PubMed · 9276997
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Y Kamikawa. 1997. [Drug interaction].. https://pubmed.ncbi.nlm.nih.gov/9276997/
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Activation of mitogen-activated protein kinase (MAPK) and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) are required for numerous forms of neuronal plasticity, including long-term potentiation (LTP). We induced LTP in rat hippocampal area CA1 using theta-pulse stimulation (TPS) paired with beta-adrenergic receptor activation [isoproterenol (ISO)], a protocol that may be particularly relevant to normal patterns of hippocampal activity during learning. This stimulation resulted in a transient phosphorylation of p42 MAPK, and the resulting LTP was MAPK dependent. In addition, CaMKII was regulated in two, temporally distinct ways after TPS-ISO: a transient rise in the fraction of phosphorylated CaMKII and a subsequent persistent increase in CaMKII expression. The increases in MAPK and CaMKII phosphorylation were strongly colocalized in the dendrites and cell bodies of CA1 pyramidal cells, and both the transient phosphorylation and delayed expression of CaMKII were prevented by inhibiting p42/p44 MAPK. These results establish a novel bimodal regulation of CaMKII by MAPK, which may contribute to both post-translational modification and increased gene expression.
This study examined whether cardiac beta-adrenoceptor (beta-AR) function was altered in conscious rats with lesions surrounding the anteroventral third ventricle (AV3V). The findings were: (1) beta(1,2)-AR-mediated tachycardia was similar in sham and AV3V-lesion rats, (2) beta(3)- and/or atypical beta-AR-mediated tachycardia elicited by isoproterenol (10 microg/kg, i.v.; ISO) was diminished in AV3V-lesion rats treated with beta(1,2)-AR antagonists, but was not in similarly-treated sham-lesion rats, and (3) the tachycardia elicited by the membrane permeable cAMP-analogue, 8-(4-chlorophenylthiol)-cAMP (10 micromol/kg, i.v.), was similar in AV3V- and sham-lesion rats. The possibility that increased plasma sodium/osmolality in AV3V-lesion rats down-regulated cardiac beta(3)- and/or atypical beta-ARs, but not beta(1,2)-ARs or intracellular cAMP signaling is discussed.
The mode of action of estrogen on beta-adrenoceptor-mediated relaxation was investigated by using isolated ring preparations of thoracic aorta from ovariectomized rats. Administration of 17beta-estradiol to ovariectomized rats significantly suppressed isoprenaline-induced relaxation of aortic rings. There was no alteration in the beta-adrenoceptor binding characteristics. The suppressing action of 17beta-estradiol on the N(G)-nitro-L-arginine and indomethacin-resistant relaxation induced by isoprenaline disappeared after pretreatment with N,N-diethylaminoethyl-2,2-diphenylvalerate hydrochloride (SKF 525A), an inhibitor of cytochrome P450 (CYP). The levels of CYP2C11 expression were the highest of the CYP mRNAs examined in rat aorta. 17beta-Estradiol replacement increased the expression of CYP2C11 mRNA in the aorta, compared with that in ovariectomized rats. These results suggest that estrogen suppresses beta-adrenoceptor-mediated vasorelaxation, and that the mechanisms may be associated with alterations in CYP2C11 metabolites.