Captopril Risk Summary

Risk Factor: CM*
Class: Cardiovascular drugs / Antihypertensives / Angiotensin-converting enzyme inhibitors

Fetal Risk Summary

Captopril, a competitive inhibitor of angiotensin I-converting enzyme (ACE), is used for the treatment of hypertension and in the management of heart failure. The drug is embryocidal in animals and has been shown to cause an increase in stillbirths in some species (1,2 and 3). In pregnant sheep and rabbits, the use of captopril was associated with a decrease in placental blood flow and oxygen delivery to the fetus (4,5).

Because of the toxicity identified in early animal studies, a committee of the National Institutes of Health recommended in 1984 that captopril be avoided during pregnancy (6). A 1985 review on the treatment of hypertension in pregnancy also stated the opinion that captopril should not be used in pregnancy because of the animal toxicity (7). However, use of captopril limited to the 1st trimester does not appear to present a significant risk to the fetus. Fetal exposure after this time has been associated with teratogenicity and severe toxicity in the fetus and newborn, including death.

A number of reports have described the use of captopril, usually in combination with other antihypertensive agents and often after the failure of other medications, for the treatment of resistant hypertension during human pregnancy (8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27 and 28). Included among these is a 1991 review that summarized those cases of captopril-exposed pregnancies published before January 1, 1990 (28). Some of these reports are reviewed below.

In a surveillance study of Michigan Medicaid recipients involving 229,101 completed pregnancies conducted between 1985 and 1992, 86 newborns had been exposed to captopril during the 1st trimester (Franz Rosa, personal communication, FDA, 1993). Four (4.7%) major birth defects were observed (three expected). Specific data were available for six defect categories, including (observed/expected) 1/1 cardiovascular defects, 0/0 oral clefts, 0/0 spina bifida, 1/0 polydactyly, 1/0 limb reduction defects, and 1/0 hypospadias. These data do not support an association between 1st trimester use of captopril and congenital defects.

One pregnancy treated with captopril was reported in a 1997 study of 19 pregnancies exposed to ACE inhibitors (8). Captopril therapy was stopped at 8 weeks' gestation. No congenital anomalies or renal dysfunction was noted in the newborn (8).

A malformed fetus was discovered after voluntary abortion in a patient with renovascular hypertension (9). The patient had been treated during the 1st trimester with captopril, propranolol, and amiloride. The left leg ended at midthigh without distal development, and no obvious skull formation was noted above the brain tissue. However, because of the very small size of the fetus (1.5 cm), the pathologist could not be certain that the defects were not a result of the abortion (10).

A mother with a history of renal artery stenosis and malignant hypertension was treated throughout gestation with captopril, minoxidil, and propranolol (11). Three of her four previous pregnancies had ended in midgestation stillbirths. The most recent stillbirth, her fourth pregnancy, involved a 500g male infant with lowset ears but no gross anomalies. The mother had been treated with the above regimen plus furosemide. In her second pregnancy, she had been treated only with hydrochlorothiazide and she had delivered a normal term infant. No information was available on the first and third pregnancies, both of which ended in stillbirths. In her latest pregnancy, daily doses of the three drugs were 50 mg, 10 mg, and 160 mg, respectively. The infant, delivered by cesarean section at 38 weeks, had multiple abnormalities including an omphalocele (repaired on the 2nd day), pronounced hypertrichosis of the back and extremities, depressed nasal bridge, lowset ears, micrognathia, bilateral fifth finger clinodactyly, undescended testes, a circumferential midphallic constriction, a large ventriculoseptal defect, and a brain defect consisting of slightly prominent sulci, especially the basal cisterns and interhemispheric fissure. Growth retardation was not evident, but the weight (3170 g, 60th percentile), length (46 cm, 15th percentile), and head circumference (32.5 cm, 25th percentile) were disproportionate. Neurologic examinations, as well as examinations of the skeleton and kidneys, were normal. Marked hypotension (3050 mm Hg systolic) was present, which resolved after 24 hours. Heart rate, blood glucose, and renal function were normal. The infant's hospital course was marked by failure to thrive, congestive heart failure, prolonged physiologic jaundice, and eight episodes of hyperthermia (>38.5C without apparent cause) between 2 and 6 weeks of age. The hypertrichosis, which was much less prominent at 2 months of age, is a known adverse effect of minoxidil therapy in both children and adults, and the condition in this infant was thought to be caused by that drug. The cause of the other defects could not be determined, but a chromosomal abnormality was excluded on the basis of a normal male karyotype (46,XY), determined after a midgestation amniocentesis (11).

