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W B Severs

Publications and source records attributed to W B Severs.

At least 91 records · Page 5Linked to original sources

Effects of subfornical organ extracts of salt-water balance in the rat.

The subfornical organ (SFO) is regarded as a neurosecretory structure but no information is available on the nature or biological effects of the secretory products(s). Supernatants of water homogenates of rat SFO were lyophilized and reconsittuted in artificial cerebrospinal fluid (CSF). Intracerebroventricular (IVT), but not subcutaneous, administration of this material to rats produced diuresis, natriuresis and kaliuresis in the following 8 h daylight period. During the overnight cycle, consummatory behavior and excretion of sodium and potassium were reduced. Similar responses were obtained after IVT administration of cerebellar cortex (CB) or large amounts of plasma. SFO, CB and cerebral cortex (CC) were incubated in potassium-enriched CSF to enhance release of secretory products. Urine volume was increased 8 h after IVT injection of SFO media; in the overnight cycle, food consumption, absolute urinary sodium and potassium, and [Na+-a1 were reduced. These effects were not produced by IVT injection of CC or CB media, or equal amounts of plasma proteins. Additional experiments demonstrated that choroid plexi and SFO effects were similar and that the active SFO material was dialyzable and thermal stable. These data suggest that SFO contains a water-soluble substance which is released into a posassium-enriched medium. The material is heat stable, has a relatively low molecular weight, and alters salt-water balance after injection into ventricular cerebrospinal fluid.

Animals↗

Release of vasopressin by angiotensin II.

To test the hypothesis that angiotensin II releases antidiuretic hormone (ADH) after injection into ventricular cerebrospinal fluid, conscious adult male Sprague-Dawley rats with a lateral cerebroventricular cannula received an intraventricular injection of 0, 10, 50, or 100 ng angiotensin II. Trunk blood was collected 90 seconds later for radioimmunoassay of ADH. Plasma ADH, pg/ml (mean plus or minus S. E.), for the four dose levels were 2.8 plus or minus 0.7, 9.6 plus or minus 2.5, 22.6 plus or minus 5.6 and 25.0 plus or minus 5.0, respectively. The increases produced by angiotensin were statistically significant (p smaller than 0.05). Plasma ADH of the 10 ng group was intermediate between control and the two highest angiotensin doses (p smaller than 0.05), suggesting a dose-response relationship. These data provide direct evidence that angiotensin releases ADH by central mechanisms.

Angiotensin II↗

Renin release from the ischaemic kidney.

1. We have confirmed that spinal section, and also pithing, inhibits the pressor response associated with the release of renin that follows re-establishment of circulation to the ischaemic rat kidney. Brain transections at bulbar and midthalamic levels did not modify the blood pressure elevation.2. Several pharmacological antagonists of the sympathetic nervous system did not modify the blood pressure response. These observations are not consistent with the view that a neural element is necessary for renin release.3. Constant flow perfusion of the ischaemic kidney in the intact and spinal sectioned rat was performed to evaluate haemodynamic factors involved in renin release. The pressor response was present in spinal sectioned animals under these conditions.4. These results suggest that the nervous system is necessary to maintain adequate blood flow for renin ;washout' into the systemic circulation rather than to release renin from juxtaglomerular cells.

Animals↗