Skip to main content

A COMPARATIVE PHARMACOLOGICAL STUDY OF DIURETIC DRUGS

 

Clinical courses

{ DOWNLOAD AS PDF }

ABOUT AUTHORS
Bharat Lal Naik, Chaitanya Prasad Meher
Department of Pharmacology
The Pharmaceutical College (TPC), Tingipali, Barpali, Odisha
chaitanyameher84@gmail.com

ABSTRACT
Diuretic are the drugs that promote the output of urine excreted by kidney. The increased excretion of water & electrolytes by the kidney is dependent on 3 different process viz. glomerular filtration, tubular reabsorption & tubular secretion. Diuretic are very effective in the treatment of cardiac oedema, specifically the one related  with congestive heart failure(C.H.F). They are extensively used in various type of disorders for ex. Cirrhosis of liver, Hypertension,Nephritic syndrome, diabetes insipidus, nutritional oedema, oedema of pregnancy & also to lower intraocular & cerebrospinal fluid pressure. The presented article is based on comprehensive idea about the pharmacology of various diuretic drugs.

REFERENCE ID: PHARMATUTOR-ART-2440

PharmaTutor (ISSN: 2347 - 7881)

Volume 4, Issue 10

Received On: 03/05/2016; Accepted On: 27/05/2016; Published On: 01/10/2016

How to cite this article: Naik BL, Meher CP; A Comparative Pharmacological Study of Diuretic Drugs; PharmaTutor; 2016; 4(10); 10-20

INTRODUCTION    
All soluble constituents of blood minus the plasma proteins and lipids are filtered at the glomerulus. More than 99% of the glomerular filtrate is reabsorbed in the tubules, about 1.5L urine is produced in 24 hours

Three different process that involve in urine formation are glomerular filtration  (180L/day), tubular re-absorption  (around 98%) & tubular secretion. Reabsorption occur in Proximal convoluted tubule, thick portion of ascending limb of the loop of Henle, distal convoluted tubule & in cortical collecting tubule is 60-70%, 25%, 5-10%, 5% respectively.

The purpose of using diuretics is to maintain urine volume (e.g.: renal failure), to mobilize edema fluid (e.g.: heart failure,liver failure, nephrotic syndrome), to control high blood pressure. Potency of a diuretic is related to the absolute amount of drug (e.g mg/Kg) required to produce an effect. While efficacy relates to the maximum diuretic effect (usually measured in terms of urine volume/time or urine loss of Na+or NaCl/time).  Diuretics may be broadly classified under the following two categories. (a) Mercurial diuretics: It contain Hg2+. These are not very much used in clinical practices due to their pronounced and marked side-effects viz., mercurialism, hypersensitivity and excessive diuresis which may lead to electrolyte depletion and vascular complications. Most of the mercurials are administered by intramuscular route and the availability of orally active diuretics has limited their use. diuretics come under this are Chlormerodrin Hg 197, Meralluride, Mercaptomerin sodium, Merethoxylline procaine  Mersalyl and Mercumatilin sodium etc. (b) Non-mercurial diuretics: It is having wider applications due to fewer side-effects1. It may be classified into following type:

1. Thiazides (Benzothiadiazines),

2. Carbonic-Anhydrase Inhibitors,

3. Miscellaneous Sulphonamide Diuretics,

4. Aldosterone Inhibitors,

5. ‘Loop’ or ‘High-Ceiling’ Diuretics,

6. Purine or Xanthine Derivatives,

7. Pyrimidine Diuretics,

8. Osmotic Diuretics,

9. Acidotic Diuretics and

10. Miscellaneous Diuretics.

Diuretics are acting at different sites in the nephron. Carbonic anhydrase inhibitors acting at the proximal convoluted tubule (site1 diuretics). Loop diuretics acting at the Henle’s loop (site 2 diuretics). Thiazides and thiazide-like diuretics acting at distal convoluted tubule (site 3 diuretics). Potassium-sparing diuretics acting at collecting tubule(site 4 diuretics). Osmotic diuretics act at proximal tubules, loop of henle, collecting tubule. According to type of electrolyte excreted it may be named as follows:

