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 journalArticlepeer-review

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

Keywords

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

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

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