Received June 23, 2006
Revised August 1, 2006
Accepted after revision September 18, 2006
Autonomic Neuroscience [200]
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Paraventricular nucleus influence on renal sympathetic activity in vasopressin gene-deleted rats
Zhuo Yang 1
John H. Coote 2*
1 Medical College, University of Nankai, Tianjin 300071, PR China
2 University of Birmingham
* To whom correspondence should be addressed. E-mail: j.h.coote{at}bham.ac.uk.
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Abstract |
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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 are dependent on the release of vasopressin and glutamate at spinal synapses. The significance of the supraspinal pathway and the cooperative interaction with an excitatory amino acid, is unclear. The present study examines this using Brattleboro rats that have a natural vasopressin gene deletion. The responses were compared with Long Evans rats from which Brattleboro rats are derived. All rats were anaesthetised with a mixture of urethane (650mg kg-1) and chloralose (50mg kg-1). Recordings were made of blood pressure, heart rate and renal sympathetic nerve activity (RSNA). Microinjection of D-L homocysteic acid (DLH, 0.2M, 100nl) 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 V1a antagonist or a glutamate antagonist (kynurenic acid), whereas in Brattleboro rats the changes were only significantly reduced (p < 0.05) by kynurenic acid. Removal of 1ml 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 V1a 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 V1a antagonist, only being significantly reduced (p < 0.01) 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 and might indicate that in normal rats vasopressin is more important in maintaining longer term adjustments to stressors.
Key Words:
Hypothalamus, Sympathetic activity
