Unaltered dopaminergic modulation of aldosterone secretion in cirrhosis

Author:

Bernardi M.1,De Palma Rossana2,Trevisani F.3,Malatesta R.4,Baraldini M.5,Cursaro Carmela6,Gasbarrini G.7

Affiliation:

1. 1Patologia Speciale Medica I, University of Bologna, Bologna, Italy

2. 3Patologia Speciale Medica I, University of Bologna, Bologna, Italy

3. 4Patologia Speciale Medica I, University of Bologna, Bologna, Italy

4. Patologia Speciale Medica II, University of Bologna, Bologna, Italy

5. 6Patologia Speciale Medica I, University of Bologna, Bologna, Italy

6. 7Patologia Speciale Medica I, University of Bologna, Bologna, Italy

7. 8Patologia Speciale Medica I, University of Bologna, Bologna, Italy

Abstract

1. The responses of plasma aldosterone and plasma prolactin concentrations to metoclopramide (10 mg intravenously) were evaluated over 2 h in eight healthy controls and in 23 patients with cirrhosis (10 without and 13 with ascites). Plasma renin activity, glomerular filtration rate and renal sodium excretion were also determined. 2. Metoclopramide did not significantly influence plasma renin activity, whereas both plasma aldosterone and plasma prolactin rose significantly. The incremental areas under the curves did not differ among controls and cirrhotic patients without and with ascites. No significant correlations between plasma prolactin and aldosterone, either under basal conditions or after metoclopramide administration, were found in either controls or patients. 3. Glomerular filtration rate did not change after metoclopramide. Renal sodium excretion in controls and cirrhotic patients without ascites was also unaffected, whereas it decreased significantly in cirrhotic patients with ascites. In the latter, renal sodium excretion was inversely correlated with plasma aldosterone both under basal conditions and after metoclopramide administration. 4. The dopaminergic control of aldosterone secretion does not appear to be significantly altered in cirrhosis. Metoclopramide administration to cirrhotic patients with ascites leads to an increase in plasma aldosterone that may enhance renal sodium retention.

Publisher

Portland Press Ltd.

Subject

General Medicine

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