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Effects of hydralazine and sodium nitroprusside on plasma catecholamines and heart rate
Author(s) -
Lin MinShung,
McNay John L,
Shepherd Alexander M M,
Keeton T Kent
Publication year - 1983
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1983.200
Subject(s) - hydralazine , sodium nitroprusside , mean arterial pressure , heart rate , chemistry , hemodynamics , anesthesia , medicine , sodium , blood pressure , endocrinology , pharmacology , nitric oxide , organic chemistry
Hydralazine and sodium nitroprusside induce different effects on systemic hemodynamics, but their effects on sympathetic neuronal activity have not been compared. Five hypertensive subjects receiving only hydrochlorothiazide were studied during two sessions. During one session, four doses of hydralazine, 0.1 to 0.6 mg/kg, were given intravenously at least 3 days apart, and during the other session, sodium nitroprusside was infused in stepwise doses, 0.05 to 4.8 μg/kg/min for 10 min per dose. Mean arterial pressure (MAP), heart rate (HR), and plasma norepinephrine (NE) and epinephrine concentrations were determined before and after dosing. The following correlated linearly for hydralazine and sodium nitroprusside: ΔHR/ΔMAP, ΔNE/ΔMAP, and ΔHR/ΔNE. Comparison of these relationships, however, indicated significant differences between the sympathetic neuronal and hemodynamic responses to hydralazine and sodium nitroprusside. Increase in HR relative to decrease in MAP was greater for hydralazine than for sodium nitroprusside. There were greater increases in plasma NE concentration relative to falls in MAP with sodium nitroprusside than with hydralazine, but increases in HR relative to increases in plasma NE concentration were smaller for sodium nitroprusside than for hydralazine. Such responses may reflect differential effects of hydralazine and sodium nitroprusside on the systemic clearance of NE or of the activity of cardiopulmonary baroreceptors. Clinical Pharmacology and Therapeutics (1983) 34, 474–480; doi: 10.1038/clpt.1983.200

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