Development of insulin sensitivity in rat aorta after chronic propranolol treatment.
Spontaneously hypertensive rats and normotensive Kyoto Wistar controls were divided into 3 groups of 10 animals each and treated with phenoxybenzamine (5 mg/kg once daily), propranolol (25 mg/kg twice daily) or saline (once daily). After 5 weeks the in vitro incorporation of D-[U-14C]-glucose into aortic lipids and glycogen was measured in the presence and absence of insulin (1 mU/ml). In both normotensive and hypertensive rats treated with propranolol 14C-incorporation into triglycerides was reduced. Furthermore, insulin significantly stimulated 14C-incorporation into triglycerides, phospholipids and glycogen in propranolol-treated hypertensive rats. This effect was not statistically significant (0.05 less than p less than 0.1) in propranolol-treated normotensives. Phenoxybenzamine treatment did not significantly modify aortic lipogenesis or glycogen synthesis from glucose. Chronic propranolol treatment of spontaneously hypertensive rats resulted in aortic tissue becoming sensitized to insulin. Possible mechanisms and explanations for this are discussed.
D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002855:Chromatography, Thin Layer; D004347:Drug Interactions; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000096:biosynthesis; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology; D066298:In Vitro Techniques; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D010743:Phospholipids / Q000096:biosynthesis; D011433:Propranolol / Q000494:pharmacology*; D051381:Rats; D011941:Receptors, Adrenergic / Q000187:drug effects; D014280:Triglycerides / Q000096:biosynthesis
D007328:Insulin; D010743:Phospholipids; D011941:Receptors, Adrenergic; D014280:Triglycerides; D006003:Glycogen; D011433:Propranolol; D005947:Glucose