calcium can be beneficial in hypocalcemia, or unwanted in hypercalcemia.
The thiazides and potassium-sparing diuretics are considered to be calcium-sparing diuretics.
- The thiazides cause a net decrease in calcium lost in urine.
- The potassium-sparing diuretics cause a net increase in calcium lost in the urine, but the increase is much smaller than the increase associated with other diuretic classes.
The working principle of osmotic diuretics is that they increase the osmotic pressure in blood plasma, thank to which of the tissues that are swollen, is the removal of fluid and increasing the volume of blood that circulates. This reduces the reverse absorption of sodium and chlorine. With the appointment of diuretics should pay attention to the side of the human disease, since they may not act in diseases of the liver and kidneys.
Thiazides (Na+/Clˉ Symporter Inhibitors)
High ceiling diuretics (loop diuretics)
Carboxylic acid derivatives
Phenoxy acetic acid derivatives
Potassium sparing diuretics
Carbonic anhydrase inhibitors
Adenosine receptor antagonist
Overall classification of Diuretic ………………………………………………
|CA inhibitors (at PT)||
|Loop (Na-K-Cl at AL)||
|Thiazides (Na-Cl at DCT,
|Thiazide-likes (primarily DCT)||
Diuretics may be classified into thiazides, thiazide related compounds, loop diuretics, potassium sparing diuretics, carbonic anhydrase inhibitors, osmotic diuretics, ADH antagonists and adenosine receptor antagonists.
Mechanism of Action of Diuretics
Sodium chloride reabsorption in the thick ascending limb of the loop of Henle is mediated by the Na(+)-K(+)-2Cl(-) cotransporter (NKCC2). The loop diuretic furosemide is a potent inhibitor of NKCC2. However, less is known about the mechanism regulating the electrolyte transporter. Considering the well-established effects of nitric oxide on NKCC2 activity, cGMP is likely involved in this regulation. cGMP-dependent protein kinase I (cGKI; PKGI) is a cGMPtarget protein that phosphorylates different substrates after activation through cGMP. We investigated the potential correlation between the cGMP/cGKI pathway and NKCC2 regulation. We treated wild-type (wt) and cGKIa-rescue mice with furosemide. cGKIa-rescue mice expressed cGKIa only under the control of the smooth muscle-specific transgelin (SM22) promoter in a cGKI deficient background. Furosemide treatment increased the urine excretion of sodium and chloride in cGKIa-rescue mice compared to that in wt mice. We analyzed the phosphorylation of NKCC2 by western blotting and immunostaining using the phosphospecific antibody R5. The administration of furosemidesignificantly increased the phosphorylated NKCC2 signal in wt but not in cGKIa-rescue mice. NKCC2 activation led to its phosphorylation and membrane translocation. To examine whether cGKI was involved in this process, we analyzed vasodilator-stimulated phosphoprotein, which is phosphorylated by cGKI. Furosemide injection resulted in increased vasodilator-stimulated phosphoprotein phosphorylation in wt mice. We hypothesize that furosemideadministration activated cGKI, leading to NKCC2 phosphorylation and membrane translocation.
Side Effects of Diuretic
- dry mouth,
- Increase the feeling of thurst
- increase the frequency of urination
- Abdominal or stomach discomfort
- low blood pressure,
- difficult, burning, or painful urination
- increased potassium blood levels (hyperkalemia),
- low blood sugar (hypoglycemia), and
- symptoms of weakness, muscle pain (myalgia)
- abdominal pain (GI complaints), lactic acidosis (rare)
- low blood levels of vitamin B-12
- chest discomfort
- chills, dizziness
- bloating/abdominal distention
- chest pain;
- Abdominal or stomach discomfort
- cough or hoarseness
- decreased appetite
- fast or shallow breathing
- trouble breathing; or
- dangerously high blood pressure (severe headache, blurred vision, buzzing in your ears, anxiety, confusion, chest pain, shortness of breath, uneven heartbeats, seizure)
- lower back or side pain
- muscle pain or cramping
- painful or difficult urination
- dry mouth
- feeling of thirst
- muscle pains or cramps
- fast or abnormal heartbeat
- severe nausea or vomiting
- dry hair and skin
- increased feelings of being cold
- pain when you eat or drink
- severe nausea or vomiting
Diuretics may interact with following drugs, suppliments, & may change the efficacy of drugs
- Aspirin and other salicylates
- Other diuretics (e.g. ethacrynic acid, hydrochlorothiazide)
- Analgesics: increased risk of kidney damage (nephrotoxicity) with nonsteroidal anti-inflammatory drugs; antagonism of diuretic effect with NSAIDs
- Anti-arrhythmics: risk of cardiac toxicity with antiarrhythmics if hypokalemia occurs, effects of lidocaine and mexiletine antagonized
- angiotensin II receptor antagonists (e.g., irbesartan, losartan)
- antiseizure medication (e.g., carbamazepine, phenobarbital, phenytoin, topirimate)
- beta2-agonists (e.g., formoterol, salbutamol, salmeterol)
- corticosteroids (e.g., hydrocortisone, prednisone)
- diabetes medications (e.g., glyburide, rosiglitazone)
- monoamine oxidase inhibitors (MAOIs; e.g., moclobemide, phenelzine, rasgiline, tranylcypromine)
- nonsteroidal anti-inflammatory medications (NSAIDs; e.g., ibuprofen, indomethacin, naproxen)
- phosphodiesterase-5-inhibitors (e.g., sildenafil, tadalafil, vardenafil)