Chloruretic

Cl-

Natriuretic

Na+

Saluretic

Nacl

Kaliuretic

K+

Bicarbonaturetic

HCO3-

 

Some of the diuretic drugs with their pharmacological action are tabulated as below:

S.N

DRUG

MECHANISM OF ACTION

PHARMACOKINETIC

ADVERSE EFFECT

CLINICAL USES

REFERENCE

1

FURESEMIDE

4-chloro-2-[(furan-2 ylmethyl)amino]- 5-sulfamoylbenzoic acid

Inhibit Na+-k+-2Cl- co-transporter of ascending loop of henle

Administer orally, IV& IM ,

Plasma t½ is 1- 2 hours,

Low lipid solubility,

Protein binding 91–99%,

Hypokalaemia ,  Metabolic alkalosis, Hypovolaemia,  Hyperuricaemia, Allergy  Excreted unchanged in urine 80–90 %,  Volume of distribution (L/kg) 0.07–0.2%

Used in pulmonary & cerebral Oedema, Hypertension,

Hypercalcaemia of malignancy

Tripathy et al2

 

2

TORASEMIDE

N[(isopropylamino)carbonyl]-4-[(3-methylphenyl)amino]pyridine-3-sulfonamide

Inhibit Na +-k+-2Cl-  co- transporter of ascending loop of henle

Administer orally, IV, plasma t½ -3.5 hours ,dose(2.5-5mg in hypertension,

5-20mg in oedema

Hypokalaemia, Metabolic alkalosis,  Hypovolaemia,  Hyperuricaemia,  Allergy

Mainly used in the management of edema associated with C.H.F ,

used at low doses for the management of hypertension

Dunn CJ et al 3

3

BUMETAMIDE

butylamino-4-phenoxy-5-sulfamoyl-benzoic acid

Inhibit the Na+-k+-2Cl- co-transporter of ascending loop of henle.

Use orally,IV&IM ,

Plasma t½ -1 hours, Bioavailability- 80 to 100%

Hypokalaemia, Metabolic Alkalosis, Hypovolaemia,  Hyperuricaemia,  Allergy

Pulmonary & cerebral Oedema, Hypertension, Hypercalcaemia of malignancy

Rang et al4

4

HYDROCHLOROTHAIZIDE

6-chloro-1,1-dioxo-3,4-dihydro-2H-1,2,4-benzothiadiazine-7-sulfonamide

Inhibit Na+-2Cl-symporter in DCT(site -3)

Use orally, bioaviability-70%,

On set of action-4-6 hours, Duration of action-8-12 hours,

Excreted 95% unchanged in urine.

Hypokalemia, Hyperuricemia, Hyperglycemia Hyperlipidemia, Headache, Nausea/vomiting, Photosensitivity, Weight gain, Gout, Pancreatitis

Hypertension,  Congestive Heart Failure, Symptomatic  edema, Diabetes, Insipidus, 

Renal Tubular Acidosis.

R.A Harvey et al5

5

CHLOROTHAIZIDE

(RS)-2-Chloro-5-(1-hydroxy-3-oxo-2,3-dihydro-1H-isoindol-1-yl)benzene-1-sulfonamide

Inhibit Na+-2Cl-symporter in DCT(site -3)

Absorbed orally,

Action starts within 1 hour, but the duration varies from 8–48 hours

Nausea, Vomiting, Headache, Dizziness, Excess urine production, Dehydration, Hypoelectrolytemia

Used to treat Edema in people with C.H.F,

 Cirrhosis of  liver,

Kidney disorders or edema caused by taking steroids or oestrogen,

Used to treat hypertension

Tripathy et al2

 

6

BENDROFLUMETHIAZIDE

Benzyl-1,1-dioxo-6-(trifluoromethyl)-3,4-dihydro-2H-1,2,4- benzothiadiazine-7-sulfonamide

Inhibit sodium reabsorption at the beginning of the DCT.

