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 language | English |
|---|---|
| Pages (from-to) | 281-285 |
| Number of pages | 5 |
| Journal | Journal of Cardiovascular Pharmacology |
| Volume | 7 |
| Issue number | 2 |
| Publication status | Published - 1985 |
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Keywords
- Diuretics
- Hemodynamics
- Hypertension
- Indapamide
- Tilt
- Vasodilators
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Pharmacology
Cite this
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 journal › Article
}
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
C2 - 2581081
AN - SCOPUS:0021869132
VL - 7
SP - 281
EP - 285
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
SN - 0160-2446
IS - 2
ER -