One case involved a mother with polyarteritis nodosa treated throughout gestation with captopril, hydralazine, and furosemide (12). The pregnancy was electively terminated at approximately 31 weeks' gestation because of worsening maternal disease. A normal, non-growth-retarded infant was delivered who did well in the neonatal period (12).

Oligohydramnios developed after 3 weeks of therapy with captopril in a woman who was treated at 25 weeks' gestation (13). Cesarean section at 29 weeks' gestation produced a 1040-g infant with dehydration, marked peripheral vasodilation, severe hypotension, respiratory distress, and anuria. Epidermolysis of the trunk and extremities appeared after birth. Diagnostic studies indicated a normal bladder, but neither kidney was perfused. ACE activity was reported as very low. The infant died on day 8 as a result of persistent anuria. At autopsy, hemorrhagic foci were discovered in the renal cortex and medulla, but nephrogenesis was adequate for the gestational age.

A woman was treated at 27 weeks' gestation with daily doses of captopril (200 mg), labetalol (1600 mg), and furosemide (80 mg) (14). Fourteen days after treatment was begun, signs of fetal distress, attributed to the maternal hypertension, appeared and the infant was delivered by cesarean section. No adverse effects of the drug treatment were observed in the infant (14).

Captopril and acebutolol were used throughout pregnancy to treat a woman with nephrotic syndrome and arterial hypertension (15). Intrauterine growth retardation (IUGR), most probably because of the severe maternal disease (although a contribution from drug therapy could not be excluded), was identified early in the 2nd trimester and became progressively worse. The growth-retarded male infant was delivered prematurely at 34 weeks by cesarean section. Captopril was found in the cord blood with levels in the mother and fetus less than 100 ng/mL, 4 hours after the last dose. Angiotensin-converting enzyme activity was below normal limits in both the mother and the newborn. Neonatal respiratory arrest occurred 15 minutes after delivery with varying degrees of hypotension persisting over the first 10 days. A patent ductus arteriosus was also present (15).

A woman with hypertension secondary to bilateral renal artery stenosis was treated with captopril, 150 mg/day, beginning 6 weeks before conception (16). Daily drug therapy during pregnancy consisted of captopril (600 mg), methyldopa (750 mg), and furosemide (80 mg). Oligohydramnios and IUGR were diagnosed at 35 weeks' gestation, at which time a cesarean section was performed to deliver the 2120-g male infant. Some of the abnormalities in the infant, such as pulmonary hypoplasia, small skull circumference (28.5 cm,<3rd percentile), hypoplastic skull bones with wide sutures, and contractures of the extremities, were probably caused by captopril-induced oligohydramnios and fetal hypotension. The severe neonatal hypotension (27/20 mm Hg), which slowly resolved over 5 days despite volume expansion and pressor agents, and the anuria were also most likely caused by captopril. The infant was anuric for 7 days, then oliguric with 710 mL/day output for the next 12 days. All diagnostic tests during the first 10 days after birth indicated apparently normal kidneys. Peritoneal dialysis was commenced on the 20th day, but the infant died at 1 month of age (16).

A 1985 case report described a woman with twins treated throughout pregnancy with captopril (75100 mg/day), hydralazine (75 mg/day), metoprolol (200 mg/day), and chlorthalidone (25 mg/day; stopped after 3 months) (17). Three previous pregnancies complicated by severe hypertension had ended with one term, mentally retarded infant and two spontaneous abortions, one at 5 months and one at 7 months. Two weeks before term the dose of captopril was reduced to 37.5 mg/day. Other than their small size (weight and length of both were less than the 10th percentile), both infants were normal and had normal mental and physical growth at 10 months (17).

