Medical Journals

Endothelin-1 and Pancreatic Islet Vasculature: Studies in Vivo and on Isolated, Vascularly Perfused Pancreatic Islets.

Authors:
  • Lai En Yin
  • Persson A Erik G
  • Bodin Birgitta
  • Källskog Orjan
  • Andersson Arne
  • Pettersson Ulrika
  • Hansell Peter
  • Jansson Leif

From: Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden. Enyin.Lai@mcb.uu.se

American journal of physiology. Endocrinology and metabolism

  • Publish Date: Jun 2007
  • ISSN: 0193-1849
  • Volume: 292
  • Issue: 6
  • Pages: E1616-23
  • Medium: Print
  • Language: English
  • Citation (JAMA): Lai En Yin, Persson A Erik G, Bodin Birgitta, et al. Endothelin-1 and Pancreatic Islet Vasculature: Studies in Vivo and on Isolated, Vascularly Perfused Pancreatic Islets.. Am. J. Physiol. Endocrinol. Metab. Jun 2007;292:E1616-23

Abstract

Endothelin-1 (ET-1) is a potent endothelium-derived vasoconstrictor, which also stimulates insulin release. The aim of the present study was to evaluate whether exogenously administered ET-1 affected pancreatic islet blood flow in vivo in rats and the islet arteriolar reactivity in vitro in mice. Furthermore, we aimed to determine the ET-receptor subtype that was involved in such responses. When applying a microsphere technique for measurements of islet blood perfusion in vivo, we found that ET-1 (5 nmol/kg) consistently and markedly decreased total pancreatic and especially islet blood flow, despite having only minor effects on blood pressure. Neither endothelin A (ET(A)) receptor (BQ-123) nor endothelin-B (ET(B)) receptor (BQ-788) antagonists, alone or in combination, could prevent this reduction in blood flow. To avoid confounding interactions in vivo, we also examined the arteriolar vascular reactivity in isolated, perfused mouse islets. In the latter preparation, we demonstrated a dose-dependent constriction in response to ET-1. Administration of BQ-123 prevented this, whereas BQ-788 induced a right shift in the response. In conclusion, the pancreatic islet vasculature is highly sensitive to exogenous ET-1, which mediates its effect mainly through ET(A) receptors.

Mesh Headings (Keywords): Adrenal Glands, Animals, Arterioles, Blood Glucose, Blood Pressure, Colon, Drug Synergism, Duodenum, Endothelin-1, Insulin, Islets of Langerhans, Male, Mice, Mice, Inbred C57BL, Oligopeptides, Pancreas, Peptides, Cyclic, Piperidines, Rats, Rats, Sprague-Dawley, Receptor, Endothelin A, Receptor, Endothelin B, Regional Blood Flow, Vasoconstriction


Check for Full Text / PubMed Unique Identifier (PMID): 17284574


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