ArticleJournal of anesthesia2010
The cellular mechanisms underlying the inhibitory effects of isoflurane and sevoflurane on arginine vasopressin-induced vasoconstriction.
Article in Journal of anesthesia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Establishment and validation of a predictive nomogram for polyuria during general anesthesia in thoracic surgery.Journal of cardiothoracic surgery · 2024Article
- Occipital Artery Function during the Development of 2-Kidney, 1-Clip Hypertension in Rats.International journal of vascular medicine · 2014Article
- Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat.Journal of anesthesia · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeArginine vasopressin (AVP) is a potent vasoconstrictor that is sometimes used for the treatment of refractory vasodilatory shock. AVP constricts vascular smooth muscle by increasing both intracellular calcium concentration ([Ca(2+)](i)) and myofilament Ca(2+) sensitivity. However, the modulation of AVP-mediated vasoconstriction by volatile anesthetics remains to be determined. This study investigates the effects of isoflurane and sevoflurane on AVP-induced vasoconstriction and elucidates the underlying mechanisms, with an emphasis on the Ca(2+)-mediated pathways and Ca(2+) sensitization pathways of rat aortic smooth muscle.
methodsThe effects of isoflurane and sevoflurane on AVP-induced vasoconstriction and on the AVP-induced increase in [Ca(2+)](i) and Rho activity in rat aorta were investigated by isometric force recording, by measuring [Ca(2+)](i) using fluorescence dye, and by Western blotting techniques.
resultsArginine vasopressin (10⁻⁷M) elicited a transient contractile response that was inhibited by isoflurane and sevoflurane in a concentration-dependent manner. AVP (10⁻⁷ M) induced a transient increase in intracellular Ca(2+) concentration ([Ca(2+)](i)). Isoflurane and sevoflurane also inhibited an AVP-induced increase in [Ca(2+)](i) in a concentration-dependent manner. AVP (10⁻⁷ M) increased the Rho activity that was attenuated by 2 minimum alveolar concentration of sevoflurane (P < 0.01), but not by an equipotent concentration of isoflurane.
conclusionArginine vasopressin-induced vasoconstriction is mediated by an increase in [Ca(2+)](i) and by the activation of the Rho-Rho kinase pathway in rat aortic smooth muscle. Although both isoflurane and sevoflurane, at clinically relevant concentrations, attenuate AVP-induced contraction, the cellular mechanisms of their inhibitory effects appear to differ.
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