title: Effect of a 14-day hindlimb suspension on cytosolic Ca2+ concentration in rat portal vein myocytes.
abstract: Effects of a 14-day hindlimb suspension were examined on increases in cytosolic Ca2+ concentration ([Ca2+]i) evoked by vasoactive compounds and on Ca2+ channels in rat portal vein myocytes. The maximal increases in [Ca2+]i elicited by caffeine, norepinephrine, and angiotensin II were reduced by 30-50% in suspended rats, and complete recovery was obtained 4 days after suspension removal. In contrast, voltage-gated Ca2+ channels were unaffected by hindlimb suspension. Using both confocal microscopy and the patch-clamp technique, we measured local increases in [Ca2+]i which corresponded to activation of a small number of ryanodine-sensitive Ca(2+)-release channels (Ca2+ sparks) and D-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]-gated Ca2+ channels. After hindlimb suspension, these local Ca2+ events, as well as the Ca2+ sensitivity of ryanodine-sensitive Ca2+ release channels, remained unchanged. In contrast, the propagated Ca2+ responses (Ca2+ waves) were significantly reduced in parallel with a noticeable inhibition of [3H]ryanodine binding to vascular membranes. Taken together, these results suggest that inhibition of the vasoconstrictor-induced increases in [Ca2+]i during long-term suspension may be related to a reduction of the number of functional ryanodine-sensitive and Ins(1,4,5)P3-gated channels in the sarcoplasmic reticulum of rat portal vein myocytes.
authors.affiliation: Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, Centre National de la Recherche Scientifique ESA 5017, Université de Bordeaux II, France.
authors.forename: J L
authors.initials: JL
authors.lastname: Morel
authors.forename: F X
authors.initials: FX
authors.lastname: Boittin
authors.forename: G
authors.initials: G
authors.lastname: Halet
authors.forename: S
authors.initials: S
authors.lastname: Arnaudeau
authors.forename: C
authors.initials: C
authors.lastname: Mironneau
authors.forename: J
authors.initials: J
authors.lastname: Mironneau
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001464:Barium / Q000494:pharmacology; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism; D006614:Hindlimb / Q000098:blood supply*; D019417:Hindlimb Suspension; D066298:In Vitro Techniques; D007700:Kinetics; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008861:Microsomes / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D010782:Photolysis; D011169:Portal Vein / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012433:Ryanodine / Q000378:metabolism; D019837:Ryanodine Receptor Calcium Release Channel / Q000502:physiology; D014466:Ultraviolet Rays; D016474:Weight-Bearing
chemical_list: D015220:Calcium Channels; D019837:Ryanodine Receptor Calcium Release Channel; D000804:Angiotensin II; D012433:Ryanodine; D001464:Barium; D002110:Caffeine; D002118:Calcium; D009638:Norepinephrine