In another case report, a woman who had had a renal transplant was treated throughout gestation with daily doses of captopril (75 mg), cyclosporine (200 mg), atenolol (200 mg), cimetidine, and amoxicillin (18). Oligohydramnios was diagnosed at 18 weeks' gestation and IUGR with gross oligohydramnios was discovered at 26 weeks. Ultrasound scanning at 27 weeks indicated renal dysplasia. Intrauterine fetal death occurred at 29 weeks. No congenital anomalies were found at autopsy. The kidneys appeared normal, but no urine was found in the ureters or bladder. The authors attributed the renal dysgenesis to the captopril therapy (18).

An 18-year-old woman with severe chronic hypertension became pregnant while taking captopril, hydralazine, and propranolol (19). Captopril and hydralazine were discontinued on presentation at 10 weeks' gestation. Because her subsequent blood pressure control was poor, her therapy was changed at 20 weeks' gestation to captopril (37.575 mg/day), atenolol (100 mg/day), and nifedipine (40 mg/day). IUGR was identified by serial scanning. A healthy, 1590g female infant was delivered by cesarean section at 30 weeks' gestation. No other additional information was provided, other than that the infant survived (19).

Two abstracts described two pregnancies terminating with newborns exhibiting characteristic patterns of captopril-induced fetotoxicity and malformations (24,25). The fetopathy consisted of fetal hypotension, severe anuria and oligohydramnios, IUGR, hypocalvaria, renal tubular dysplasia, and pulmonary hypoplasia. Both infants died.

The result of a survey on the use of captopril during pregnancy was published in 1988 (26). The outcomes of therapy in the 37 pregnancies (38 fetuses, 1 set of twins) were 3 stillbirths, 11 premature births, 4 small-for-gestational-age infants, 4 cases of patent ductus arteriosus, and 2 neonatal deaths secondary to anuria (26).

A 1992 Reference described the effects of ACE inhibitors on pregnancy outcome (27). Among 106,813 women enrolled in the Tennessee Medicaid program who delivered either a liveborn or stillborn infant, 19 had taken either captopril, enalapril, or lisinopril during gestation. One premature newborn, exposed in utero to captopril, had microcephaly, a large occipital encephalocele, and was probably blind (27).

Investigators at the FDA summarized some of the known cases of captoprilinduced neonatal anuria in a 1989 report (29). These cases have been described above (13,15,16). The FDA authors cautioned that if captopril was used during pregnancy, then preparations should be made for neonatal hypotension and renal failure (29). Of interest, a 1991 review concluded that fetal and neonatal renal dysfunction was more common after maternal use of enalapril than with captopril (28).

A 1991 report presented two cases of fetopathy and hypocalvaria in newborns exposed in utero to ACE inhibitors, including one case in which captopril, prednisone, atenolol, and furosemide were used throughout pregnancy (same case as described in Reference 24) and one case caused by lisinopril (30). Twelve other cases of hypocalvaria or acalvaria were reviewed, three of which were thought to be caused by captopril (N=2) or enalapril (N=1) and nine others with causes that were either not drug-related or unknown. The authors speculated that the underlying pathogenetic mechanism in these cases is fetal hypotension (30).

In a 1991 article examining the teratogenesis of ACE inhibitors, the authors cited evidence linking fetal calvarial hypoplasia with the use of these agents after the 1st trimester (31). They speculated that the mechanism was related to drug-induced oligohydramnios that allowed the uterine musculature to exert direct pressure on the fetal skull. This mechanical insult, combined with drug-induced fetal hypotension, could inhibit peripheral perfusion and ossification of the calvaria (31).

Investigators in a study published in 1992 examined microscopically the kidneys of nine fetuses exposed to ACE inhibitors, one of which was enalapril (32). The researchers concluded that the renal defects associated with ACE inhibitors were caused by decreased renal perfusion and are similar to the defects seen in other conditions related to reduced fetal renal blood flow (32).

