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W B Severs

Publications and source records attributed to W B Severs.

At least 55 records · Page 3Linked to original sources
PubMed1987

Site-dependent central effects of aldosterone in rats.

A relationship between the subcommissural organ (SCO) and the adrenal glands has long been suspected. This report provides further information about the effects of a continuous D-aldosterone infusion into the SCO area of conscious, adult male Sprague-Dawley rats. A 6-day aldosterone infusion (5 ng/h) increased urinary sodium excretion, decreased adrenal medullary cross-sectional area, elevated adrenal corticosterone content and terminal plasma epinephrine concentration. Mineralocorticoid infusions directly into a lateral cerebral ventricle did not affect these parameters but, unlike SCO area infusions, decreased consummatory behavior. Infusions of tritiated aldosterone into the SCO area revealed that radioactivity was mainly confined to dorsomedial portions of the brain near the SCO, whereas the pineal body contained only background radioactivity. The data support the concept that the SCO area interacts with physiological systems related to both the adrenal cortex and medulla.

Adrenal Glands↗
PubMed1986

Blood flow and functional responses correlate in the ovine neural lobe.

Regional neurohypophyseal and cerebral blood flow were measured in 5 awake unstressed female sheep with radiolabelled microspheres before and after the intracarotid infusion of a 3% NaCl solution. Plasma arginine vasopressin (AVP) levels were concurrently measured by radioimmunoassay. Following intracarotid sodium chloride infusion, neural lobe (but not median eminence) blood flow significantly increased, as did plasma AVP levels. Directed thirst and water-seeking behavior was observed, accompanied by a global increase in cortical blood flow. We conclude that the neuroendocrine response and the behavioral display induced by intracarotid sodium chloride infusion are accompanied by increases in blood flow in selected brain regions.

Animals↗
PubMed1986

Increased delta, but not mu, opiate receptor binding in the medulla oblongata of Long-Evans rats following 5-day water deprivation.

Opiate receptors of the mu type were labeled with [125I]D-Ala2,N-Me-Phe4,Met-(O)5-ol-enkephalin (FK-33824). delta receptors were labeled with [125I]D-Ala2-D-Leu5-enkephalin (DADLE) in the presence of excess (N-Me-Phe3,D-Pro4)-morphiceptin (PL017). Since DADLE binds mu and delta receptor sites, and PL017 blocks mu receptors, this protocol improves specific labeling of delta receptors. Quantitative autoradiography showed that chronic dehydration causes no changes in mu receptor binding in the medulla oblongata of Long-Evans rats. However, there is increased delta receptor binding in the solitary, hypoglossal and gracilis nuclei, and the spinal nucleus of trigeminal system of dehydrated animals, suggesting that delta opiate receptors participate in the physiological response to dehydration.

Animals↗
PubMed1986

Effects of chronic dehydration on angiotensin II receptor binding in the subfornical organ, paraventricular hypothalamic nucleus and adrenal medulla of Long-Evans rats.

Angiotensin II (AII) is an important peptide known to regulate blood pressure and body fluid. In the present study we used a potent AII antagonist, 125I-(Sar1,Ile8)-AII (125I-SI-AII), to study AII receptor binding in Long-Evans rats 5 days after water deprivation. Specific structures evaluated include the subfornical organ (SFO) and adrenal gland. With quantitative autoradiography, we have found that there is an increase of 125I-SI-AII binding in the SFO, whereas there is a decrease in AII binding in the adrenal medulla. These observations suggest that central and peripheral AII target tissues are affected differently by dehydration. The increase in SI-AII binding in the SFO may indicate participation of this structure during dehydration, as angiotensin stimulation of SFO causes thirst and vasopressin release.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1986

Barrel rotation evoked by intracerebroventricular vasopressin injections in conscious rats. I. Description and general pharmacology.

