1. Endothelin-1 induces a strong pressor effect in ball pythons (Python regius).
- Author
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Jensen MF, Nedergaard S, Nielsen HN, Skovgaard N, Stevnsner TV, and Wang T
- Subjects
- Animals, Blood Pressure drug effects, Mesenteric Arteries drug effects, Nitric Oxide metabolism, Pulmonary Artery drug effects, Receptors, Endothelin chemistry, Receptors, Endothelin genetics, Receptors, Endothelin metabolism, Vasodilation drug effects, Boidae physiology, Endothelin Receptor Antagonists pharmacology, Endothelin-1 pharmacology, Vasoconstriction drug effects
- Abstract
Endothelin-1 (ET-1) is a very potent vasoactive peptide released from endothelial cells, and ET-1 plays an important role in the maintenance and regulation of blood pressure in mammals. ET-1 signaling is mediated by two receptors: ET
A and ETB . In mammals, ETA receptors are located on vascular smooth muscle where they mediate vasoconstriction. ETB receptors located on the endothelium mediate vasodilatation through the release of nitric oxide, whereas stimulation of ETB receptors placed on vascular smooth muscle leads to vasoconstriction. Less is known about ET-1 signaling in reptiles. In anaesthetized alligators, ET-1 elicits a biphasic blood pressure with a long-lasting initial decrease followed by a smaller increase in systemic blood pressure. In anaesthetized freshwater turtles, ET-1 causes a dose-dependent systemic vasodilatation mediated through ETB receptors. In the present study, we investigated the cardiovascular effects of ET-1 on the systemic and pulmonary vasculature of pythons. The presence of ETA and ETB receptors in the vasculature of pythons was verified by means of immunoblotting. Myography on isolated vessels revealed a dose-dependent vasoconstrictory response to ET-1 in both mesenteric and pulmonary arteries. Pressure measurements in recovered specimens revealed an ET-1-induced rise in systemic blood pressure supporting our in vitro findings. In conclusion, our study shows that ET-1 induces a strong pressor effect in the systemic circulation., (Copyright © 2019 Elsevier Inc. All rights reserved.)- Published
- 2020
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