In a retrospective 2000 study, the outcomes of 10 pregnant women treated with low-dose captopril (12.525 mg/day) for severe, unresponsive vasoconstricted hypertension were reviewed (33). Maternal hemodynamics improved without fetal or neonatal complications. Assuming an expected complication rate of 5%10%, however, the number of exposed pregnancies may have been too small to identify adverse effects (33).

In summary, captopril and other ACE inhibitors appear to be human teratogens when used in the 2nd and 3rd trimesters, producing fetal hypocalvaria and renal defects. The cause of the defects and other toxicity associated with angiotensin-converting enzyme inhibitors is probably related to fetal hypotension and decreased renal blood flow.

The use of captopril during the 1st trimester does not appear to present a risk to the fetus. Use during the 2nd and 3rd trimesters, however, may compromise the fetal renal system and result in severe, and at times fatal, anuria, both in the fetus and in the newborn. Anuria-associated oligohydramnios may produce pulmonary hypoplasia, limb contractures, persistent patent ductus areteriosus, craniofacial deformation, and neonatal death (34,35). IUGR, prematurity, and severe neonatal hypotension may also be observed. Two reviews of fetal and newborn renal function indicated that both renal perfusion and glomerular plasma flow are low during gestation and that high levels of angiotensin II may be physiologically necessary to maintain glomerular filtration at low perfusion pressures (36,37). Captopril prevents the conversion of angiotensin I to angiotensin II and, thus, may lead to in utero renal failure. In those cases in which captopril must be used to treat the mother's disease, the lowest possible dose should be used combined with close monitoring of amniotic fluid levels and fetal wellbeing. Newborn renal function and blood pressure should also be closely monitored. If oligohydramnios occurs, stopping captopril may resolve the problem but may not improve infant outcome because of irreversible fetal damage (34). Guidelines for counseling exposed pregnant patients have been published and should be of benefit to health professionals faced with this task (31,34).

[*Risk Factor DM if used in the 2nd or 3rd trimesters.]

Breast Feeding Summary

Captopril is excreted into breast milk in low concentrations. In 12 mothers given 100 mg three times/day, average peak milk levels were 4.7 ng/mL at 3.8 hours after their last dose (38,39). This represented an average milk:plasma ratio of 0.012. No differences were found in captopril levels in milk before and after the drug. No effects on the nursing infants were observed. The American Academy of Pediatrics considers captopril compatible with breast feeding (40).

