Pressure response to carotid occlusion in diabetic rats: effect of insulin therapy

• Published in: Diabetes research and clinical practice 2005-04, Vol.68 (1), p.12-17
• Main Authors: Parra, Rogério S., Mendes, Lys Angela F., Fazan, Rubens, Salgado, Hélio C.
• Format: Article
• Language: English
• Subjects: Animals; Baroreflex; Baroreflex - drug effects; Blood Glucose - drug effects; Blood Pressure - drug effects; Carotid occlusion; Carotid Stenosis - complications; Carotid Stenosis - drug therapy; Chronic Disease; Diabetes Mellitus, Experimental - complications; Diabetes Mellitus, Experimental - drug therapy; Experimental diabetes; Hypertension - complications; Hypertension - drug therapy; Hypoglycemic Agents - pharmacology; Insulin - pharmacology; Male; Rats; Rats, Wistar; Streptozotocin; Sympathetic Nervous System - physiology; Weight Gain - drug effects
• ISSN: 0168-8227; 1872-8227
• DOI: 10.1016/j.diabres.2004.08.010

Bilateral carotid occlusion (BCO) in conscious rats has been used as a maneuver to increase the sympathetic drive, producing a hypertensive response characterized by two components: an initial peak, and a maintained response of lower intensity. Acute (10–15 days) or chronic (6–13 weeks) diabetes was induced in Wistar rats with streptozotocin (STZ, 50 mg/kg, i.v.) while time-control rats received vehicle. Insulin (9 IU/kg, s.c.) was applied daily to other diabetic groups. Blood glucose was monitored three days after the administration of STZ and immediately before the experiment. Blood glucose was elevated in diabetic rats, but normal in time-control or diabetic rats treated with insulin. Basal mean arterial pressure (MAP) was reduced in diabetic as compared to time-control rats. The initial peak of the hypertensive response to BCO was blunted in either acute or chronic diabetic rats, whereas the maintained response was unaffected. Treatment of diabetic rats with insulin prevented the decrease in basal MAP and the attenuation of the initial peak caused by BCO. The maintained response was similar to that of time-control or non-treated rats. These findings suggest an abnormality of the carotid afference of the baroreflex caused by chronic hyperglycemia, which was prevented by treatment with insulin.