Enhancement by endothelin-1 of microvascular permeability via the activation of ETA receptors
| Autor: | János G. Filep, Mitsuo Yano, Anne Rousseau, Gérard E. Plante, Pierre Sirois, Alain Fournier, Éva Földes-Filep, M. G. Sirois |
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| Rok vydání: | 1993 |
| Předmět: |
Male
medicine.hormone medicine.medical_specialty Molecular Sequence Data Blood Pressure Vascular permeability Peptides Cyclic Capillary Permeability Endothelins chemistry.chemical_compound Internal medicine medicine Animals Amino Acid Sequence Plasma Volume Rats Wistar Receptor Evans Blue Pharmacology BQ-123 Endothelin-1 Receptors Endothelin Chemistry Endothelin 1 Extravasation Rats Endocrinology Regional Blood Flow cardiovascular system Endothelin receptor Research Article |
| Zdroj: | British Journal of Pharmacology. 109:880-886 |
| ISSN: | 0007-1188 |
| DOI: | 10.1111/j.1476-5381.1993.tb13657.x |
| Popis: | 1. The objective of the present experiments was to assess the involvement of endothelin-A (ETA) receptors in mediating the effects of endothelin-1 on microvascular permeability in conscious rats. 2. Bolus injection of endothelin-1 (0.1 and 1 nmol kg-1, i.v.) resulted in a dose-dependent prolonged pressor effect preceded by a transient depressor response. These changes were accompanied by a dose-dependent loss of plasma volume. Endothelin-1 (1 nmol kg-1) enhanced the vascular permeability of the upper and lower bronchi, kidney, stomach, duodenum and spleen (up to 270%) as measured by the extravasation of Evans blue dye. 3. Pretreatment of the animals with the selective ETA receptor antagonist, BQ-123 (1 mg kg-1, i.v.) significantly blunted the pressor response to endothelin-1 without affecting the depressor response. BQ-123 inhibited by 87% the endothelin-1 (1 nmol kg-1)-induced plasma volume loss. BQ-123 markedly attenuated protein extravasation elicited by endothelin-1 in the upper and lower bronchi and kidney, whereas it completely inhibited the permeability effect of endothelin-1 in the stomach and duodenum. BQ-123 by itself had no significant effect on the parameters studied. 4. The endothelin-1 analogue, [Trp(For)21]-endothelin-1, in which Trp21 is formylated, was as potent a pressor agent as endothelin-1, but had no depressor action. Bolus injection of [Trp(For)21]-endothelin-1 (0.1 and 1 nmol kg-1, i.v.) evoked similar plasma volume losses to those observed following administration of equimolar doses of endothelin-1. Furthermore, 1 nmol kg-1 [Trp(For)21]-endothelin-l evoked increases in protein extravasation similar to endothelin-l, 1 nmol kg-1.5. The present findings suggest that endothelin- 1 enhances microvascular permeability, in part, via the activation of ETA receptors. |
| Databáze: | OpenAIRE |
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