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R T Lai

Publications and source records attributed to R T Lai.

11 recordsLinked to original sources
PubMed1984

Interaction between 2-chloroadenosine and alpha-adrenoceptors in rat vas deferens.

The effect of 2-chloroadenosine (2CA) on the binding of alpha 1- and alpha 2-adrenoceptor ligands in the rat vas deferens was investigated. In homogenates of vas deferens, 2CA (10(5)M) increased 3H-clonidine maximal binding sites from an undetectable level to 0.71 +/- 0.08 pmol/g. wet weight or 10.1 +/- 1.1 fmol/mg protein (N=12). This effect lasted for at least 5 hours after removal of 2CA. Concurrent addition of 1.25 mM theophylline completely abolished the effect of 2CA. A similar effect of 2CA on 3H-clonidine binding was observed following incubation of intact tissues with 2CA prior to homogenization. The effect of 2CA were similar in potency in the homogenate to that in the intact organ, suggesting that 2CA-sensitive sites are located on the outer surface of the plasma membrane. The binding of 3H-prazosin was not influenced by the presence of 10(-5)M 2CA. Contractions of isolated vasa deferentia induced by norepinephrine and phenylephrine were not changed by 10(-5)M 2CA, but the inhibition by clonidine of contractions induced by electric stimulation was enhanced by preincubation for 30 min with 10(-5)M 2CA. The results suggest that 2CA increases the number of available alpha 2-adrenoceptors and this interactions occurs, at least in part, presynaptically.

2-Chloroadenosine↗
PubMed1983

Effect of glucocorticoids on alpha-2 adrenoceptors in vas deferens of reserpinized rat in organ culture.

The changes in alpha adrenoceptors in vasa deferentia of reserpinized rats in organ culture were examined by binding studies with 3H-clonidine, 3H-yohimbine and 3H-prazosin. On organ culture for 1 day, the 3H-clonidine binding sites decreased by 1.07 pmol/g tissue and after 2 days no binding sites were detectable. 3H-Yohimbine binding sites also decreased during culture, but in smaller extent than 3H-clonidine binding sites. On the other hand, 3H-prazosin binding sites showed no apparent change in amount during culture. Addition of 0.1 mM hydrocortisone or dexamethasone to the culture medium inhibited the decrease in 3H-clonidine binding sites (1.7 pmol/g tissue), and the effect of glucocorticoid was blocked by the inhibitors of protein synthesis, cycloheximide and puromycin. However, hydrocortisone showed no effect on the 3H-yohimbine and the 3H-prazosin binding sites. An anti-endocytotic agent, an anti-microtubular agent and protease inhibitors had no effects on the decrease of 3H-clonidine binding sites during culture. These results suggest that the amount of alpha-2 adrenoceptors can change rapidly while alpha-1 adrenoceptors are stable and that glucocorticoids are important in regulation of conformation of alpha-2 adrenoceptor through synthesis of certain protein(s).

Animals↗
PubMed1983

Effect of islet-activating protein (IAP) on contractile responses of rat vas deferens: evidence for participation of Ni (inhibitory GTP binding regulating protein) in the alpha 2-adrenoceptor-mediated response.

The effects of islet-activating protein (IAP) on the contractile responses of vas deferens to exogenous norepinephrine (NE) and electric stimulation (ES) were investigated. IAP treatment had no effect on the contractile response to NE. Pretreatment of the vas deferens with IAP (2.0 micrograms/ml) for 2 h however significantly attenuated the inhibitory effect of clonidine on ES-induced contractile responses, suggesting that feedback inhibition of presynaptic alpha 2-adrenoceptors is mediated by the Ni subunit of presynaptic adenylate cyclase.

Adenylate Cyclase Toxin↗
PubMed1982

Increase of [3H]clonidine binding sites induced by adenosine receptor agonists in rat vas deferens in vitro.

In vitro binding experiments were done to study the effects of adenosine receptor agonists on induction of [3H]clonidine binding sites in rat vasa deferentia by reserpine. In the presence of 1 microM adenosine and 2-chloroadenosine, respectively, the specific binding of [3H]clonidine to vas deferens homogenates of reserpine-treated rats increased 38 and 42% over the control value. The increase in binding sites induced by adenosine was inhibited by the adenosine receptor antagonist theophylline. No effect of 1 microM 2-chloroadenosine on the beta-adrenoceptor or alpha 1-adrenoceptor was detected. The results imply a direct interaction between alpha 2-adrenoceptor and adenosine receptor and suggest that stimulated adenosine receptors unmasked [3H]clonidine binding sites in membranes of rat vas deferens.

