Defect in deamination of biogenic amines in spontaneous hypertension

Makarova T.A., Smirnov I.E., Verevkina I.V., Shatemirova K.K., Markov K.M.
PubMed Id: 3953019
Year: 1986  Volume: 32  Issue: 1  Pages: 93-97
Activity of monoamine oxidases (MAO) of the types A and B (substrates: 5-hydroxytryptamine, 2-phenylethylamine, tyramine) has been studied in mitochondrial fractions from brain, heart, liver and kidney of 24-week-old rats of the normotonic strain Wistar Kyoto (WKY) and spontaneously hypertonic rats (SHR). As compared with the WKY rats, in the SHR strain the activity of MAO-A in heart mitochondria was increased 1.5-1.7-fold; in liver mitochondria the activities of both MAO-A and -B were increased 2.6-2.7-fold. In brain mitochondria there was noted only slight tendency towards an increase in MAO-A (substrate: 5-hydroxytryptamine) and MAO-B (substrate: 2-phenylethylamine) activities in the SHR strain as compared with the normotonic animals of the same age. However, in experiments with tyramine as a substrate of MAO the enzymatic activity in SHR brain mitochondria was increased 1.5-fold (P less than 0.05) as compared with the WKY rats. In kidney mitochondria of SHR the activity of MAO (substrates: 5-hydroxytryptamine, 2-phenylethylamine, tyramine) did not exhibit any alterations as compared with the control WKY rats.
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Makarova, T. A., Smirnov, I. E., Verevkina, I. V., Shatemirova, K. K., Markov, K. M. (1986). Defect in deamination of biogenic amines in spontaneous hypertension. Voprosy Meditsinskoi Khimii, 32(1), 93-97.
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