This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Oliveira, V. L. L. Articles by Irigoyen, M. C. Search for Related Content PubMed PubMed Citation Articles by Oliveira, V. L. L. Articles by Irigoyen, M. C. Pubmed/NCBI databases Compound via MeSH Substance via MeSH

(Hypertension. 1999;34:813-817.)
© 1999 American Heart Association, Inc.

Scientific Contributions

Cardiopulmonary Reflex Impairment in Experimental Diabetes in Rats

Vera Lucia Longo Oliveira; Edson Dias Moreira; Vera de Moura Azevedo Farah; Fernanda Consolim-Colombo; Eduardo Moacyr Krieger; Maria Claudia Irigoyen

From the Experimental Division and Hypertension Unit, Heart Institute, University of São Paulo, Brazil.

Correspondence to Maria Claudia Irigoyen, Experimental Division and Hypertension Unit, Heart Institute, University of São Paulo, Rua Dr Eneas de Carvalho Aguiar 44, São Paulo, SP, 05403-000, Brazil. E-mail hipirigoyen{at}incor4.incor.usp.br

Abstract—The aim of the present study was to evaluate the sensitivity of the cardiopulmonary receptors in experimental diabetes induced by streptozotocin by the use of 2 different methods: (1) administration of increasing doses of serotonin to analyze peak changes of arterial pressure and heart rate for each given dose in conscious intact normal and diabetic rats; (2) expanding blood volume with the use of dextran (6%) to produce similar increases in left ventricular end-diastolic pressure to quantify the arterial pressure, heart rate, and renal sympathetic nerve activity in sinoaortic, denervated, anesthetized normal and diabetic rats. Blood samples were collected to measure blood glucose. Diabetic rats showed hyperglycemia (22±0.7 versus 7±0.2 mmol/L), reduced body weight (226±12 versus 260±4 g) and heart rate (294±14 versus 350±10 bpm), and similar arterial pressure (104±4 versus 113±4 mm Hg) when compared with control rats. Serotonin induced significant bradycardia and hypotension, which were similar and proportional to the dose injected in both groups. Mean arterial pressure and heart rate decreases in response to volume overload were significantly lower in diabetic than in control rats. The reflex reduction of the renal sympathetic nerve activity as expressed by percentage changes in nerve activity in response to increasing left end-diastolic pressure was abolished in diabetic animals (1.9±0.8% versus -14±4%/mm Hg in controls). These results showed an impairment of cardiopulmonary reflex control of circulation in diabetes during acute volume expansion. The normal responses to serotonin administration indicated that the cardiopulmonary reflex is still preserved in diabetic rats.

Key Words: cardiac function • diabetes mellitus • blood pressure • renal nerve • reflex

This article has been cited by other articles:

				C. Lau, I. Sudbury, M. Thomson, P. L. Howard, A. B. Magil, and W. A. Cupples Salt-resistant blood pressure and salt-sensitive renal autoregulation in chronic streptozotocin diabetes Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2009; 296(6): R1761 - R1770. [Abstract] [Full Text] [PDF]

				R. B. Wichi, V. Farah, Y. Chen, M. C. Irigoyen, and M. Morris Deficiency in angiotensin AT1a receptors prevents diabetes-induced hypertension Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2007; 292(3): R1184 - R1189. [Abstract] [Full Text] [PDF]