Animals↗
PubMed1982

Reserpine and sympathetic denervation cause an increase of postsynaptic alpha 2-adrenoceptors.

The changes in alpha-adrenoceptors in rat vasa deferentia after injections of reserpine and 6-hydroxydopamine (6-OHDA) were examined in binding studies with [3H]WB4101 and [3H]clonidine. On intraperitoneal injection of reserpine (0.5 mg/kg body weight per day, 2 days), [3H]clonidine binding sites increased by about 2.0 pmol/g wet weight; the binding sites were not detectable in vasa from control rats. [3H]WB4101 binding sites showed no apparent change in amount. After a single injection of 6-OHDA (30 mg/kg body weight), [3H]clonidine binding sites amounted to about 1.1 pmol/g wet weight. The data suggest that both reserpine treatment and incomplete chemical denervation with 6-OHDA cause an increase of [3H]clonidine binding sites in the postsynaptic region of rat vasa deferentia. The possibility was tested by completely denervating rat vasa deferentia by chemical treatment and operation. The treatments increased the binding sites to about 0.9 and 1.0 pmol/g wet weight, respectively over the control level. The results imply that the binding sites indeed also increased in the postsynaptic area.

Animals↗
PubMed1981

Role of alpha-adrenergic receptors in denervation supersensitivity of rat vas deferens.

Contractile responses of rat vas deferens were studied with particular attention directed to the role of receptors and neuronal control. Marked contraction of the vas deferens was observed with alpha-adrenergic agonists, depending on their concentrations. This tissue had a low sensitivity to ACh. Four days after denervation, this tissue showed a supersensitivity to alpha-adrenergic agonists and a high K+ concentration, but not to ACh. The increase in sensitivity to alpha-agonists resulted in an enhancement of the maximal response and a shift of the concentration response curve to lower concentrations of these reagents. Alterations were seen in the alpha-adrenergic receptors in the rat vas deferens, assayed by measuring the binding of [3H]WB4101. The maximal binding sites decreased significantly to 86 from 142 fmoles per mg protein. The affinity of the receptors for alpha-agonist, determined by measuring the ability of agonists to displace bound [3H] WB4101, increased significantly, while the affinity to alpha-antagonists remained unchanged. Studies on [3H]QNB binding indicated no significant change in muscarinic ACh receptors after denervation. Thus, supersensitivity of the alpha-adrenergic mechanism mediated by a specific change in affinity of alpha-receptors occurs after denervation of rat vas deferens. These changes in sensitivity and in receptors are discussed in relation to the characteristics and roles of alpha-receptors in the rat vas deferens.

Acetylcholine↗
PubMed1980

Specific changes in the cholinergic system in guinea-pig vas deferens after denervation.

A small rapid phase (1st phase) was distinguished from a concomitant phase (2nd phase) in contraction of guinea-pig vas deferens. The vas deferens 4 days after denervtion exhibited supersensitivity to stimulants. The supersensitivity in the 2nd phase of contraction was nonspecific, but that in the 1st phase was specific to muscarinic cholinergic agonists. The increase in sensitivity resulted in a shift of the dose-response curve to lower concentrations without significant change in the maximal response. Muscarinic cholinergic receptors in the vas deferens, determined by measuring binding of [3H]quinuclidinyl benzilate, changed after denervation. The maximal binding sites increased from 115 to 165 fmol/mg of protein with no significant change in the dissociation constant. The affinity of the receptor for agonist also did not change significantly. Studies on [3H]WB4101 binding indicated no significant change in alpha adrenergic receptors after denervation. Thus, specific supersensitivity of the cholinergic mechanism mediated by muscarinic acetylcholine receptors occurred after denervation of guinea-pig vas deferens. This increased sensitivity is discussed in relation to the amount of receptor.

Acetylcholine↗
PubMedDate not supplied

The beta-adrenoreceptor in human lymphocytes.

The beta-adrenoreceptors of human lymphocytes were investigated by binding assays using a radiolabelled beta-adrenoreceptor agonist, 3H-hydroxybenzylisoproterenol, in an intact cell system. Intact human lymphocytes had binding sites for the ligand, which seemed to represent physiological beta-adrenoreceptors. Thus, assay of binding of the beta-adrenergic agonist, 3H-HBI, by intact lymphocytes can be used to study beta-adrenoreceptors in human tissue and to elucidate possible beta-adrenoreceptor disorders in human diseases.

Humans↗