Oral use,Adverse interaction with alcohol, not be used by pregnant women

Common adverse effects: Postural Hypotension, hyponatraemia, Hypokalaemia, Hypercalcaemia,Gout, Impaired glucose tolerance, impotence, fatigue, Pulmonary Oedema, Pneumonitis  Rare

adverse effects: Thrombocytopenia, Agranulocytosis, Photosensitivity, Rash, Pancreatitis, Renal Insufficiency

Used for the treatment of mild heart failure, hypertension

Satoskar et al6

7

CHLORTHALIDONE

(RS)-2-Chloro-5-(1-hydroxy-3-oxo-2,3-dihydro-1H-isoindol-1-yl)benzene-1-sulfonamide

Inhibit Na+-Cl- symporter in  DCT

Oral use,dose-50-100mg/day, Duration of action is48 hours, Excreted unchanged in urine,

t½ 40–50 hours

Hypokalemia,  Hypochloremia,  mild metabolic alkalosis.

Used

exclusively as antihypertensive.

Tripathy et al2

8

XIPAMIDE

4-chloro-N-(2,6-dimethylphenyl)-2-hydroxy-5-sulfamoylbenzamide

Acts on kidney to reduce sodium reabsorption in DCT

After oral administration 20 mg are reabsorbed quickly & reach the plasma cocn. Of 3 mg/l with in 1hr.

Diuretic effect start after 1 hr of administration & lasts for nearly 24 hr.

Plasma clearance is 30-40 ml/min.

Hypokalaemia,  Hyponatraemia,  Thrombocytopenia,  Leucopenia,  Acute interstitial nephritis  Hyperlipidemia,  Orthostatic hypotension

Used for cardiac edema caused by decompensation of heart failure,

Renal edema, chronic renal disease,

Hepatic edema caused by cirrhosis ascites lymphoedema,

Hypertension

Jasek et al7,

Klopp et al8

9

METALAZONE

7-chloro-2-methyl-4-oxo-3-o-tolyl-1,2,3,4-tetrahydroquinazoline-6-sulfonamide

Inhibit sodium-chloride symporter

Oral use, Excreted unchanged in urine,

Duration of action 12-24 hours

Aplastic anaemia, Pancreatitis, Agranulocytosis, Angioedema, Abnormalities of water balance, electrolyte levels.

Used mainly for

edema (5–10 mg/day, rarely 20 mg), and

occasionally for hypertension (2.5–5 mg/day).

Tripathy et al2

10

INDAPAMIDE

4-chloro-N-(2-methyl-2,3-dihydroindol-1-yl)-3-sulfamoyl-benzamide

Inhibit Na+-Cl- symporter in  DCT

Oral use, highly lipid soluble,dose-2.5-5mg/day, duration of action-12-24 hours

Hypokalemia, Fatigue, Orthostatic hypotension, Allergic  menifestations

Hypertension,

Decompensated hypertension.

Tripathy et al2

11

CLOPAMIDE

4-chloro-N-(2,6-dimethyl-1-piperidyl)-3-sulfamoyl-
benzamide

It act in kidney at PCT of nephron where it Na+-Cl- symporter

Oral absorption 100 %,

Plasma protein binding is < 50%,

Plasma half life is 10 hr.

Hypokalemia, hyperglycemia Nausea, Vomiting, Diarrhoea, Loss of appetite, Blurred vision, Dizziness.

Used in hypertension ,

Edema associated with heart failure

Tripathy et al2

12

SPIRONOLACTONE

7α-Acetylthio-17α-hydroxy-3-oxopregn-4-ene-21-carboxylic acid γ-lactone

It is a competitive antagonist to the mineralocorticoids such as aldosterone.

The mineralocorticoid receptor is an intracellular protein in nature that can bind aldosterone.

Spironolactone binds to the receptor and competitively inhibits aldosterone binding the the receptor. The inability of aldosterone to bind to its receptor prevents reabsorption of Na+& Cl-and associated water.

The oral bioavailability from microfine powder tablet is 75%,

It is highly bound to plasma proteins,

Completely metabolized in liver,

The most important active metabolite

is Canrenone.