References

1. Broughton Pipkin F, Turner SR, Symonds EM. Possible risk with captopril in pregnancy: some animal data. Lancet 1980;1:1256.
2. Broughton Pipkin F, Symonds EM, Turner SR. The effect of captopril (SQ14,225) upon mother and fetus in the chronically cannulated ewe and in the pregnant rabbit. J Physiol 1982;323:41522.
3. Keith IM, Will JA, Weir EK. Captopril: association with fetal death and pulmonary vascular changes in the rabbit (41446). Proc Soc Exp Biol Med 1982;170:37883.
4. Lumbers ER, Kingsford NM, Menzies RI, Stevens AD. Acute effects of captopril, an angiotensin-converting enzyme inhibitor, on the pregnant ewe and fetus. Am J Physiol 1992;262 (Regul Integrative Comp Physiol 31):R754R60.
5. Binder ND, Faber JJ. Effects of captopril on blood pressure, placental blood flow and uterine oxygen consumption in pregnant rabbits. J Pharmacol Exp Ther 1992;260:294-9.
6. Anonymous. The 1984 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1984;144:10456.
7. Lindheimer MD, Katz AI. Current concepts. Hypertension in pregnancy. N Engl J Med 1985;313:67580.
8. Lip GYH, Churchill D, Beevers M, Auckett A, Beevers DG. Angiotensin-converting-enzyme inhibitors in early pregnancy. Lancet 1997;350:14462.
9. Duminy PC, Burger PT. Fetal abnormality associated with the use of captopril during pregnancy. S Afr Med J 1981;60:805.
10. Broude AM. Fetal abnormality associated with captopril during pregnancy. S Afr Med J 1982;61:68.
11. Kaler SG, Patrinos ME, Lambert GH, Myers TF, Karlman R, Anderson CL. Hypertrichosis and congenital anomalies associated with maternal use of minoxidil. Pediatrics 1987;79:4346.
12. Owen J, Hauth JC. Polyarteritis nodosa in pregnancy: a case report and brief literature review. Am J Obstet Gynecol 1989;160:6067.
13. Guignard JP, Burgener F, Calame A. Persistent anuria in a neonate: a side effect of captopril? (abstract). Int J Pediatr Nephrol 1981;2:133.
14. Millar JA, Wilson PD, Morrison N. Management of severe hypertension in pregnancy by a combined drug regimen including captopril: case report. NZ Med J 1983;96:7968.
15. Boutroy MJ, Vert P, Hurault de Ligny B, Miton A. Captopril administration in pregnancy impairs fetal angiotensin converting enzyme activity and neonatal adaptation. Lancet 1984;2:9356.
16. Rothberg AD, Lorenz R. Can captopril cause fetal and neonatal renal failure? Pediatr Pharmacol 1984;4:18992.
17. Coen G, Cugini P, Gerlini G, Finistauri D, Cinotti GA. Successful treatment of longlasting severe hypertension with captopril during a twin pregnancy. Nephron 1985;40:498500.
18. Knott PD, Thorpe SS, Lamont CAR. Congenital renal dysgenesis possibly due to captopril. Lancet 1989;1:451.
19. Smith AM. Are ACE inhibitors safe in pregnancy? Lancet 1989;2:7501.
20. Fiocchi R, Lijnen P, Fagard R, Staessen J, Amery A, Van Assche F, Spitz B, Rademaker M. Captopril during pregnancy. Lancet 1984;2:1153.
21. Caraman PL, Miton A, Hurault de Ligny B, Kessler M, Boutroy MJ, Schweitzer M, Brocard O, Ragage JP, Netter P. Grossesses sous captopril. Therapie 1984;39:5963.
22. Plouin PF, Tchobroutsky C. Angiotensin converting-enzyme inhibition during human pregnancy: fifteen cases. Presse Md 1985;14:21758.
23. Ducret F, Pointet Ph, Lauvergeon B, Jacoulet C, Gagnaire J. Grossesse sous inhibiteur de l'enzyme de conversion. Presse Md 1985;14:897.
24. Barr M. Fetal effects of angiotensin converting enzyme inhibitor (abstract). Teratology 1990;41:536.
25. Pryde PG, Nugent CE, Sedman AB, Barr M Jr. ACE inhibitor fetopathy (abstract). Am J Obstet Gynecol 1992;166:348.
26. KreftJais C, Plouin PF, Tchobroutsky C, Boutroy J. Angiotensinconverting enzyme inhibitors during pregnancy: a survey of 22 patients given captopril and nine given enalapril. Br J Obstet Gynaecol 1988;95:4202.
27. Piper JM, Ray WA, Rosa FW. Pregnancy outcome following exposure to angiotensin-converting enzyme inhibitors. Obstet Gynecol 1992;80:42932.
28. Hanssens M, Keirse MJNC, Vankelecom F, Van Assche FA. Fetal and neonatal effects of treatment with angiotensin-converting enzyme inhibitors in pregnancy. Obstet Gynecol 1991;78:12835.
29. Rosa FW, Bosco LA, Graham CF, Milstien JB, Dreis M, Creamer J. Neonatal anuria with maternal angiotensin-converting enzyme inhibition. Obstet Gynecol 1989;74:3714.
30. Barr M Jr, Cohen MM Jr. ACE inhibitor fetopathy and hypocalvaria: the kidney-skull connection. Teratology 1991;44:48595.
31. Brent RL, Beckman DA. Angiotensin-converting enzyme inhibitors, an embryopathic class of drugs with unique properties: information for clinical teratology counselors. Teratology 1991;43:5436.
32. Martin RA, Jones KL, Mendoza A, Barr M Jr, Benirschke K. Effect of ACE inhibition on the fetal kidney: decreased renal blood flow. Teratology 1992;46:31721.
33. Easterling TR, Carr DB, Davis C, Diederichs C, Brateng DA, Schmucker B. Low-dose, short-acting, angiotensin-converting enzyme inhibitors as rescue therapy in pregnancy. Obstet Gynecol 2000;96:95661.
34. Barr M Jr. Teratogen Update: angiotensin-converting enzyme inhibitors. Teratology 1994;50:399409.
35. Shotan A, Widerhorn J, Hurst A, Elkayam U. Risks of antiotensin-converting enzyme inhibition during pregnancy: experimental and clinical evidence, potential mechanisms, and recommendations for use. Am J Med 1994;96:4516.
36. Robillard JE, Nakamura KT, Matherne GP, Jose PA. Renal hemodynamics and functional adjustments to postnatal life. Semin Perinatol 1988;12:14350.
37. Guignard JP, Gouyon JB. Adverse effects of drugs on the immature kidney. Biol Neonate 1988;53:24352.
38. Devlin RG, Fleiss PM. Selective resistance to the passage of captopril into human milk. Clin Pharmacol Ther 1980;27:250.
39. Devlin RG, Fleiss PM. Captopril in human blood and breast milk. J Clin Pharmacol 1981;21:1103.
40. Committee on Drugs, American Academy of Pediatrics. The transfer of drugs and other chemicals into human milk. Pediatrics 1994;93:13750.

