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This Article Full Text Full Text (PDF) All Versions of this Article: 92/1/109    most recent expphysiol.2006.034884v1 Alert me when this article is cited Alert me if a correction is posted 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yang, Z. Articles by Coote, J. H. Search for Related Content PubMed PubMed Citation Articles by Yang, Z. Articles by Coote, J. H.

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

In Wistar rats, an increase in renal sympathetic activity is induced by activation of presympathetic neurones in the paraventricular nucleus (PVN) and reflexly by a mild venous haemorrhage. Both stimuli are dependent on the release of vasopressin and glutamate at spinal synapses. The significance of the supraspinal pathway and the co-operative interaction of vasopressin with an excitatory amino acid is unclear. The present study examines this in Brattleboro rats, which have a natural vasopressin gene deletion. The responses were compared with Long–Evans rats, from which Brattleboro rats are derived. All rats were anaesthetized with a mixture of urethane (650 mg kg^–1 I.V.) and chloralose (50 mg kg^–1 I.V.). Recordings were made of blood pressure, heart rate and renal sympathetic nerve activity (RSNA). Microinjection of D,L-homocysteic acid (DLH, 0.2 M, 100 nl) at sites restricted to the PVN elicited significant increases in RSNA (P < 0.001) in both strains of rats. These changes were significantly reduced (P < 0.01) in Long–Evans rats by intrathecal application to the spinal cord of either a V_1a antagonist or a glutamate antagonist (kynurenic acid), whereas in Brattleboro rats the changes were significantly reduced (P < 0.05) only by kynurenic acid. Removal of 1 ml of venous blood in Long–Evans rats increased RSNA by 28 ± 4% (P < 0.01), which was significantly reduced (P < 0.05) by prior intrathecal application of either the V_1a antagonist or by kynurenic acid. The same test in Brattleboro rats caused a significanty greater (P < 0.05) increase (63 ± 14.7%) in RSNA which, in contrast to Long–Evans rats, was unchanged by intrathecal application of the V_1a antagonist, being significantly reduced (P < 0.01) only by intrathecal kynurenic acid. Thus, in Brattleboro rats, the lack of vasopressin in the brain sympathetic pathways appears to be compensated, acutely, by glutamate-releasing pathways. This might indicate that, in normal rats, vasopressin is more important in maintaining longer term adjustments to stressors.

(Received 23 June 2006; accepted after revision 18 September 2006; first published online 28 September 2006)
Corresponding author J. H. Coote: Division of Neuroscience, The Medical School, University of Birmingham, Birmingham B15 2TT, UK. Email: j.h.coote{at}bham.ac.uk

This article has been cited by other articles:

				T. Zhang, Z. Yang, and J. H. Coote Autonomic Neuroscience: Cross-sample entropy statistic as a measure of complexity and regularity of renal sympathetic nerve activity in the rat Exp Physiol, July 1, 2007; 92(4): 659 - 669. [Abstract] [Full Text] [PDF]