Vasopressorische Wirkung von Extrakten aus humaner Nebenschilddrüse

Zusammenfassung

In der Pathogenese der essentiellen Hypertonie werden bisher unidentifizierte, zirkulierende, vasopressorisch wirkende Faktoren diskutiert. Benishin [2] beschrieb kürzlich einen solchen Vasopressor. Es wird vermutet, daß dieser Faktor in der Nebenschilddrüse gebildet wird [6]. Bisher gab es jedoch keine Informationen, ob ein solcher Faktor auch in menschlichem Nebenschilddrüsengewebe gebildet wird. Aus diesem Grund wurde in dieser Studie Nebenschilddrüsengewebe auf die Existenz eines Vasopressors hin untersucht.

Abstract

Recently, a parathyroid hypertensive factor was postulated to play a role in the pathogenesis of hypertension in genetically hypertensive rats. Therefore it was examined, whether in human parathyroid adenomas a vasopressor substance can be detected and if so, whether this factor is identical with the human plasmaderived hypertensive factor demonstrated by our group. To this purpose, homogenates of parathyroid adenomas from 22 patients with primary or tertiary hyperparathyroidism were fractionated with chromatographic techniques. The vasopressor action of the fractions was tested in an isolated perfused rat kidney (constant flow system, measurement of perfusion pressure). One of the fractions obtained from size exclusion chromatography developed an increase of perfusion pressure of 17 mmHg ± 1.9 mmHg. This fraction contained substances in a mass range between 0.6 and 2.5 kDa, based on column calibration and mass spectrometry. According to the elution time in size exclusion chromatography, it is unlikely that the vasopressor factor from human parathyroid glands is identical with the hypertensive factor derived from human plasma. Experiments with alpha-adreno- and angiotensin II-receptor inhibitors excluded the identity of the parathyroid gland-derived vasopressor factor with the catecholamines and angiotensin II. The results demonstrate the existence of a yet unknown vasopressor agent in parathyroid adenomas from patients with primary or tertiary hyperparathyroidism.