TY - JOUR
T1 - Paraventricular nucleus influence on renal sympathetic activity in vasopressin gene-deleted rats
AU - Yang, Z
AU - Coote, John
PY - 2007/1/1
Y1 - 2007/1/1
N2 - 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.
AB - 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.
U2 - 10.1113/expphysiol.2006.034884
DO - 10.1113/expphysiol.2006.034884
M3 - Article
C2 - 17012145
SN - 1469-445X
VL - 92
SP - 109
EP - 117
JO - Experimental Physiology
JF - Experimental Physiology
IS - 1
ER -