The t½ of spironolactone is

1–2 hours, while that canrenone is ~18 hours.

Drowsiness,  Ataxia,  Mental confusion, Epigastric distress  and loose motions.

Edema,

Hypertension,

C.H.F,

It is a weak diuretic and is used only in combination with

other more efficacious diuretics.

Tripathy et al2

13

EPLERENONE

pregn-4-ene-7,21-dicarboxylic acid, 9,11-epoxy-17-hydroxy-3-oxo, γ-lactone, methyl ester (7α, 11α, 17α)

It is an antagonist of the mineralocortecoid receptor.

well absorbed orally,

t½ is

4–6 hours,

Plasma protein binding is 50 %,

Oral bioavailability is 69% following administration of 100 mg oral tablet,

Metabolism is mediated via CYP3A4,

 

Hyperkalemia,  Hypotension,  Dizziness,  Altered renal function,  Increased creatinine concentration.

Used in moderate

to severe CHF,

 Post-infarction left ventricular

dysfunction,

Hypertension,

can be used

as alternative to spironolactone.

Rossi et al9

14

TRIAMTERENE

6-phenylpteridine-2,4,7-triamine

It acts by blocking the epithelial sodium channel on the lumen side of the kidney collecting tubule.

It is incompletely absorbed orally,

partly bound to plasma proteins, largely

metabolized in liver to an active metabolite and

excreted in urine. Plasma t½ is 4 hours, effect of

a single dose lasts 6–8 hours.

Nausea,  Dizziness,   Muscle cramps,   Rise in blood urea.  Impaired glucose tolerance and photosensitivity

 

Hypertension,

Edema

Tripathy et al2

15

AMILORIDE

3,5-diamino-6-chloro-N-(diaminomethylene)pyrazine-2-carboxamide

Act by directly blocking the epithelial sodium channel in the late DCT in the kidney

Only ¼ of an oral dose is absorbed,

It is not

bound to plasma proteins and not metabolized,

The t½ (20 hours) and duration of action are

longer than triamterene.

Nausea,  Headache,  Diarrhoea.

Hypertension,

C.H.F,

Cystic fibrosis.

Tripathy et al2

16

MANNITOL

(2R,3R,4R,5R)-Hexane-1,2,3,4,5,6-hexol

It is act on the proximal tubules & inhibit both water & solute reabsorption in the kidney tubule by increasing the osmolarity of the renal tubular fluid.

It is not absorbed orally,

Has to be given i.v. as 10–20% solution,

It is

excreted with a t½ of 0.5–1.5 hour.

Pulmonary congestion,  Fluid & electrolyte imbalance,  Dryness of mouth,  Thrist,  Edema,  Urinary retention,  Headache,  Blurred vision

Used in acute congestive heart, Glaucoma,

Head injury, Shock , Severe trauma, Cardiac surgery

Satoskar et al6

17

GLYCEROL

propane-1,2,3-triol

It acts by expanding extracellular fluid & plasma volume, therefore increasing blood flow to the kidney

Orally active osmotic diuretics,

Dose: 0.5–1.5 g/kg as oral solution

Intravenous glycerol can cause  haemolysis.

Used to reduce intraocular or

intracranial tension

Satoskar et al6

18

ISOSORBIDE

1,4:3,6-Dianhydro-D-sorbitol; 1,4-Dianhydrosorbitol

No direct effect on transport but cause shift of ions by inducing bulk water flow & changing steady state water concentration in body compartment.

Orally active osmotic Diuretics,

Dose: 0.5–1.5 g/kg as oral solution

Hypotension,  Hypovolemia,  Heart failure,  Pulmonary congestion,  Headache, blurred vision,  Nausea, vomitting

Used to reduce intraocular or

intracranial tension

Tripathy et al2

19

ACETAZOLAMIDE

N-(5-sulfamoyl-1,3,4-thiadiazol-2-yl)acetamide

Inhibits CAse (type II) in PT Cells,

Inhibition of CAse (type IV), The net effect

is inhibition of HCO¯ (and accompanying Na+) reabsorption in PT.

