ArticlePloS one2010
Stimuli of sensory-motor nerves terminate arterial contractile effects of endothelin-1 by CGRP and dissociation of ET-1/ET(A)-receptor complexes.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 34 citations in OpenAlex.
- Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026Review
- Pharmacological Gq inhibition induces strong pulmonary vasorelaxation and reverses pulmonary hypertension.EMBO molecular medicine · 2024Article
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- The role of TRPV1 channels in atherosclerosis.Channels (Austin, Tex.) · 2020Review
- Vascular actions of peripheral CGRP in migraine-like photophobia in mice.Cephalalgia : an international journal of headache · 2020Article
- Endothelin-1 Regulation of Exercise-Induced Changes in Flow: Dynamic Regulation of Vascular Tone.Frontiers in pharmacology · 2017Article
- Distinct ETA receptor binding mode of macitentan as determined by site directed mutagenesis.PloS one · 2014Article
- Endothelin-1 and endothelin-2 initiate and maintain contractile responses by different mechanisms in rat mesenteric and cerebral arteries.British journal of pharmacology · 2013Article
- Angiotensinergic innervation of the kidney: present knowledge and its significance.Current hypertension reports · 2013Review
- Article
- Agonist-dependent modulation of arterial endothelinA receptor function.British journal of pharmacology · 2012Article
- G-protein βγ subunits in vasorelaxing and anti-endothelinergic effects of calcitonin gene-related peptide.British journal of pharmacology · 2012Article
- Role of calcitonin gene-related peptide in cerebral vasospasm, and as a therapeutic approach to subarachnoid hemorrhage.Frontiers in endocrinology · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndothelin-1 (ET-1), a long-acting paracrine mediator, is implicated in cardiovascular diseases but clinical trials with ET-receptor antagonists were not successful in some areas. We tested whether the quasi-irreversible receptor-binding of ET-1 (i) limits reversing effects of the antagonists and (ii) can be selectively dissociated by an endogenous counterbalancing mechanism. METHODOLOGY/PRINCIPAL
findingsIn isolated rat mesenteric resistance arteries, ET(A)-antagonists, endothelium-derived relaxing factors and synthetic vasodilators transiently reduced contractile effects of ET-1 but did not prevent persistent effects of the peptide. Stimuli of peri-vascular vasodilator sensory-motor nerves such as capsaicin not only reduced but also terminated long-lasting effects of ET-1. This was prevented by CGRP-receptor antagonists and was mimicked by exogenous calcitonin gene-related peptide (CGRP). Using 2-photon laser scanning microscopy in vital intact arteries, capsaicin and CGRP, but not ET(A)-antagonism, were observed to promote dissociation of pre-existing ET-1/ET(A)-receptor complexes.
conclusionsIrreversible binding and activation of ET(A)-receptors by ET-1 (i) occur at an antagonist-insensitive site of the receptor and (ii) are selectively terminated by endogenously released CGRP. Hence, natural stimuli of sensory-motor nerves that stimulate release of endogenous CGRP can be considered for therapy of diseases involving ET-1.
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