Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1832588 (PSS)
 2,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of substrate condition and ADP beta S on the pCa2+-tension relationships were investigated, using alpha-toxin permeabilized rabbit mesenteric artery at 37 degrees C. The contraction induced by 10 microM Ca2+ solution after permeabilization was as large as that induced by 145 mM K+ PSS solution containing 10 microM NE in the intact tissue, indicating that the majority of the cells were permeabilized. The Ca2+ sensitivity was greatly affected by the substrate condition and increasing the ratio of ATP/CP induced a leftward shift of the pCa2+-tension curve. Addition of 100 microM ADP beta S had a similar effect. When the ATP/CP ratio was high, the 0.1 microM Ca2+ solution relaxed the tissue precontracted by 10 microM Ca2+ solution more slowly showing hysteresis. One mM vanadate, which is reported to relax muscle by forming actomyosin-ADP-Vi (AM-ADP-Vi), completely inhibited both contractions induced by 0.18 microM Ca2+ solution containing 2 mM MgADP and 0.3 microM Ca2+ solution containing 0.3 microM PDBu. These results indicated that the population of AM-ADP complex in the crossbridge had increased due to the accumulation of ADP inside the tissue or activation of PKC and that the inhibition of ADP release from AM-ADP complex may be playing a key role in increasing Ca2+ sensitivity of myofilaments.
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PMID:Possible involvement of actomyosin ADP complex in regulation of Ca2+ sensitivity in alpha-toxin permeabilized smooth muscle. 259 Feb 38

31P-NMR spectroscopy was performed on vascular smooth muscle (VSM; porcine carotid artery) superfused with a substrate-free high K(+)-PSS. Scans were collected before (control), during (hypoxia), and after (post-control) hypoxia, and chemical measurements of ATP (0.070 +/- 0.13 mumoles/g wet wt.) and creatine (2.04 +/- 0.14 mumol/g wet wt.) were made. During hypoxia, well-defined beta-ADP signals were consistently resolved. Their areas indicated that after 30, 60, and 90 min of hypoxia, free ADP was 0.05 +/- 0.01, 0.09 +/- 0.01, and 0.12 +/- 0.01 mumol/g wet wt., respectively. The apparent tissue equilibrium constant (Kck) for creatine kinase (CK) was calculated using 90 min hypoxic data and was 7.6 +/- 0.6 x 10(8) M-1. It was used to compute free ADP levels (mumol/g wet wt.) for control (0.028 +/- 0.002) and post-control (0.23 +/- 0.003) periods, since ADP signals could not be directly detected, and for the 30 and 60 min hypoxic periods (0.05 +/- 0.01 and 0.08 +/- 0.01, respectively). The Kck-dependent ADP values for the 30 and 60 min hypoxic periods periods were the same as the ADP values determined directly from the beta-ADP peak areas, suggesting that the CK reaction is in equilibrium in smooth muscle. These data show that 31P-NMR provides a means of directly measuring free ADP in hypoxic smooth muscle and a more accurate means of computing free ADP levels in normoxic VSM through the use of an in situ tissue Kck vs an assumed or in vitro Kck.
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PMID:Direct determination of ADP in hypoxic porcine carotid artery using 31P NMR. 327 22