Intracerebroventricular (i.c.v.) arginine-vasopressin (AVP) injections in rats evoke an unusual motor response termed 'barrel rotation' (BR). This report documents several aspects of BR after i.c.v. AVP in conscious, adult male Sprague-Dawley rats: single i.c.v. AVP injections (100-1000 ng/5 microliters) evoke BR in about 50% of naive rats with no relationship to dose and 20% mortality; no directional preference exists for BR, and sensitivity to BR does not vary over a weight range of 301-475 g; continuous i.c.v. AVP infusions at doses of 50-2500 ng/h evoked BR in 13 and 50% of rats tested at the extreme ranges; latency to BR was always within 3-6 min in infusion experiments; a protocol where rats received a single i.c.v. AVP injection (1 microgram) on day 1 followed on day 3 by 0.5 micrograms, increased the proportion of rats with BR from 51% to 83% (P less than 0.05), indicating a sensitization phenomenon; latency to BR after single i.c.v. injections did not fit the assumption of single underlying normal distribution; a novel method to analyze these data, hazard plotting, revealed two phases to the BR latency under ambient illumination. The following paper presents evidence of visual/vestibular involvement and the efficacy of anti-seizure drugs. Collectively, the data are compatible with the hypothesis that brain vasopressin pathways are involved in some abnormalities of motor output.

Animals↗
PubMed1986

Barrel rotation evoked by intracerebroventricular vasopressin injections in conscious rats. II. Visual/vestibular interactions and efficacy of antiseizure drugs.

Intracerebroventricular (i.c.v.) arginine-vasopressin (AVP) injections evoke 'barrel rotation' (BR) in rats. This motor system abnormality was studied in a protocol where conscious rats were injected on day 1 with 1 microgram i.c.v. AVP and reexposed to 0.5 micrograms on day 3. Three paradigms modifying visual/vestibular systems were employed: labyrinthectomy, 3-acetylpyridine (3-AP) destruction of the inferior olive and atropine pretreatment. Ambient illumination (light vs dark) was also modified. Initial (day 1) incidence of BR, increased incidence (i.e. sensitization) on day 3, and day 3 BR latency were differentially affected by the various paradigms and suggest a complex role of visual/vestibular input in modifying i.c.v. AVP-induced BR. For example, 3-AP rats tested in light and atropinized rats had a reduced responsiveness to the peptide on day 1. 3-AP-treated rats tested in dark conditions showed a normal incidence of BR on day 1, but the expected sensitization to AVP on day 3 did not occur. Combined labyrinthectomy and darkness did not modify BR incidence on either day, but altered the distribution of latency data. Four diverse antiepileptic drugs were tested for efficacy against i.c.v. AVP-induced BR in sensitized rats: phenytoin, diazepam, valproic acid and phenobarbital; all drugs reduced the proportion of rats with BR and prolonged the latency. We conclude that brain AVP may be involved in abnormal motor conditions that are modified by visual/vestibular neuronal circuits. The unusual motor output (barrel rotation) can be inhibited by diverse antiepileptic drugs.

Animals↗
PubMed1984

A specific harmaline-evoked increase in cerebellar 5'-nucleotidase activity.

This study examines harmaline-induced changes in 5'-nucleotidase (5'-ND) activity in cerebellar fractions from rats with an intact inferior olive (IO) or prior destruction of the IO by 3-acetylpyridine (3-AP) intoxication. Harmaline markedly increased 5'-ND activity in the crude homogenate (P less than 0.05) and P2 fraction (P less than 0.001) of cerebella from rats with an intact IO. This increase was absent in the P1, P3 and S3 fractions and it was abolished by 3-AP olivectomy. It was also absent in basal ganglia P2 fractions. Since harmaline produces rhythmic complex spike discharges of Purkinje cells by activating IO neurons [4, 18], these data suggest that climbing fiber activation per se increases 5'-ND activity in the P2 fraction. This raises the possibility that a climbing fiber-induced local increase in 5'-ND activity at parallel fiber-Purkinje cell synapses results in a local increase in adenosine concentration. This may account for climbing fiber-evoked suppression of simple spike activity [12, 13, 28].

