Effects of amlodipine, nifedipine GITS, and indomethacin on angiotensin- converting enzyme inhibitor-induced cough: A randomized, placebo-controlled, double-masked, crossover study

Roberto Fogari, Annalisa Zoppi, Amedeo Mugellini, Paola Preti, Alessandra Banderali, Antonio Salvetti

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Prostaglandins (PGs) are thought to play a role in the genesis of cough induced by angiotensin-converting enzyme (ACE) inhibitors, whereas inhibition of PG synthesis can reduce or abolish the incidence of this side effect. Experimental and clinical data suggest that nifedipine, a dihydropyridine calcium channel blocker, can inhibit PG synthesis. Therefore, the aim of the present study was to determine whether treatment with amlodipine would also reduce cough induced by an ACE inhibitor and to compare the efficacy of amlodipine with that of indomethacin, a known inhibitor of PG synthesis. Thirty-three patients with hypertension who developed cough during chronic benazepril therapy were allocated randomly to receive slow-release nifedipine gastrointestinal therapeutic system (GITS) 30 mg once daily, amlodipine 5 mg once daily, indomethacin 50 mg twice dally, or placebo twice dally for 2 weeks. This was according to a double-masked, double-dummy, crossover, Latin square design. At the end of each phase, cough was assessed by means of a self-administered questionnaire with an ordinal 10-point visual analogue scale for rating daily cough intensity and frequency. Indomethacin eliminated or markedly reduced cough induced by the ACE inhibitor, whereas nifedipine GITS and amlodipine reduced it to a lesser degree. These findings suggest that PGs play a role in cough caused by ACE inhibitors and that a dihydropyridine calcium channel blocker can reduce the occurrence of this side effect.

Original languageEnglish
Pages (from-to)121-128
Number of pages8
JournalCurrent Therapeutic Research
Volume60
Issue number3
DOIs
Publication statusPublished - 1999

Fingerprint

Amlodipine
Nifedipine
Double-Blind Method
Angiotensin-Converting Enzyme Inhibitors
Cough
Indomethacin
Cross-Over Studies
Placebos
Prostaglandins
Calcium Channel Blockers
Therapeutics
Prostaglandin Antagonists
Visual Analog Scale
Hypertension
Incidence

Keywords

  • Amlodipine
  • Angiotensin-converting enzyme inhibitors
  • Cough
  • Indomethacin
  • Nifedipine

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Effects of amlodipine, nifedipine GITS, and indomethacin on angiotensin- converting enzyme inhibitor-induced cough : A randomized, placebo-controlled, double-masked, crossover study. / Fogari, Roberto; Zoppi, Annalisa; Mugellini, Amedeo; Preti, Paola; Banderali, Alessandra; Salvetti, Antonio.

In: Current Therapeutic Research, Vol. 60, No. 3, 1999, p. 121-128.

Research output: Contribution to journalArticle

@article{d94409c3311f4bd384089fff81020b88,
title = "Effects of amlodipine, nifedipine GITS, and indomethacin on angiotensin- converting enzyme inhibitor-induced cough: A randomized, placebo-controlled, double-masked, crossover study",
abstract = "Prostaglandins (PGs) are thought to play a role in the genesis of cough induced by angiotensin-converting enzyme (ACE) inhibitors, whereas inhibition of PG synthesis can reduce or abolish the incidence of this side effect. Experimental and clinical data suggest that nifedipine, a dihydropyridine calcium channel blocker, can inhibit PG synthesis. Therefore, the aim of the present study was to determine whether treatment with amlodipine would also reduce cough induced by an ACE inhibitor and to compare the efficacy of amlodipine with that of indomethacin, a known inhibitor of PG synthesis. Thirty-three patients with hypertension who developed cough during chronic benazepril therapy were allocated randomly to receive slow-release nifedipine gastrointestinal therapeutic system (GITS) 30 mg once daily, amlodipine 5 mg once daily, indomethacin 50 mg twice dally, or placebo twice dally for 2 weeks. This was according to a double-masked, double-dummy, crossover, Latin square design. At the end of each phase, cough was assessed by means of a self-administered questionnaire with an ordinal 10-point visual analogue scale for rating daily cough intensity and frequency. Indomethacin eliminated or markedly reduced cough induced by the ACE inhibitor, whereas nifedipine GITS and amlodipine reduced it to a lesser degree. These findings suggest that PGs play a role in cough caused by ACE inhibitors and that a dihydropyridine calcium channel blocker can reduce the occurrence of this side effect.",
keywords = "Amlodipine, Angiotensin-converting enzyme inhibitors, Cough, Indomethacin, Nifedipine",
author = "Roberto Fogari and Annalisa Zoppi and Amedeo Mugellini and Paola Preti and Alessandra Banderali and Antonio Salvetti",
year = "1999",
doi = "10.1016/S0011-393X(00)88520-3",
language = "English",
volume = "60",
pages = "121--128",
journal = "Current Therapeutic Research - Clinical and Experimental",
issn = "0011-393X",
publisher = "Excerpta Medica",
number = "3",

