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  2. [The role of beta 2-adrenoceptor on the pathogenesis of insulin resistance in essential hypertension]

[The role of beta 2-adrenoceptor on the pathogenesis of insulin resistance in essential hypertension]

  • Nihon Naibunpi Gakkai Zasshi. 1994 Jun 20;70(5):521-8. doi: 10.1507/endocrine1927.70.5_521.
J Kim 1 S Shigetomi K Tanaka Z O Yamada S Hashimoto S Fukuchi
Affiliations

Affiliation

  • 1 Third Department of Internal Medicine, Fukushima Medical College.
Abstract

The role of beta 2-adrenoceptor on the pathogenesis of Insulin resistance in essential hypertension (EH) was explored. After the measurement of blood pressure in 15 EH patients and 8 control subjects, EH patients were divided into two groups by the elevation of plasma NE (delta NE) 5 min after standing: 7 normoadrenergic EH (delta NE < 140 pg/ml) and 8 hyperadrenergic EH (delta NE > or = 140 pg/ml). On the morning after a 12-h overnight fast, regular Insulin (0.1 U/kg) was injected intravenously, and glucose disappearance rate (GDR) was measured and used as an index of Insulin sensitivity. On the following day, the test was reinvestigated following the administration of mabuterol, a beta 2 agonist. Plasma growth hormone (GH), cortisol, norepinephrine (NE) and epinephrine (Epi) were measured before and after the mabuterol administration. Although there were no significant differences of basal GDR among these three groups, mabuterol induced a considerable decrease in GDR in EH patients but not in control subjects. There was no significant difference in the decrease of GDR between normo- and hyperadrenergic EH. The decrease in GDR tended to correlate with the mean blood pressure at rest in EH but not in normal subjects. Plasma glucose and serum Insulin in EH patients were increased more than in normal subjects. Plasma GH, cortisol and Epi were not elevated by mabuterol, but plasma NE increased in each group, significantly in hyperadrenergic EH. There was no correlationship between the increase in plasma NE and the decrease in GDR after mabuterol.(ABSTRACT TRUNCATED AT 250 WORDS)

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