Well

absorbed orally,

Excreted unchanged in urine.

Action of a single dose lasts 8–12 hours.

Acidosis,  Hypokalaemia, Drowsiness,  Paresthesias, Fatigue,  Abdominal Discomfort.  Hypersensitivity reaction,  Bone marrow depression.

Glaucoma,

To alkalinise urine,

Epilepsy,

Acute mountain sickness,

Periodic paralysis

Tripathy et al2

20

THEOPHYLLINE

1,3-Dimethyl-7H-purine-2,6-dione

Mechanism unclear, may be related to inhibition of phosphodiesterase and/ or antagonism of adenosine receptor

Bioavailability is 100% in case of IV,

Metabolized in liver (70%),

Excreted unchanged in urine,

 

Nausea, diarrhoea,  Abnormal heart rhythm, CNS excitation, seizure

Increasing renal blood flow,

Relaxing bronchial smooth muscle,

COPD.

 

Rieg T et al11 ,

Yoshikawa et al12

21

CAFFINE

1,3,7-Trimethylpurine-2,6-dione

Mechanism unclear, may be related to inhibition of phosphodiesterase and/ or antagonism of adenosine receptor

Metabolized in the liver,

In healthy adults

t1/2  is 3-7 hr,

Nicotine decrease the half life by 30-50 %

 

Increase  metabolic rate,  Anxiety,  Vasoconstriction,

Relax smooth muscle of bronchi & is used to treat Asthma

 

Rieg T et al11

22

ETHACRYNIC ACID

[2,3-dichloro-4-(2-methylenebutanoyl)phenoxy]acetic acid

Inhibit the Na +-k+-2Cl-  co transporter of ascending loop of henle  (site-2)

Oral use,

t1/2-~1 hr, Metabolised ~33% in liver,

 Excreted in urine ~62%.

Hypokalaemia, metabolic alkalosis, Hypovolaemia , Hyperuricaemia, Allergy

Oedema like (pulmonary, cerebral), hypertension

Goodman et al10

23

AZOSEMIDE

2-chloro-5-(2H-tetrazol-5-yl)-4-[(thiophen-2-ylmethyl)amino]benzenesulfonamide

It is a high ceiling diuretic.

Exact mechanism is not understood

But it mainly act on both medullary & cortical segment of thick ascending limb of the loop of henle.

Oral boavailability in human is aprox. 20.4%,

It’s effect is 5.5-8 time greater than furosemide.

Apparent post-pseudodistribution volume is 0.0262 l/kg,

In human total body clearance, renal clearance, terminal half life is 112ml/min, 41.6 ml/min, 2.03 hr respectively.

Panic disorder,  Liver disorder,  Blood creatine phosphokinase increased

Used in the treatment of oedematous states,

Hypertension.

Kim et al13

24

PIRETANIDE

3-(aminosulfonyl)-4-phenoxy-5-pyrolidin-1-yl benzoic acid.

Site of action is thick ascending limb of the loop of henle.

Oral use ,

t1/2-~0.6-1.5 hours, Metabolised ~50% in liver,

Excreted in urine ~50%.

Excess loss of fluid & electrolyte.

Use for the treatment of hypertension,

C.H.F & edematous state caused by renal & hepatic disease.

Goodman et al10

25

MUZOLIMINE

3-Amino-1-(3,4-dichloro-á-methylbenzyl)-2-pyrazolin-5-one

It is a loop diuretic

Effect is slow,

It’s action is long lasting.

 

Used for hypertension but was withdrawn because of severe neurological side effect.

Reyes et al14

26

TRIPAMIDE

3-(aminosulfonyl)-4-chloro-N-[(3aR,4S,7R,7aS)-octahydro-2H-4,7-methanoisoindol-2-yl]benzamide

Inhibitory effect on solute reabsorption  at the cortical segment of thick ascending limb of loop of henle.

Oral use, Metabolised in liver

Hypokalaemia, metabolic alkalosis, Hypovolaemia , Hyperuricaemia, Allergy

Hypertension,

Edema.

