Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Uhlig, S. et al.

Pharmacologic characterization of endothelin receptor responses in the isolated perfused rat lung.

Endothelin receptor subtypes were characterized in isolated perfused rat lungs using the peptide ETA-receptor antagonists BQ 610 and BQ 123, the nonpeptide mixed ETA-/ETB-receptor antagonist bosentan, and the ETB-receptor agonist IRL 1620. Intra-arterial injection of 1 nmol IRL 1620 caused an enhanced reduction in pulmonary conductance compared with 1 nmol endothelin (ET-1) or 0.33 nmol IRL 1620. Pretreatment of lungs with BQ 610, BQ 123, or bosentan aggravated the bronchoconstriction induced by 1 nmol ET-1 so that it was comparable to that induced by 1 nmol IRL 1620. Although perfusion with 1 nmol IRL 1620 had only minor effects on vascular conductance, 1 nmol ET-1 caused a marked decrease in this parameter. This vasonconstriction was prevented by BQ 610, BQ 123, or bosentan. High concentrations of the stable prostacyclin metabolite, 6-keto-PGF1 alpha, were found in the perfusate of lungs treated with 1 nmol IRL 1620 or 1 nmol ET-1. The ET-1-induced release of 6-keto-PGF1 alpha was blocked by bosentan, but not by BQ 610. ET-1, but not IRL 1620, provoked the release of thromboxane B2. The main effect of ETA-receptor stimulation is vasoconstriction, whereas ETB-receptor stimulation causes bronchoconstriction. Both actions, however, are attenuated by the other receptor, i.e., the ETA- induced vasoconstriction is attenuated by ETB-receptor-induced release of vasodilators such as prostacyclin, whereas the ETB-receptor- induced bronchoconstriction is attenuated by an unknown ETA-receptor-dependent bronchodilatory mechanism.[1]

References

Pharmacologic characterization of endothelin receptor responses in the isolated perfused rat lung. Uhlig, S., von Bethmann, A.N., Featherstone, R.L., Wendel, A. Am. J. Respir. Crit. Care Med. (1995) [Pubmed]

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