Sustained norepinephrine contraction in the rat portal vein is lost when Ca(2+) is replaced with Sr(2+) |
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Authors: | Bonnevier Johan Malmqvist Ulf Sonntag Dagmar Schroeter Mechthild Nilsson Holger Pfitzer Gabriele Arner Anders |
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Affiliation: | Department of Physiological Sciences, Lund University, Tornav?gen 10, SE-221 Lund, Sweden. |
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Abstract: | Agonist-induced activation of smoothmuscle involves a rise in intracellular Ca2+ concentrationand sensitization of myosin light chain phosphorylation toCa2+. Sr2+ can enter through Ca2+channels, be sequestered and released from sarcoplasmic reticulum, andreplace Ca2+ in activation of myosin light chainphosphorylation. Sr2+ cannot replace Ca2+ infacilitation of agonist-activated Ca2+-dependentnonselective cation channels. It is not known whether Sr2+can replace Ca2+ in small G protein-mediated sensitizationof phosphorylation. To explore mechanisms involved in-receptor-activated contractions in smooth muscle, effects ofreplacing Ca2+ with Sr2+ were examined in ratportal vein. Norepinephrine (NE) at >3.0 × 107 Min the presence of Ca2+ resulted in a strong sustainedcontraction, whereas this sustained component was absent in thepresence of Sr2+; only the amplitude of phasic contractionsincreased. Pretreatment with low (~0.05 mM) free Ca2+followed by 2.5 mM Sr2+ resulted in a sustained componentof the NE response. In -escin-permeabilized preparations,phenylephrine in the presence of GTP or guanosine 5'-O-(3-thiotriphosphate) alone induced sensitization toSr2+. In conclusion, a Ca2+-regulatedmembrane/channel process is required for the sustained component of NEresponses in rat portal vein. Sensitization alone is not responsiblefor the sustained phase of the NE contraction. |
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