Goodman et al 10

27

QUINETHAZONE

7-chloro-2-ethyl-4-oxo-1,2,3,4-tetrahydroquinazoline-
6-sulfonamide

It inhibit active chloride reabsorption at the early distal tubule via Na-Cl cotransporter

Onset of action 2 hr,

Duration of action 18-24 hr.

Time to peak effect 6 hr.

Dizziness,  Dry mouth,  Nausea,  Low potassium level.

Diuretic and antihypertensive properties similar to those of the thiazides.

Satoskar et al6

28

TRICHLORMETHIAZIDE

6-Chloro-3-(dichloromethyl)-1,1-dioxo-3,4-dihydro-2H-benzo[e] [1,2,4]thiadiazine-7-sulfonamide

Inhibit Na+/2Cl_symporter in DCT(site -3)

Oral use ,

t1/2-~2.3-7.3 hours,

Excreted in urine

Hypokalemia,  Hyperurecaemia,  Hyperlipidimia,  Hyperglycemia,  Hypersensitivity,  Thrombocytopenia,  Volume depletion, Hyponatraemia

Hypertension,

Heart failure,

Diabetes insipidus,

Hypercalciurea

Goodman et al 10

29

POLYTHIAZIDE

6-chloro-2-methyl-3-{[(2,2,2-trifluoroethyl)thio]methyl}-3,4-dihydro-2H-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide

Enhance urinary excretion of both Na and H2O by specifically inhibiting Na reabsorption located in the cortical (thick) portion of the ascending

limb of Henle’s loop and also in the early distal tubules.

Normal human subjects receiving single 1mg oral dose, the mean plasma half life for absorption & elimination were 1.2 & 25.7 hr respectively,

25 % excreted unchanged in urine.

Abdominal or stomach pain,  Bleeding gum,  Blurred vision,  Chest pain,  Blood in urine or stool.

Long-acting diuretic and anti-hypertensive agent.

As diuretic, usual, 1 to 4 mg per day

 As antihypertensive, 2 to 4 mg

Hobbs et al15

30

METHYCLOTHIAZIDE

6-Chloro-3-(chloromethyl)-2-methyl-3,4-dihydro-2H-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide

Enhance urinary excretion of both Na and H2O by specifically inhibiting Na reabsorption located in the cortical (thick) portion of the ascending

limb of Henle’s loop and also in the early distal tubules.

Given orally,

Rapid absorption,

Cross the placenta,

Elimination through kidney.

Duration of action 6 hr

 

Anxiety,  Sweating,  Severe shortness of breath,  Cough with foamy mucus,  Increased thrist,  Drowsiness,  Muscle pain,  Fainting or seizure,  Nausea,  Vomiting.

Diuretic and an antihypertensive agent.

2.5 to 10 mg once per day

Asutosh et al1

31

CANRENONE

10,13-Dimethylspiro[2,8,9,11,12,14,15,16-octahydro-1H-cyclopenta[a]phenanthrene-17,5'-oxolane]-2',3-dione

Inhibit binding of aldosterone with mineralocorticoid receptor.

Oral use,

t1/2-~16.5 hours,

Drowsiness,  Ataxia,  Mental confusion

Oedema, hypertension, CHF

Goodman et al10

32

UREA

No direct effect on transport but cause shift of ions by inducing bulk water flow & changing steady state water concentration in body compartment.

Used intravenously,

It penetrate total body water, short half life,

 

Hypotension,  Hypovolemia,  Heart failure,  Pulmonary congestion,  Headache, blurred vision,  Nausea, vomitting

Approved to reduce intraocular pressure, intracranial pressure,

Cerebral edema

Goodman et al10

33

POTASSIUM CANRENOATE

potassium 3-[(8R,9S,10R,13S,14S,17R)-
17-hydroxy-10,13-dimethyl-3-oxo-2,8,9,
11,12,14,15,16-octahydro-1H-cyclopenta[a]
phenanthren-17-yl]propanoate

It is an aldosterone antagonist.

