ISSN:
1432-1106
Keywords:
Osmotic stimuli
;
Hemorrhage
;
Angiotensin II
;
Unit activity
;
Paraventricular nucleus
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Antidromically identified paraventricular neurosecretory cells were recorded extracellularly in urethane-anesthetized female rats. Their activity was examined for response to 0.3 M NaCl (0.1 ml, intracarotid injection) and hemorrhage (10 ml/kg b.w.) applied separately or in combination, and was also investigated for the interaction of these stimuli with angiotensin II (AII). About half (51%) of the 106 neurosecretory cells recorded were excited both by osmotic stimuli and by hemorrhage. The remaining cells exhibited various combinations of responses such as no change after 0.3 M NaCl and excitation after hemorrhage (24.5%), no change after either stimulus (19.8%), no change after 0.3 M NaCl and inhibition after hemorrhage (3.8%), and excitation after 0.3 M NaCl and no change after hemorrhage (0.9%). When the neurosecretory cells which did not respond to the 0.3 M NaCl were tested for response to the combined application of 0.3 M NaCl and subthreshold bleeding stimulus (2.5–5.0 ml/kg b.w.), 65.4% of them (n = 26) showed an excitatory response. A subthreshold dose (5 ng) of AII injected into the third ventricle (IVT) potentiated the response to 0.3 M NaCl in 61.8% of the neurosecretory cells (n = 34), whereas the same dose of AII had no effect on the response to hemorrhage (10 ml/kg b.w.). An AII antagonist, saralasin (1 μg, IVT), inhibited a response to 0.3 M NaCl in 80.8% of the neurosecretory cells (n = 26), while it affected a response to hemorrhage (10 ml/kg b.w.) in none of them. However, when the dose of saralasin was increased to 4 or 5 μg, it inhibited not only a response to 0.3 M NaCl but also a spontaneous firing activity and a response to hemorrhage of the neurosecretory cells (n = 5). These results suggest that an osmotic stimulus interacts with hemorrhage or AII in stimulating the neurosecretory cell and that endogenous AII is involved in the mechanism for osmotic activation of the neurosecretory cell. On the other hand, hemorrhage seemed hardly to interact with AII, although a dose of saralasin large enough to inhibit the spontaneous activity of neurosecretory cells suppressed their excitatory response to hemorrhage.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00239579
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