5'-Nucleotidase↗
PubMed1984

Effects of dehydration and renin on vasopressin concentration in the subfornical organ area.

The subfornical organ (SFO), one of the brain circumventricular organs, contains immuno-reactive arginine-vasopressin (AVP). AVP in the SFO area may originate in neurons of the hypothalamo-neurohypophysial system. If AVP in the SFO area is part of the magnocellular neuroendocrine system and is important in the regulation of hydration, then its concentration [(]) should change during prolonged dehydration. The SFO is also a target for angiotensin II when the peptide stimulates drinking and releases AVP from the hypothalamo-neurohypophysial system. For these reasons, it was reasoned that hormones of the renin-angiotensin system may also influence [AVP] in the SFO area. To test these hypotheses [AVP] was measured in the SFO area, hippocampal commissure-fornix (HC-F), neural lobe and plasma of rats after 24, 48 and 72 h of water deprivation and at various times after intracerebroventricular (i.v.t.) administration of 5 milli -Goldblatt Units of renin. Before examining the responsiveness of [AVP] in these brain regions to stimulation, we characterized the extraction and recovery of AVP from brain tissue and determined the variance of [AVP] in the SFO area and HC-F among different groups of animals. AVP was extracted from pooled brain tissue into 0.1 N HCl. The homogenate was centrifuged and AVP in the supernatant was quantified by radioimmunoassay either directly or after bentonite extraction. AVP extracted from the SFO area and HC-F displaced labelled antigen bound to antisera in a manner similar to that displaced by standard AVP. The recovery of AVP, added to the 0.1 N HCl extract and assayed directly, averaged 78-108%, whereas 51% was recovered after bentonite extraction. [AVP] in the SFO area from 47 or more groups of 2-6 organs each, averaged 16 +/- 5 pg/organ, 16 +/- 4 pg/mg wet wt, 153 +/- 31 pg/mg protein, and was not significantly different from that contained in the HC-F, 10 +/- 1 pg/mg wet wt and 111 +/- 16 pg/mg protein. A frequency histogram of these data revealed a normal (HC-F) and skewed distribution (SFO). Water deprivation for 24, 48 and 72 h stimulated drinking and increased plasma [AVP]. The elevation in plasma [AVP] plateaued after 48 and 72 h of water deprivation, whereas [AVP] in the neural lobe was reduced (P less than 0.05). Water deprivation increased [AVP] in the HC-F (control vs 72 h water deprivation), but did not alter hormone in the SFO area when expressed as pg/mg protein or pg/mg wet wt.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiotensin I↗
PubMed1984

Catecholamine synapses and contents in the paraventricular hypothalamic nucleus and nucleus tractus solitarius of DOCA-salt hypertensive rats.

Central catecholamine (CA) neurons in the nucleus tractus solitarius (NTS) and paraventricular hypothalamic nucleus (PVN) were studied in Wistar rats that had been unilaterally nephrectomized. The experimental animals were then treated with deoxycorticosterone acetate (DOCA) and salt water. The control animals were treated with the vehicle and tap water. Blood pressure of animals 4 weeks after DOCA/salt treatment was significantly elevated when compared to control rats. Morphologically, CA terminals showed no noticeable changes in the DOCA/salt hypertensive rats. Furthermore, the density of CA terminals either in the NTS or in the PVN of the DOCA/salt hypertensive rats was not statistically different from that of normotensive controls, suggesting that salt does not cause lesions or destruction of CA terminals. However, an extensive electron-microscopic morphometric analysis indicated that there was an enhancement of CA synaptogenesis (expressed by increased synaptic frequency among all CA boutons labeled with 5-hydroxydopamine) in the PVN, but not in the NTS of DOCA/salt hypertensive rats. In addition, the high-performance liquid chromatography revealed decreased CA contents in the PVN, but not in the NTS, of DOCA/salt hypertensive animals. Since synapses are primary sites for neurotransmitter release, the above results collectively suggest that more CA synapses formed in the PVN may reflect a net CA release from CA terminals resulting in the decreased CA content in the axonal terminals. Such an increased CA release and enhanced CA synaptogenesis may consequently enhance CA function in the PVN of hypertensive rats 4 weeks after DOCA/salt treatment, and relate to the development and/or maintenance of hypertension in the DOCA/salt rats.

