Blunted natriuretic response and low blood pressure after atrial natriuretic factor in early cirrhosis

Authors

  • Jaap J. Beutler M.D.,

    Corresponding author
    1. Departments of Nephrology and Hypertension and Gastroenterology, University Hospital Utrecht, 3500 GV Utrecht, The Netherlands
    • Department of Nephrology and Hypertension, University Hospital Utrecht, Catharijnesingel 101, 3511 GV Utrecht, The Netherlands
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  • Hein A. Koomans,

    1. Departments of Nephrology and Hypertension and Gastroenterology, University Hospital Utrecht, 3500 GV Utrecht, The Netherlands
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  • Ton J. Rabelink,

    1. Departments of Nephrology and Hypertension and Gastroenterology, University Hospital Utrecht, 3500 GV Utrecht, The Netherlands
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  • Carlo A. Gaillard,

    1. Departments of Nephrology and Hypertension and Gastroenterology, University Hospital Utrecht, 3500 GV Utrecht, The Netherlands
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  • Jan van Hattum,

    1. Departments of Nephrology and Hypertension and Gastroenterology, University Hospital Utrecht, 3500 GV Utrecht, The Netherlands
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  • Peter Boer,

    1. Departments of Nephrology and Hypertension and Gastroenterology, University Hospital Utrecht, 3500 GV Utrecht, The Netherlands
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  • Evert J. Dorhout Mees

    1. Departments of Nephrology and Hypertension and Gastroenterology, University Hospital Utrecht, 3500 GV Utrecht, The Netherlands
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Abstract

We compared the natriuretic response to a standard dose of atrial natriuretic factor in nine patients with early cirrhosis (no ascites or edema) with the response in normal subjects displaying a range of baseline sodium excretions due to different sodium intakes (20 mmoles per day, n = 9; 100 mmoles per day, n = 9, and 200 mmoles per day, n = 9). In these normal subjects, sodium output rose, in the same order, from 49 ± 12 to 177 ± 26, from 116 ± 21 to 365 ± 106 and from 228 ± 29 to 901 ± 85 μmoles per min in the first 20 min after 100 μg atrial natriuretic factor (human atrial natriuretic factor 99–126). Thus, irrespective of basal excretion, natriuresis rose by at least 2-fold. In the cirrhotic patients, natriuresis rose from 173 ± 42 to 305 ± 77 μmoles per min, that is by hardly 1-fold, significantly less than in the normal subjects (p < 0.01). Renal function studies indicated that atrial natriuretic factor caused less rise in glomerular filtration rate and in fractional sodium excretion. Atrial natriuretic factor induced a fall in blood pressure only in the cirrhotic group, from 130 ± 4/81 ± 2 to 108 ± 4/68± 3 mmHg (p < 0.001). Plasma atrial natriuretic factor was not low in the cirrhotic patients. Although these data are compatible with a primary disturbance of sodium excretion in early cirrhosis without ascites, such an explanation is complicated by the concomitant drop in blood pressure after atrial natriuretic factor. Whether this hypotensive reaction reflects impending underfill, or rather an abnormality in the regulation of vascular tone specific for cirrhosis, is obscure.

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