}

TY - JOUR

T1 - Effects of amlodipine, nifedipine GITS, and indomethacin on angiotensin- converting enzyme inhibitor-induced cough

T2 - A randomized, placebo-controlled, double-masked, crossover study

AU - Fogari, Roberto

AU - Zoppi, Annalisa

AU - Mugellini, Amedeo

AU - Preti, Paola

AU - Banderali, Alessandra

AU - Salvetti, Antonio

PY - 1999

Y1 - 1999

N2 - Prostaglandins (PGs) are thought to play a role in the genesis of cough induced by angiotensin-converting enzyme (ACE) inhibitors, whereas inhibition of PG synthesis can reduce or abolish the incidence of this side effect. Experimental and clinical data suggest that nifedipine, a dihydropyridine calcium channel blocker, can inhibit PG synthesis. Therefore, the aim of the present study was to determine whether treatment with amlodipine would also reduce cough induced by an ACE inhibitor and to compare the efficacy of amlodipine with that of indomethacin, a known inhibitor of PG synthesis. Thirty-three patients with hypertension who developed cough during chronic benazepril therapy were allocated randomly to receive slow-release nifedipine gastrointestinal therapeutic system (GITS) 30 mg once daily, amlodipine 5 mg once daily, indomethacin 50 mg twice dally, or placebo twice dally for 2 weeks. This was according to a double-masked, double-dummy, crossover, Latin square design. At the end of each phase, cough was assessed by means of a self-administered questionnaire with an ordinal 10-point visual analogue scale for rating daily cough intensity and frequency. Indomethacin eliminated or markedly reduced cough induced by the ACE inhibitor, whereas nifedipine GITS and amlodipine reduced it to a lesser degree. These findings suggest that PGs play a role in cough caused by ACE inhibitors and that a dihydropyridine calcium channel blocker can reduce the occurrence of this side effect.

AB - Prostaglandins (PGs) are thought to play a role in the genesis of cough induced by angiotensin-converting enzyme (ACE) inhibitors, whereas inhibition of PG synthesis can reduce or abolish the incidence of this side effect. Experimental and clinical data suggest that nifedipine, a dihydropyridine calcium channel blocker, can inhibit PG synthesis. Therefore, the aim of the present study was to determine whether treatment with amlodipine would also reduce cough induced by an ACE inhibitor and to compare the efficacy of amlodipine with that of indomethacin, a known inhibitor of PG synthesis. Thirty-three patients with hypertension who developed cough during chronic benazepril therapy were allocated randomly to receive slow-release nifedipine gastrointestinal therapeutic system (GITS) 30 mg once daily, amlodipine 5 mg once daily, indomethacin 50 mg twice dally, or placebo twice dally for 2 weeks. This was according to a double-masked, double-dummy, crossover, Latin square design. At the end of each phase, cough was assessed by means of a self-administered questionnaire with an ordinal 10-point visual analogue scale for rating daily cough intensity and frequency. Indomethacin eliminated or markedly reduced cough induced by the ACE inhibitor, whereas nifedipine GITS and amlodipine reduced it to a lesser degree. These findings suggest that PGs play a role in cough caused by ACE inhibitors and that a dihydropyridine calcium channel blocker can reduce the occurrence of this side effect.

KW - Amlodipine

KW - Angiotensin-converting enzyme inhibitors

KW - Cough

KW - Indomethacin

KW - Nifedipine

UR - http://www.scopus.com/inward/record.url?scp=0032994496&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032994496&partnerID=8YFLogxK

U2 - 10.1016/S0011-393X(00)88520-3

DO - 10.1016/S0011-393X(00)88520-3

M3 - Article

AN - SCOPUS:0032994496

VL - 60

SP - 121

EP - 128

JO - Current Therapeutic Research - Clinical and Experimental

JF - Current Therapeutic Research - Clinical and Experimental

SN - 0011-393X

IS - 3

ER -