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1 ts recorded from CN21 cells expressing human postjunctional acetylcholine receptors (hnAChR) with an
2 ypothesis that this is due to a reduction in postjunctional alpha-adrenergic responsiveness to endoge
3 ng is associated with a reduction in forearm postjunctional alpha-adrenergic responsiveness to endoge
4 ndings indicate that the ability to modulate postjunctional alpha-adrenergic vasoconstriction during
5 pothesis that exogenous ATP can blunt direct postjunctional alpha-adrenergic vasoconstriction in huma
6 we tested the hypothesis that modulation of postjunctional alpha-adrenergic vasoconstriction to exog
7 exogenous ATP is capable of blunting direct postjunctional alpha-adrenergic vasoconstriction, that t
8 present study, we tested the hypothesis that postjunctional alpha-adrenergic vasoconstrictor responsi
9 ageing is associated with a reduction in leg postjunctional alpha-adrenoceptor responsiveness to endo
10 Whether this involves direct modulation of postjunctional alpha-adrenoceptor responsiveness, or is
12 enteric NEJ consists of enteric neurons and postjunctional cells of the SIP syncytium, including smo
13 ch occurred ahead of other prejunctional and postjunctional components, suggesting that LRP4 may regu
14 cles, but not the p1 muscle, by activating a postjunctional conductance increase that was blocked by
16 compared beta-NAD(+) and ATP metabolism and postjunctional effects of the primary extracellular meta
18 ucturally simplified and the organization of postjunctional folds is aberrant in mice lacking tyrosin
19 istributions of acetylcholine receptors, and postjunctional folds that are generally less organized a
23 adenosine receptors are exerted not only on postjunctional M1/M3 receptors but also at M2 presynapti
24 an inhibitory neurotransmitter rather than a postjunctional mediator; (b) VIP is a prejunctional neur
25 eptor tyrosine kinases, are localized at the postjunctional membrane presumably to ensure localized s
28 pse that is formed by motor nerve terminals, postjunctional muscle membranes, and terminal Schwann ce
29 Autoantibodies with reactivity against the postjunctional muscle receptor for acetylcholine recepto
34 ooth muscle is consistent with its role as a postjunctional receptor in autonomic transmission, while
35 this does not appear to be due to changes in postjunctional receptors, or to a depletion of transmitt
37 through gap junctions conditionally trigger postjunctional spikes, depending on both neurons being c
38 n in isolated PDGFRalpha(+) cells, which are postjunctional targets for purinergic neurotransmission.