(Hypertension. 1995;25:1053-1057.)
© 1995 American Heart Association, Inc.
Articles |
From the Cardiovascular Unit, Istituto di Medicina Interna (G. La V., C.L., C.F., L.S., G.S., F.F.); Nuclear Medicine Unit, Dipartimento di Fisiopatologia Clinica (G. Bisi); Cardiovascular Unit, Clinica Medica I (G. Barletta, R. Del B.), University of Florence School of Medicine; and Laboratorio di Endocrinologia, U.S.L. 10D (G.M.), Florence, Italy.
Abstract We evaluated the cardiovascular effects of pathophysiological plasma levels of brain natriuretic peptide in seven patients with mild to moderate essential hypertension by performing equilibrium radionuclide angiocardiography at baseline and during brain natriuretic peptide infusion at increasing doses (4, 8, 10, and 12 pmol/kg per minute for 20 minutes each). Brain natriuretic peptide induced a progressive reduction of left ventricular end-diastolic volume (from 107.5±10.3 to 89.0±11.0 mL at the end of all infusion periods) and end-systolic volume, whereas stroke volume did not show any significant change (from 64.9±5.9 to 62.7±7.8 mL). Cardiac output, arterial pressure, and peripheral vascular resistance did not change significantly. The lack of effects on systemic hemodynamics was probably due to compensatory activation of the sympathetic nervous system, as indicated by the significant increase in plasma norepinephrine levels (from 1.75±0.18 to 2.19±0.21 nmol/L), heart rate (from 68±6 to 81±6 beats per minute), peak ejection rate, and peak filling rate. These results indicate that brain natriuretic peptide, at the pathophysiological plasma concentrations reached in this study, influences cardiovascular homeostasis mainly by reducing cardiac preload.
Key Words: natriuretic peptides, brain hypertension, essential radionuclide imaging cardiac output hemodynamics
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