Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension

Fabio Magrini, Giuliano Buzzetti, Francesco De Giovanni, Donatella Cerati, Giovanna Macchi, Cristina Mondadori

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

We studied the hemodynamic mechanism responsible for the antihypertensive effect of indapamide in eight patients with mild essential hypertension. Systemic and pulmonary hemodynamics were measured using direct techniques (right heart catheterization and thermodilution method), before and 7-10 days after oral treatment with indapamide (2.5 mg/day). Indapamide reduced mean arterial blood pressure from 120 ± 1.6 (mean ± SE) to 101 ± 1.4 mm Hg (p <0.01), and mean pulmonary artery pressure from 21 ± 0.59 to 17 ± 1.05 mm Hg (p <0.01). Total peripheral vascular resistance (TPR) and pulmonary vascular resistance were reduced from 36 ± 0.85 to 29 ± 0.72 U/m2 (p <0.01) and from 4.3 ± 0.17 to 3.8 ± 0.18 U/m2 (p <0.01), respectively. Indapamide did not change cardiac index (CI) (3.311 ± 61.6 vs. 3,325 ± 72.1 ml/min/m2), heart rate (HR) (75 ± 1.7 vs. 75 ± 9 beats/min), mean rate of left ventricular ejection index 140 ± 2.04 vs. 139 ± 1.99 ml/s/m2, and stroke index (44 ± 5.6 vs. 43 ± 5.8 ml/m2). Mean pulmonary wedge pressure decreased from 7 ± 0.6 to 5 ± 0.5 mm Hg (p <0.05). Body weight. 24-h urinary volume, and hematocrit were unchanged after treatment. We conclude that the hemodynamic mechanism responsible for the antihypertensive action of indapamide is a reduction in TPR without changes in CI and HR.

Original languageEnglish
Pages (from-to)281-285
Number of pages5
JournalJournal of Cardiovascular Pharmacology
Volume7
Issue number2
Publication statusPublished - 1985

Fingerprint

Indapamide
Vascular Resistance
Hemodynamics
Hypertension
Lung
Antihypertensive Agents
Arterial Pressure
Heart Rate
Thermodilution
Pulmonary Wedge Pressure
Cardiac Catheterization
Hematocrit
Pulmonary Artery
Stroke
Body Weight
Pressure
Therapeutics

Keywords

  • Diuretics
  • Hemodynamics
  • Hypertension
  • Indapamide
  • Tilt
  • Vasodilators

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Magrini, F., Buzzetti, G., De Giovanni, F., Cerati, D., Macchi, G., & Mondadori, C. (1985). Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension. Journal of Cardiovascular Pharmacology, 7(2), 281-285.

Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension. / Magrini, Fabio; Buzzetti, Giuliano; De Giovanni, Francesco; Cerati, Donatella; Macchi, Giovanna; Mondadori, Cristina.

In: Journal of Cardiovascular Pharmacology, Vol. 7, No. 2, 1985, p. 281-285.

Research output: Contribution to journalArticle

Magrini, F, Buzzetti, G, De Giovanni, F, Cerati, D, Macchi, G & Mondadori, C 1985, 'Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension', Journal of Cardiovascular Pharmacology, vol. 7, no. 2, pp. 281-285.
Magrini F, Buzzetti G, De Giovanni F, Cerati D, Macchi G, Mondadori C. Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension. Journal of Cardiovascular Pharmacology. 1985;7(2):281-285.
Magrini, Fabio ; Buzzetti, Giuliano ; De Giovanni, Francesco ; Cerati, Donatella ; Macchi, Giovanna ; Mondadori, Cristina. / Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension. In: Journal of Cardiovascular Pharmacology. 1985 ; Vol. 7, No. 2. pp. 281-285.
@article{e951dc9f173a4462a911a7f393343118,
title = "Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension",
abstract = "We studied the hemodynamic mechanism responsible for the antihypertensive effect of indapamide in eight patients with mild essential hypertension. Systemic and pulmonary hemodynamics were measured using direct techniques (right heart catheterization and thermodilution method), before and 7-10 days after oral treatment with indapamide (2.5 mg/day). Indapamide reduced mean arterial blood pressure from 120 ± 1.6 (mean ± SE) to 101 ± 1.4 mm Hg (p <0.01), and mean pulmonary artery pressure from 21 ± 0.59 to 17 ± 1.05 mm Hg (p <0.01). Total peripheral vascular resistance (TPR) and pulmonary vascular resistance were reduced from 36 ± 0.85 to 29 ± 0.72 U/m2 (p <0.01) and from 4.3 ± 0.17 to 3.8 ± 0.18 U/m2 (p <0.01), respectively. Indapamide did not change cardiac index (CI) (3.311 ± 61.6 vs. 3,325 ± 72.1 ml/min/m2), heart rate (HR) (75 ± 1.7 vs. 75 ± 9 beats/min), mean rate of left ventricular ejection index 140 ± 2.04 vs. 139 ± 1.99 ml/s/m2, and stroke index (44 ± 5.6 vs. 43 ± 5.8 ml/m2). Mean pulmonary wedge pressure decreased from 7 ± 0.6 to 5 ± 0.5 mm Hg (p <0.05). Body weight. 24-h urinary volume, and hematocrit were unchanged after treatment. We conclude that the hemodynamic mechanism responsible for the antihypertensive action of indapamide is a reduction in TPR without changes in CI and HR.",
keywords = "Diuretics, Hemodynamics, Hypertension, Indapamide, Tilt, Vasodilators",
author = "Fabio Magrini and Giuliano Buzzetti and {De Giovanni}, Francesco and Donatella Cerati and Giovanna Macchi and Cristina Mondadori",
year = "1985",
language = "English",
volume = "7",
pages = "281--285",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Systemic and pulmonary hemodynamic effects of indapamide in patients with mild arterial hypertension

