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Showing papers by "Gang Wang published in 2002"


Journal ArticleDOI
TL;DR: A linear correlation was found between the thermal denaturation temperature (T(m)) and the logarithm of the refolding rate of the slow folding phase of hen egg white lysozyme (lnk(2).

33 citations


Journal ArticleDOI
TL;DR: It is concluded that adenosine, acting via A1 receptors, specifically blocks the terminal N‐type Ca2+ channel thus leading to inhibition of the release of both AVP and OT.
Abstract: Effects of adenosine on voltage-gated Ca(2+) channel currents and on arginine vasopressin (AVP) and oxytocin (OT) release from isolated neurohypophysial (NH) terminals of the rat were investigated using perforated-patch clamp recordings and hormone-specific radioimmunoassays. Adenosine, but not adenosine 5'-triphosphate (ATP), dose-dependently and reversibly inhibited the transient component of the whole-terminal Ba(2+) currents, with an IC(50) of 0.875 microM. Adenosine strongly inhibited, in a dose-dependent manner (IC(50) = 2.67 microM), depolarization-triggered AVP and OT release from isolated NH terminals. Adenosine and the N-type Ca(2+) channel blocker omega-conotoxin GVIA, but not other Ca(2+) channel-type antagonists, inhibited the same transient component of the Ba(2+) current. Other components such as the L-, Q- and R-type channels, however, were insensitive to adenosine. Similarly, only adenosine and omega-conotoxin GVIA were able to inhibit the same component of AVP release. A(1) receptor agonists, but not other purinoceptor-type agonists, inhibited the same transient component of the Ba(2+) current as adenosine. Furthermore, the A(1) receptor antagonist 8-cyclopentyltheophylline (CPT), but not the A(2) receptor antagonist 3, 7-dimethyl-1-propargylxanthine (DMPGX), reversed inhibition of this current component by adenosine. The inhibition of AVP and OT release also appeared to be via the A(1) receptor, since it was reversed by CPT. We therefore conclude that adenosine, acting via A(1) receptors, specifically blocks the terminal N-type Ca(2+) channel thus leading to inhibition of the release of both AVP and OT.

33 citations


Journal ArticleDOI
TL;DR: Exogenous agmatine is co-expressed in AVP-containing, hypothalamic magnocellular neurons of the SON/PVN and in neurohypophysial nerve terminals of posterior pituitary gland, and may serve as a physiological neuromodulator by regulating the voltage-gated Ca(2+) channel and, as a result, the release of AVP from neurohypophysical nerve terminals.

24 citations