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Experimental Physiology 91.4 pp 791-797
DOI: 10.1113/expphysiol.2006.034082
© The Physiological Society 2006
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The role of supraspinal vasopressin and glutamate neurones in an increase in renal sympathetic activity in response to mild haemorrhage in the rat

Zhou Yang1 and J. H. Coote2

1 Medical College, University of Nankai, Tianjin 300071, PR China 2 Division of Neuroscience, The Medical School, University of Birmingham, Birmingham B15 2TT, UK

This study investigated the importance of supraspinal vasopressin and glutamate neurones in regulating renal sympathetic activity as part of the response to an acute reduction in blood volume. Wistar rats anaesthetized with chloralose and urethane were instrumented to record arterial blood pressure, heart rate and left renal sympathetic nerve activity. Pharmacological agonists and antagonists to glutamate and vasopressin were applied to the renal outflow of the spinal cord via an intrathecal catheter inserted at the foramen magnum and with the tip at the level of T10. Both glutamate and vasopressin increased renal sympathetic activity, and these actions were shown to be selectively blocked by their respective antagonists. Removing 1 ml of venous blood from a femoral venous catheter elicited an increase of 26 ± 2% in renal sympathetic activity. This response to mild haemorrhage was halved to 13 ± 4% by prior intrathecal application of a selective V1a antagonist. Similarly, prior intrathecal application of kynurenic acid reduced the response to the mild haemorrhage from 28 ± 2 to 12.6 ± 2.8%. Intrathecal application of both antagonists together reduced the haemorrhage response even further to 8 ± 3%. All the changes were statistically significant at P < 0.01. It is concluded that a small reduction in blood volume induces an increase in renal sympathetic activity dependent on vasopressin and glutamate release from terminals of supraspinal neurones. It is suggested that the vasopressin neurones most probably originate from the paraventricular nucleus of the hypothalamus.

(Received 22 March 2006; accepted after revision 10 May 2006; first published online 12 May 2006)
Corresponding author J. H. Coote: Division of Neuroscience, The Medical School, University of Birmimngham, Birmingham B15 2TT, UK. Email: j.h.coote{at}bham.ac.uk




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