Reflex control of arterial pressure and heart rate in short-term streptozotocin diabetic rats

Impaired baroreflex sensitivity in diabetes is well described and has been attributed to autonomic diabetic neuropathy. In the present study conducted on acute (10-20 days) streptozotocin (STZ)-induced diabetic rats we examined: 1) cardiac baroreflex sensitivity, assessed by the slope of the linear...

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Published in:	Brazilian journal of medical and biological research Vol. 35; no. 7; pp. 843 - 849
Main Authors:	Dall'Ago, P, Silva, V O K, De Angelis, K L D, Irigoyen, M C, Fazan, Jr, R, Salgado, H C
Format:	Journal Article
Language:	English
Published:	Brazil Associação Brasileira de Divulgação Científica 01-07-2002
Subjects:	Animals Baroreceptors Baroreflex Baroreflex - drug effects Baroreflex - physiology BIOLOGY Blood Pressure - drug effects Diabetes Mellitus, Experimental - physiopathology Heart Rate - drug effects Heart Rate - physiology Linear Models Male MEDICINE, RESEARCH & EXPERIMENTAL Pressoreceptors - drug effects Pressoreceptors - physiology Rats Rats, Wistar Streptozocin Streptozotocin Vagus nerve Vagus Nerve - drug effects Baroreceptors Vagus nerve Streptozotocin Baroreflex
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Summary:	Impaired baroreflex sensitivity in diabetes is well described and has been attributed to autonomic diabetic neuropathy. In the present study conducted on acute (10-20 days) streptozotocin (STZ)-induced diabetic rats we examined: 1) cardiac baroreflex sensitivity, assessed by the slope of the linear regression between phenylephrine- or sodium nitroprusside-induced changes in arterial pressure and reflex changes in heart rate (HR) in conscious rats; 2) aortic baroreceptor function by means of the relationship between systolic arterial pressure and aortic depressor nerve (ADN) activity, in anesthetized rats, and 3) bradycardia produced by electrical stimulation of the vagus nerve or by the iv injection of methacholine in anesthetized animals. Reflex bradycardia (-1.4 +/- 0.1 vs -1.7 +/- 0.1 bpm/mmHg) and tachycardia (-2.1 +/- 0.3 vs -3.0 +/- 0.2 bpm/mmHg) were reduced in the diabetic group. The gain of the ADN activity relationship was similar in control (1.7 +/- 0.1% max/mmHg) and diabetic (1.5 +/- 0.1% max/mmHg) animals. The HR response to vagal nerve stimulation with 16, 32 and 64 Hz was 13, 16 and 14% higher, respectively, than the response of STZ-treated rats. The HR response to increasing doses of methacholine was also higher in the diabetic group compared to control animals. Our results confirm the baroreflex dysfunction detected in previous studies on short-term diabetic rats. Moreover, the normal baroreceptor function and the altered HR responses to vagal stimulation or methacholine injection suggest that the efferent limb of the baroreflex is mainly responsible for baroreflex dysfunction in this model of diabetes.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0100-879X 1414-431X 0100-879X 1414-431X
DOI:	10.1590/s0100-879x2002000700013