Paraventricular nucleus influence on renal sympathetic activity in vasopressin gene-deleted rats.
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 significantly 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.
Yang
Zhou
Z
Division of Neuroscience, The Medical School, University of Birmingham, Birmingham B15 2TT, UK.
Coote
J H
JH
D000818:Animals; D001794:Blood Pressure; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism; D006339:Heart Rate; D006470:Hemorrhage / Q000503:physiopathology; D006710:Homocysteine / Q000031:analogs & derivatives / Q000494:pharmacology; D007668:Kidney / Q000294:innervation*; D007736:Kynurenic Acid / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011910:Rats, Brattleboro; D020318:Rats, Long-Evans; D013127:Spinal Nerves / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D014667:Vasopressins / Q000172:deficiency* / Q000235:genetics / Q000494:pharmacology
D018691:Excitatory Amino Acid Antagonists; D006710:Homocysteine; C007956:homocysteic acid; D014667:Vasopressins; D018698:Glutamic Acid; D007736:Kynurenic Acid