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)

1. A novel slowly activating voltage-dependent K+ current was observed in isolated nerve terminals from rat neurohypophysis using the whole-cell configuration of the patch-clamp technique. 2. The activation kinetics of the slow current could be fitted assuming Hodgkin--Huxley-type kinetics, an exponential, n, of 1.3 and activation time constants decreasing from 4 s at -50 mV to 0.7s at +40 mV. 3. A positive shift of reversal potential was observed when [K+] was increased in the bath solution. The current is carried mainly but not exclusively by K+ ions. 4. When intracellular free [Mg2+] was low (approximately 60 microM), average current density was 74 pA pF-1 at membrane potentials around 0 mV. In 83% of nerve terminals current amplitude was > 10 pA pF-1. 5. The slow current was never observed when the pipette contained 4.6 mM free Mg2+. At a physiological level of free Mg2+ (0.5 mM) the average current density was 16 pA pF-1. 6. When nerve terminals were analysed after patch-clamp experiments for vasopressin content by immunodetection, no difference in current amplitude was found between the terminals containing vasopressin and all analysed terminals. 7. The voltage dependence of activation was fitted by a Boltzmann equation giving a half-activation potential of -37 mV and a slope factor of about 9 mV. 8. Tail current deactivation kinetics was biexponential with time constants of 0.12 and 1.5s. Kinetics was dependent on the duration of the activating pulse. 9. Noise analysis of the slow current indicated a single-channel current of 0.33 pA at +6 mV, corresponding to a single-channel conductance of 4.3 pS. 10. This is the first demonstration of a current similar to the slow K+ current, IKs, in a neurone, suggesting that a protein similar to the IKs-inducing channel protein IsK (minK) may be present in peptidergic nerve terminals. 11. The activation properties are consistent with a role of the slow current in inhibition of excitability, at least at the level of the nerve terminal.
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PMID:A slowly activating voltage-dependent K+ current in rat pituitary nerve terminals. 900 56

Strial marginal cells are known to secrete K+ into endolymph via apical IsK/KvLQT1 (IKs) channels. Regulation of K+ secretion by several hormones is important for inner ear homeostasis but the role of vasopressin in the cochlea is still controversial. We examined the effect of arginine vasopressin (AVP) on marginal cells in the middle turn of the neonatal rat cochlea using nystatin-perforated whole-cell recordings at 24 degrees C. Whole-cell capacitance was 27.3 + 1.1 pF (n = 31). AVP(10(-8) M) gradually increased the IKs channel current in 30 min from the basal (1.1 +/- 0.3 pA; n = 6) to the peak level (714.7 +/- 197.5 pA; n = 6). The deactivation curve of the IKs channel current was best fitted to a biexponential function. 1-Deamino-D-arginine vasopressin (DDAVP; 10(-8) M; n = 5) and 8-bromo-cAMP (10(-4) M; n = 5) also mimicked the effect of AVP with similar time courses. However, 10(-9) M AVP (n = 7) and DDAVP (n = 5) showed no response. The majority of the increase in the IKs channel current caused by 10(-8) M AVP, 10(-8) M DDAVP or 10(-4) M cAMP was blocked within 2 min by the application of chromanol 293B (10(-5) M), a selective blocker of the IKs channel. Our results demonstrate that AVP increases the IKs channel current in marginal cells of the neonatal rat at a concentration of 10(-8) M, and the fact that 8-bromo-cAMP (10(-4) M) and DDAVP (10(-8) M) also showed similar effects at 24 degrees C may suggest the involvement of V2 receptors and the subsequent activation of the cAMP signal pathway.
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PMID:Effect of vasopressin on marginal cells of neonatal rat cochlea in vitro. 1181 92