The role of the anteroventral third ventricle (AV3V) region in mediating hypertonic sodium chloride-induced pressor responses was investigated in conscious rats. Sham- and AV3V-lesioned rats were prepared with femoral artery and vein catheters and subjected to bilateral nephrectomy under gaseous anesthesia. After recovery, animals were infused intravenously with isotonic (0.5 meq/kg) or hypertonic (10 meq/kg) saline at a rate of 0.0103 ml/min over 2 h. Isotonic saline infusion did not affect arterial pressure or heart rate in either group of rats. Hypertonic saline increased arterial pressure 35 ± 3 mmHg in sham-lesioned rats and only 10 ± 4 mmHg in AV3V-lesioned animals (P < 0.0005). Sham-lesioned rats infused with hypertonic saline had a greater vasopressin-dependent component maintaining arterial pressure than the other groups of rats. Conversely, the sympathetic nervous system-dependent component of blood pressure was suppressed in the hypertonic saline-infused sham-lesioned animals compared with the other animals. However, when the vasopressin receptors were blocked, the neurally mediated portion of blood pressure was similar in all four groups of rats. These results emphasize that circulating vasopressin is important for the rise in arterial pressure accompanying the osmotic stimulus. Furthermore, this study demonstrates that the AV3V region is necessary for vasopressin-dependent pressor responses caused by an osmotic stimulus.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|Issue number||3 (21/3)|
|State||Published - 1987|
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