AU - Magrini, Fabio

AU - Buzzetti, Giuliano

AU - De Giovanni, Francesco

AU - Cerati, Donatella

AU - Macchi, Giovanna

AU - Mondadori, Cristina

PY - 1985

Y1 - 1985

N2 - We studied the hemodynamic mechanism responsible for the antihypertensive effect of indapamide in eight patients with mild essential hypertension. Systemic and pulmonary hemodynamics were measured using direct techniques (right heart catheterization and thermodilution method), before and 7-10 days after oral treatment with indapamide (2.5 mg/day). Indapamide reduced mean arterial blood pressure from 120 ± 1.6 (mean ± SE) to 101 ± 1.4 mm Hg (p <0.01), and mean pulmonary artery pressure from 21 ± 0.59 to 17 ± 1.05 mm Hg (p <0.01). Total peripheral vascular resistance (TPR) and pulmonary vascular resistance were reduced from 36 ± 0.85 to 29 ± 0.72 U/m2 (p <0.01) and from 4.3 ± 0.17 to 3.8 ± 0.18 U/m2 (p <0.01), respectively. Indapamide did not change cardiac index (CI) (3.311 ± 61.6 vs. 3,325 ± 72.1 ml/min/m2), heart rate (HR) (75 ± 1.7 vs. 75 ± 9 beats/min), mean rate of left ventricular ejection index 140 ± 2.04 vs. 139 ± 1.99 ml/s/m2, and stroke index (44 ± 5.6 vs. 43 ± 5.8 ml/m2). Mean pulmonary wedge pressure decreased from 7 ± 0.6 to 5 ± 0.5 mm Hg (p <0.05). Body weight. 24-h urinary volume, and hematocrit were unchanged after treatment. We conclude that the hemodynamic mechanism responsible for the antihypertensive action of indapamide is a reduction in TPR without changes in CI and HR.

AB - We studied the hemodynamic mechanism responsible for the antihypertensive effect of indapamide in eight patients with mild essential hypertension. Systemic and pulmonary hemodynamics were measured using direct techniques (right heart catheterization and thermodilution method), before and 7-10 days after oral treatment with indapamide (2.5 mg/day). Indapamide reduced mean arterial blood pressure from 120 ± 1.6 (mean ± SE) to 101 ± 1.4 mm Hg (p <0.01), and mean pulmonary artery pressure from 21 ± 0.59 to 17 ± 1.05 mm Hg (p <0.01). Total peripheral vascular resistance (TPR) and pulmonary vascular resistance were reduced from 36 ± 0.85 to 29 ± 0.72 U/m2 (p <0.01) and from 4.3 ± 0.17 to 3.8 ± 0.18 U/m2 (p <0.01), respectively. Indapamide did not change cardiac index (CI) (3.311 ± 61.6 vs. 3,325 ± 72.1 ml/min/m2), heart rate (HR) (75 ± 1.7 vs. 75 ± 9 beats/min), mean rate of left ventricular ejection index 140 ± 2.04 vs. 139 ± 1.99 ml/s/m2, and stroke index (44 ± 5.6 vs. 43 ± 5.8 ml/m2). Mean pulmonary wedge pressure decreased from 7 ± 0.6 to 5 ± 0.5 mm Hg (p <0.05). Body weight. 24-h urinary volume, and hematocrit were unchanged after treatment. We conclude that the hemodynamic mechanism responsible for the antihypertensive action of indapamide is a reduction in TPR without changes in CI and HR.

KW - Diuretics

KW - Hemodynamics

KW - Hypertension

KW - Indapamide

KW - Tilt

KW - Vasodilators

UR - http://www.scopus.com/inward/record.url?scp=0021869132&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021869132&partnerID=8YFLogxK

M3 - Article

VL - 7

SP - 281

EP - 285

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 2

ER -