Given intravenously

 

Nausea, vomiting,  Confusion,  Restlessness,  Hallucination.

Oedema

Goodman et al10

34

METAZOLAMIDE

N-[5-(aminosulfonyl)-3-methyl-1,3,4-thiadiazol-2(3H)-ylidene]acetamide

Carbonic anhydrase inhibitor

Oral use,

t1/2-~14 hours, Metabolise~75%,

Renal excreation of intact drug~25%

Acidosis, drowsiness, Paresthesias , Abdominal Discomfort, Fatigue, Hypertension.

Glaucoma, Epilepsy,

periodic paralysis.

Goodman et al10

35

DICHLORPHENAMIDE

4,5-Dichlorobenzene-1,3-disulfonamide

Carbonic anhydrase inhibitor

Oral use

Dizziness, Change in the sense of test, Headache, Confusion, Weight loss, muscle pain, joint pain, Throat pain, rash

Glaucoma,

Epilepsy

Goodman et al10

Selected Drug- Diuretic Interaction:

DRUGS

DIURETCS

PROBLEMS

Digitalis

Loop & thiazide

Hypokalemia à digitalis toxicity

NSAID

Loop & thiazide

Decrease diuretic effect

Aminoglycoside

loop

Ototoxicity & nephrotoxicity

Adrenal steroids

Loop & thiazide

Severe hypokalemia

Chlorpropamide

Thiazide

Hyponatremia

Lithium

Loop & thiazide

Increased plasma (lithium)

Probenecid

Loop & thiazide

Decrease diuretic effect

ACE inhibitors

K+ sparing

Hyperkalemia à Arrhythmias

 
CONCLUSION
By increasing the urine flow rate diuretic usage leads to increase excretion of electrolytes (especially Na+ & Cl-) and water from the body without affecting protein,vitamins, glucose amino acids reabsorption & capable of solving various type of diseases mention above.

REFERENCES
1.  Asutosh kar, “Medicinal chemistry”, 4th edition, page-439,451
2.K.D,Tripathy, “Essential medical pharmacology” ,seventh edition ,page no-581,582, 583,584,587,590,
3. Dunn CJ, Fitton A, Brogden RN (January 1995). "Torasemide. An update of its pharmacological properties and therapeutic efficacy".Drugs 49 (1): 121–42
4. Rang & dale’s pharmacology,H.P.Rang,M.M.Dale,J.M.Ritter, R.J Flower,7th edition ,page no. 354
5. R.A.Harvey, Pharmacology, 5th edition.page-283
6.R.S.Satoskar,S.D.bhandarkar,S.Sainapure, Pharmacology and pharmacotherapeutic, page no.543,540,545
7. Jasek.W,ed.(2007).austria-codex (in german)1 (2007/2008 ed.).vienna,pp-600-603
8. Klopp.T, ed.(2007). Arzenemittel-interaktionen (in german) (2007/2008 ed.)
9.Rossi S,editor,Australian medicines hand book 2006,adelade.
10. Goodman & Gilman” The  Pharmacological basis of therapeutics,10thedition,Page no-767,770,774
11. Rieg T, J Pharmacol Exp Ther, 2005,Apr,313(1)403-9.Epub 2004 Dec 8.
12. Yoshika H(Apr 2007), first line therapy for theophylline associated seizure, Acta neurol scand 115 (4 suppl): 57-61
13. Suh, OK, Kim SH, Biopharm Drug Dispose,2003 Oct;24(7): 275-97.
14. reyes A.J,” Clinicopharmacologicalreappraisal of the potency of diuretics” cardiovascular dru & therapy 7:23-28.
15. Hobbs DC,Clin pharmacol ther,1978 feb:23(2):241-6

NOW YOU CAN ALSO PUBLISH YOUR ARTICLE ONLINE.

SUBMIT YOUR ARTICLE/PROJECT AT editor-in-chief@pharmatutor.org

Subscribe to Pharmatutor Alerts by Email

FIND OUT MORE ARTICLES AT OUR DATABASE