title: [Involvement of calmodulin in realization of vasoconstrictive effects of serotonin and norepinephrin].
abstract: Possible involvement ofcalmodulin in adrenergic and serotoninergic regulation of vascular contractility has been studied. Calmodulin inhibitors trifluoperazine and W-13 suppress vasoconstriction of the rat aorta in response to norepinephrine, serotonin, and serotonin 5HT1A- and 5HT2A-receptor agonists (8-OH-DPAT and DOI, respectively) and do not affect the vasodilatory effect of 5HT1B-, 5HT2B-, and 5HT4-receptors. The force of aorta contraction in response to 8-OH-DPAT increases after the activation of calcium entry through voltage-gated Ca2+-channels. This effect is not related to non-specific activation of alpha1-adrenoceptors, since it is realized in the presence of prazosin. The inhibitor of calmodulin-dependent myosin light chain kinase KN93 decreases the vasoconstrictive response in response to norepinephrine and serotonin by only 20%. Calmodulin inhibitors slightly decrease aortic constriction in response to endothelin-1, vasopressin, angiotensin II, and KCl. Trifluoperazine does not suppress vasoconstriction induced by the G-protein activator AlF4(-). It is assumed that the target of trifluoperazine and W-13 is calmodulin interacting directly with alpha1-adrenoceptors and serotonin 5HT1A- and 5HT2A-receptors.
authors.forename: L M
authors.initials: LM
authors.lastname: Kozhevnikova
authors.forename: P V
authors.initials: PV
authors.lastname: Avdonin
mesh_terms: D000804:Angiotensin II / Q000378:metabolism / Q000502:physiology; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000502:physiology*; D015220:Calcium Channels / Q000378:metabolism; D002147:Calmodulin / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000502:physiology; D019332:Endothelin-1 / Q000819:agonists / Q000378:metabolism / Q000502:physiology; D008297:Male; D009638:Norepinephrine / Q000378:metabolism / Q000502:physiology; D009924:Organ Culture Techniques; D051381:Rats; D017208:Rats, Wistar; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism / Q000502:physiology; D011985:Receptors, Serotonin / Q000378:metabolism / Q000502:physiology; D012701:Serotonin / Q000378:metabolism / Q000502:physiology; D017366:Serotonin Receptor Agonists / Q000494:pharmacology; D013449:Sulfonamides / Q000494:pharmacology; D014268:Trifluoperazine / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014667:Vasopressins / Q000378:metabolism / Q000502:physiology
chemical_list: D015220:Calcium Channels; D002147:Calmodulin; D019332:Endothelin-1; D018340:Receptors, Adrenergic, alpha-1; D011985:Receptors, Serotonin; D017366:Serotonin Receptor Agonists; D013449:Sulfonamides; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D000804:Angiotensin II; D014268:Trifluoperazine; D012701:Serotonin; C033772:N-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamide; D009638:Norepinephrine