Questions and Answers

Has anyone had trouble with taking captopril and novolog?, My levels seem to rise when taking captopril and novolog. I was wondering if anyone else had this result?

The hypoglycemic effect of insulin may be potentiated by certain drugs, including ACE inhibitors, anabolic steroids, fibrates, monoamine oxidase inhibitors (MAOIs), salicylates, selective serotonin reuptake inhibitors (SSRIs), sulfonamides, disopyramide, propoxyphene, quinine, and quinidine. These drugs may increase the risk of hypoglycemia by enhancing insulin sensitivity (ACE inhibitors, fibrates); stimulating insulin secretion (salicylates, disopyramide, quinine, quinidine, MAOIs); increasing peripheral glucose utilization (SSRIs, insulin-like growth factor); and/or inhibiting gluconeogenesis (SSRIs, MAOIs, insulin-like growth factor). Clinical hypoglycemia has been reported during use of these agents alone or with insulin and/or insulin secretagogues.

Close monitoring for the development of hypoglycemia is recommended if these drugs are coadministered with insulin, particularly in patients with advanced age and/or renal impairment. The insulin dosage may require adjustment if an interaction is suspected. Patients should be apprised of the signs and symptoms of hypoglycemia (e.g., headache, dizziness, drowsiness, nausea, hunger, tremor, weakness, sweating, palpitations), how to treat it, and to contact their physician if it occurs. Patients should be observed for loss of glycemic control when these drugs are withdrawn.

Why when taking captopril should you not touch your eyes until washing hands thoroughly ?, What is in it that affects the eyes? Can it cause floaters in the eyes?

As with any vasodilator, intercellular fluid accumulation is possible. It is not a very common side effect, but never the less, it is still a good idea to wash your hands before rubbing your eyes. If you don't, you may experience ocular angioedema through prolonged exposure.

It does not cause floaters aside from the potential that increased pressure and decreased blood flow/oxygen can result in visual disturbance.

Explain how an angiotensin-converting enzyme inhibitor (ACE inhibitor) such as captopril would be effective?, Explain how an angiotensin-converting enzyme inhibitor (ACE inhibitor) such as captopril would be effective as an antihypertensive.

One of the many systems that regulates blood pressure is the angiotensin enzymes. ACE activates these enzymes and causes them to constrict the blood vessels and raise blood pressure. ACE inhibitors prevent this from happening and prevent the blood vessels from constricting. This keeps pressure from being raised due to angiotensin enzymes. After a few weeks, the ACE inhibitor can decrease average blood pressure pretty well

Why can't you take antiacids when you are taking Captopril?,

Most antiacids have calcium carbonate in them. This is an alkaline buffer which neutralizes stomach acid to help with acid disorders (dyspepsia and esophageal reflux). Many drugs require stomach acid for absorption and this is a possible mechanism of interference. In most cases however, calcium carbonate forms complexs with drugs preventing or significantly delaying their absorption. Sometimes even the calcium from milk can interfere (tetracycline antibiotics for example)

Does captopril causes retention of bradykinin?,

Mechanism of Action

Competitive inhibitor of angiotensin-converting enzyme (ACE); prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor; results in lower levels of angiotensin II which causes an increase in plasma renin activity and a reduction in aldosterone secretion.

