Cardiovascular autonomic regulation in Non-Obese Diabetic (NOD) mice

• Published in: Autonomic neuroscience 2008-02, Vol.138 (1), p.108-113
• Main Authors: Gross, Volkmar, Tank, Jens, Partke, Hans-Joachim, Plehm, Ralph, Diedrich, André, da Costa Goncalves, Andrey C, Luft, Friedrich C, Jordan, Jens
• Format: Article
• Language: English
• Subjects: Adrenergic beta-Antagonists - pharmacology; Advanced Basic Science; Animals; Arrhythmias, Cardiac - etiology; Arrhythmias, Cardiac - physiopathology; Autonomic nervous system; Autonomic Nervous System - physiopathology; Autonomic Nervous System Diseases - etiology; Autonomic Nervous System Diseases - physiopathology; Baroreflex; Baroreflex - drug effects; Baroreflex - physiology; Biological and medical sciences; Blood Glucose - physiology; Blood pressure; Blood Pressure - drug effects; Blood Pressure - physiology; Bradycardia - etiology; Bradycardia - physiopathology; Chronobiology Disorders - etiology; Chronobiology Disorders - physiopathology; Diabetes. Impaired glucose tolerance; Diabetic Neuropathies - physiopathology; Diabetic neuropathy; Disease Models, Animal; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Female; Fundamental and applied biological sciences. Psychology; Ganglia, Sympathetic - physiopathology; Heart - drug effects; Heart - innervation; Heart - physiopathology; Heart Rate - drug effects; Heart Rate - physiology; Medical Education; Medical sciences; Mice; Mice, Inbred NOD; Muscarinic Antagonists - pharmacology; NOD mice; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; Reproducibility of Results; Spectral analysis; Telemetry; Vertebrates: nervous system and sense organs
• ISSN: 1566-0702; 1872-7484
• DOI: 10.1016/j.autneu.2007.11.006

Abstract Non-Obese Diabetic (NOD) mice show profound pathomorphological changes in sympathetic ganglia during the development of type 1 diabetes mellitus. We tested the hypothesis that NOD mice represent an experimental model to investigate cardiovascular changes seen in humans with diabetic autonomic neuropathy. Blood glucose (BG) levels were measured once a week. Diabetes mellitus was diagnosed as BG levels exceeded 250 mg/dl twice. NOD mice that did not become diabetic served as control group. Blood pressure (BP) and heart rate (HR) were monitored by telemetry and baroreflex sensitivity (BRS) was calculated with the sequence method or with cross spectral analysis. The measurements were obtained before onset of diabetes and during the 4th week of diabetes. The onset of diabetes was accompanied by a continuous decline in HR (615 ± 14 vs. 498 ± 23 bpm), whereas BP values remained stable (108 ± 2 vs. 111 ± 2 mm Hg). The circadian HR rhythm increased in diabetic NOD mice. BRS was higher in diabetic NOD mice than in controls. Atropine reduced BRS more profoundly in diabetic mice compared to non-diabetic mice. Despite pathomorphological similarities of the diabetic autonomic neuropathy between patients with diabetes and diabetic NOD mice, the changes in blood pressure regulation are different. In conclusion the use of diabetic NOD mice as a functional model for human diabetes may be questioned.