作者: J. F. KUO , CRAIG W. DAVIS , JAMES TSE
DOI: 10.1038/261335A0
关键词: Internal medicine 、 Protein kinase A 、 Guanethidine 、 Enzyme 、 Phosphodiesterase 、 Endocrinology 、 Cyclic nucleotide 、 Adenylate kinase 、 Receptor 、 In vivo 、 Chemistry
摘要: BIOCHEMICAL modifications in cardiac hyptertrophy, secondary to high blood pressure, spontaneously hypertensive (SH) rats, include reduced receptor reactivities isoproterenol1,2 and glucagon3, lower contents of cyclic AMP GMP due aberrations adenylate guanylate cyclases or phosphodiesterases, both. Also possibly affected are AMP-dependent protein kinase (A-PK) GMP-dependent (G-PK), enzymes that presumably mediate the effects respective nucleotide vivo. An accurate assay for G-PK from mammalian tissues is possible presence stimulatory modulator (specifically stimulating G-PK), either as a separated purified form4 mixture with inhibitory inhibiting A-PK) form crude modulator5,6. We have examined involvements G-PK, relative A-PK, chronic hypertension guanethidine, hypotensive drug, on two key enzymes. found level rats was than normotensive whereas A-PK same both groups. Guanethidine depressed former enzyme further without affecting latter.