Depressed cardiac cyclic GMP-dependent protein kinase in spontaneously hypertensive rats and its further depression by guanethidine

作者: J. F. KUO , CRAIG W. DAVIS , JAMES TSE

DOI: 10.1038/261335A0

关键词: Internal medicineProtein kinase AGuanethidineEnzymePhosphodiesteraseEndocrinologyCyclic nucleotideAdenylate kinaseReceptorIn vivoChemistry

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.

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