Exp Clin Endocrinol Diabetes 1985; 86(4): 79-86
DOI: 10.1055/s-0029-1210476
Original

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Clinical and Experimental Investigations of Vasopressin Secretion in Acute Porphyrias1)

U. Desaga1 , K. F.  Leonhardt2 , H. Frahm1 , M. Doss3
  • 1II. Medical Clinic of the University of Hamburg (Director: Prof. H. Frahm), Hamburg, Marburg/F.R.G.
  • 2Department of Neurology of the Landeskrankenhaus Schleswig (Director: Dr. R. Schnell), Schleswig, Marburg/F.R.G.
  • 3Department of Biochemistry of the University of Marburg (Director: Prof. M. Doss), Marburg/F.R.G.
1) The investigations were supported by Deutsche Forschungsgemeinschaft SFB 34/D4.
Further Information

Publication History

1984

Publication Date:
16 July 2009 (online)

Summary

In 41 patients suffering from acute hepatic porphyrias the arginin.vasopressin (AVP) levels in their urine were measured by RIA. In 6 patients, AVP secretion was normal; in 8 cases AVP levels were significantly elevated, while 27 cases showed decreased levels of AVP (p < 0.001). A linear correlation between AVP secretion and urine volume was not found.

In animal experiments, 20 rats were treated with δ-aminolevulinic acid (ALA), (1.5 mmol/kg/24 h and 1.5 mmol/kg/48 h) for 4 weeks. Afterwards vasopressin production in the hypothalamo-hypophyseal system was analysed by the immunperoxidase technique and a microdensitometric method.

In ALA-treated animals, AVP positive neurones showed coarse-grained granules of different intensity and a distinct increase of peroxidase positive granules in the zona interna of the eminentia mediana. Furthermore, in comparison with the control group in ALA-treated animals the mean diameter of nuclei in AVP positive neurons was greater. While animals treated daily showed an increase of transmission in the pituitary, microdensitometric findings in animals treated at 48 hourly intervals showed an equal transmission in AVP producing nuclei compared to the controlgroup.

Our results seem to point to a toxic effect of porphyrin precursors on the CNS, which may also induce via hypothalamus lesion either diabetes insipidus or a SIADH-syndrome.

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