Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of arginine-vasopressin (AVP, 0.1 microM) on elementary Ca2+ channel currents (L-type) was studied in cell-attached patches with 10 mM BaCl2 as the charge carrier. At a constant potential of -30 mV, bath applied AVP increased the channel openness (NPo) by a factor of 4.7 +/- 3.0 (mean +/- SD, n = 9), the effect resulted from an increase in the frequency of opening (factor 2.5 +/- 0.8) and from a longer mean open time. Under control, openings longer than 5 ms contributed only 4% of the total, however, with the application of AVP this contribution increased to 29%. Under control, the open times were distributed along a single exponential (tau o1 = 0.8 +/- 0.4 ms), a double exponential distribution was obtained during AVP (tau o1 = 0.8 +/- 0.5 ms, tau o2 = 7.5 +/- 0.7 ms). The Ca2+ agonist BAYk8644 (1 microM) changed the open time distribution similarly to AVP (tau o1 = 1.0 +/- 0.5 ms, tau o2 = 9 +/- 2.8 ms). With 1 microM BAYk8644 in the bath, AVP did not significantly increase the relative contribution of long openings, however, AVP increased the frequency of openings by a factor of 2.0 +/- 1 (n = 6). The results are compatible with the idea that AVP can change the gating of L-type Ca2+ channels from mode 1 to mode 2.
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PMID:Arginine-vasopressin induces mode-2 gating in L-type Ca2+ channels (smooth muscle cells of the urinary bladder of the guinea-pig). 137 16

Verapamil (ED50 = 3 x 10(-6) M) and nicardipine (ED50 = 10(-6) M) inhibited the platelet activating factor (PAF)-induced increase of free cytosolic calcium concentration [( Ca2+]i) in quin2-loaded human platelets. In a Ca-free medium containing 5 mM BaCl2, PAF stimulated the inflow of Ba2+ ions which is completely abolished by verapamil and nicardipine. Simultaneous determination of quin2 fluorescence and 45Ca absorption showed that the action of verapamil is accounted for by blocking of the Ca2+ entry. Nicardipine suppresses also Ca2+ mobilization from intracellular stores. The effects of verapamil and nicardipine are not competitive with respect to PAF. The blockers reduce the [Ca2+]i increase induced by ADP, vasopressin, and PGH2 analogue U46619.
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PMID:Blocking of the receptor-stimulated calcium entry into human platelets by verapamil and nicardipine. 323 28

To study the effects of oxytocin on both spontaneous phasic contractions and K+ outward currents (IK) of the so-called 'non-target' smooth muscle cells, physiological concentrations of oxytocin ranging between 10(-12) mol/l and 10(-8) mol/l were applied to smooth muscle preparations and single voltage-clamped cells isolated from the circular layer of the guinea-pig gastric antrum. Oxytocin (10(-12) mol/l to 10(-8) mol/l) suppressed, in a dose-dependent manner, the tetrodotoxin- and atropine-resistant spontaneous phasic contractions and shifted rightward the dose-response curves of 10(-7) mol/l charybdotoxin and 10(-3) mol/l BaCl2. In cells with preloaded intracellular Ca2+ stores, oxytocin (10(-12) mol/l to 10(-9) mol/l) caused a dose-dependent activation of the charybdotoxin-blockable non-inactivating component of IK (IK(sl)) of single voltage-clamped cells, which was accompanied by hyperpolarization of the cell membranes. 8Lys-vasopressin and 8arg-vasopressin failed to mimic the effects of oxytocin on both contraction and K+ currents. Further, the oxytocin-induced activation of IK(sl) was effectively antagonized by 5 x 10(-8) mol/l U-73122 or 5 x 10(-6) mol/l 2-nitro-4-carboxyphenyl N,N-diphenylcarbamate (inhibitors of the cell membrane phospholipase C), as well as by intracellularly applied heparin (selective inhibitor of inositol-1,4,5-trisphosphate (IP3)-induced Ca2+ release channels). In cells incubated in the absence of Ca2+ entry throughout the study, oxytocin (10(-9) mol/l) caused a slight and transient increase of IK(sl) amplitudes. Neither ryanodine (10(-6) mol/l) nor cyclopiazonic acid (10(-6) mol/l) were able to restore the IK-activating effect of oxytocin in these cells. The data obtained suggest (i) that selective oxytocin receptors are present on the membranes of guinea-pig antral smooth muscle cells, (ii) that the oxytocin-related relaxation may result from the activation of Ca(2+)-sensitive K+ conductivity via activation of IP3-induced release of Ca2+ from the submembrane located cisternae of the sarcoplasmic reticulum Ca2+ stores and (iii) in turn, this evokes a non-inactivating component of IK, hyperpolarizing the cell membrane.
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PMID:Oxytocin-induced changes in single cell K+ currents and smooth muscle contraction of guinea-pig gastric antrum. 918 74