Yes it causes urinary retention.

Captopril drug for child?, My 6 yr old son is going on this (captopril) drug next week as he has narrow heart valves i've read that this drug will lower his blood pressure! And am wondering if there is anyone on here who is on this drug who can advise me on it and its side effects especially in children? thanks

Sorry, I do not have any specific information regarding pediatric use of this drug.

Two main things to look out for in terms of side effects:

1) angioedema - a rare allergy-swelling of the lips, that can extend to the breathing tubes, see :

http://www.merck.com/mmpe/sec13/ch165/ch...

The FDA reciently revised the topic on angioedema to also include 'intestinal' angioedema, something I never had heard of before.

2) persistant coughing due to a build of bradykinin a natural substance that the body normally makes and destroys but captopril inhibits its destruction.

Captopril is classified as an ACE inhibitor

is Metroprolol and captopril the same thing ? if not can they be taken together?,

No and yes. Metoprolol is a beta blocker, it slows your heart rate helping to control your BP(it also decreases contractility of the heart). Captopril is an ace inhibitor, it helps lower BP by blocking angiotensin effects. The combination often lowers BP greater than either drug alone

Help with drug captopril?, My 6 yr old son is going on this (captopril) drug next week as he has narrow heart valves i've read that this drug will lower his blood pressure! And am wondering if there is anyone on here who is on this drug who can advise me on it and its side effects especially in children? thanks

As mentioned, a dry, non-productive cough is a potenital side effect of this class of medication. I thought it was interesting that it was being given to a 6 year old. I looked around the internet and cannot find anything showing that it is approved in children. Actually, The safety and effectiveness of Capoten (captopril) in children has not been established.

what is "captopril"? for wha desease is it?,

This topic is discussed in detail:
It's an ACE inhibitor.
Diseases:

1)Hypertension

Captopril (captopril tablets, USP) is indicated for the treatment of hypertension.

It can be given sublingual to lower BP/Angina.

2)Captopril may be used as initial therapy for patients with normal renal function, in whom the risk is relatively low. In patients with impaired renal function, particularly those with collagen vascular disease, captopril should be reserved for hypertensives who have either developed unacceptable side effects on other drugs, or have failed to respond satisfactorily to drug combinations.

Captopril is effective alone and in combination with other anti-hypertensive agents, especially thiazide-type diuretics. The blood pressure lowering effects of captopril and thiazides are approximately additive.

3)Heart Failure/CCF.

Captopril is indicated in the treatment of congestive heart failure usually in combination with diuretics and digitalis. The beneficial effect of captopril in heart failure does not require the presence of digitalis, however, most controlled clinical trial experience with captopril has been in patients receiving digitalis, as well as diuretic treatment.

4)Left Ventricular Dysfunction After Myocardial Infarction

Captopril is indicated to improve survival following myocardial infarction in clinically stable patients with left ventricular dysfunction manifested as an ejection fraction ≤40% and to reduce the incidence of overt heart failure and subsequent hospitalizations for congestive heart failure in these patients.

In considering use of captopril tablets, USP it should be noted that in controlled trials ACE inhibitors have an effect on blood pressure that is less in black patients than in non-blacks. In addition, ACE inhibitors cause a higher rate of angioedema in black than in non-black patients.

Determine the absolute configuration (R,S) for the indicated chiral centers in captopril and ephedrine. a. __,

captopril IUPAC name: (2S)-1-[(2S)-2-methyl-3-sulfanylpropanoy...
pyrrolidine-2-carboxylic acid

ephedrine: (1R,2S)-2-methylamino-1-phenylpropan-1-o...

Continue reading here: Clavulanate Potassium Risk Summary

Was this article helpful?

0 0