Sustained norepinephrine contraction in the rat portal vein is lost when Ca(2+) is replaced with Sr(2+).
Agonist-induced activation of smooth muscle involves a rise in intracellular Ca(2+) concentration and sensitization of myosin light chain phosphorylation to Ca(2+). Sr(2+) can enter through Ca(2+) channels, be sequestered and released from sarcoplasmic reticulum, and replace Ca(2+) in activation of myosin light chain phosphorylation. Sr(2+) cannot replace Ca(2+) in facilitation of agonist-activated Ca(2+)-dependent nonselective cation channels. It is not known whether Sr(2+) can replace Ca(2+) in small G protein-mediated sensitization of phosphorylation. To explore mechanisms involved in alpha-receptor-activated contractions in smooth muscle, effects of replacing Ca(2+) with Sr(2+) were examined in rat portal vein. Norepinephrine (NE) at >3.0 x 10(-7) M in the presence of Ca(2+) resulted in a strong sustained contraction, whereas this sustained component was absent in the presence of Sr(2+); only the amplitude of phasic contractions increased. Pretreatment with low (approximately 0.05 mM) free Ca(2+) followed by 2.5 mM Sr(2+) resulted in a sustained component of the NE response. In beta-escin-permeabilized preparations, phenylephrine in the presence of GTP or guanosine 5'-O-(3-thiotriphosphate) alone induced sensitization to Sr(2+). In conclusion, a Ca(2+)-regulated membrane/channel process is required for the sustained component of NE responses in rat portal vein. Sensitization alone is not responsible for the sustained phase of the NE contraction.[1]References
- Sustained norepinephrine contraction in the rat portal vein is lost when Ca(2+) is replaced with Sr(2+). Bonnevier, J., Malmqvist, U., Sonntag, D., Schroeter, M., Nilsson, H., Pfitzer, G., Arner, A. Am. J. Physiol., Cell Physiol. (2002) [Pubmed]
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