Animals↗
PubMed1984

Central effects of aldosterone infused into the rat subcommissural organ region.

D-Aldosterone (5 ng/microliter/h) was infused for 6 days into the region of the subcommissural organ (SCO) of conscious, adult male Sprague-Dawley rats. Aldosterone increased urinary sodium loss and the sodium/potassium ratio. Although probably central in origin, these effects still occurred when cannulae were displaced up to 1 mm from the targeted SCO placement. Aldosterone decreased adrenal medullary cross-sectional area without affecting cell density. This effect was highly dependent on proper cannula placement and was not observed when the cannula tip was not in contact with the cerebrospinal fluid of the pineal recess over the rostral two-thirds of the SCO. We conclude that aldosterone increases sodium excretion by an action in the SCO and/or adjacent structures. We also postulate a negative trophic relationship between mineralocorticoids and the adrenal medulla mediated by the SCO.

Adrenal Glands↗
PubMed1983

Cerebrospinal fluid pressure during cerebroventricular infusion of angiotensin and vasopressin.

Rationale exists for suspecting that angiotensin (Ang) and arginine vasopressin (AVP) given by the intracerebroventricular (IVT) route can affect cerebrospinal fluid (CSF) pressure. This hypothesis was tested in conscious, unrestrained adult male Sprague-Dawley rats with IVT and left carotid arterial catheters. The rats were infused (IVT) for 30 min with artificial CSF followed by 30 additional minutes with CSF, Ang, (0.6 micrograms/h) AVP (5 or 50 ng/h), or AVP (5 or 50 ng/h) + Ang, (0.6 micrograms/h). Angiotensin evoked a central hypertensive effect (+ 16 mm Hg) and increased CSF pressure from 10 to 16 cm H2O (P less than 0.05). Neither dose of AVP affected blood or CSF pressures. The AVP (5 ng/h) prevented Ang-induced changes in blood and CSF pressures and AVP (50 ng/h) blocked only the Ang-induced rise in CSF pressure. These results raise the possibility that angiotensin and vasopressin participate in the regulation of CSF pressure.

Angiotensin II↗
PubMed1983

Cerebroventricular sites for enkephalin inhibition of the central actions of angiotensin.

The effect of leucine5-enkephalin (Leu-enkephalin) administered into the lateral (LV) or fourth (4V) cerebroventricle on angiotensin II (ANG II)-stimulated increase in blood pressure, plasma vasopressin concentration ([AVP]), and drinking behavior was determined in conscious rats. Leu-enkephalin (20, 50, or 100 micrograms) was injected into the LV (5 microliters) or 4V (2 microliters) less than or equal to 15 s before ANG II (50 or 500 ng, LV). LV and 4V administration of Leu-enkephalin (100 or 50 micrograms) significantly (P less than 0.05) delayed the drinking onset, decreased the number of animals drinking, and reduced the volume consumed (100 micrograms, 30 min) in response to ANG II (50 ng). ANG II-stimulated increases in plasma [AVP] and blood pressure were inhibited by 50 or 100 micrograms, respectively, of Leu-enkephalin administered into LV but not 4V. Decreased motor activity occurred after Leu-enkephalin (100 micrograms) administration into LV and 4V, whereas head shakes were more consistent after the former. Fast green dye administered into 4V did not reach anterior periaqueductal, third, or lateral cerebroventricular sites. Thus opioid peptide receptors inhibiting ANG II-stimulated drinking, vasopressin release, and pressor response are postulated to be in brain structures accessible from lateral or third cerebroventricles. Opiate receptors inhibitory to drinking are also reached from peri-4V sites.

Angiotensin II↗
PubMed1983

Vasopressin release induced by water deprivation: effects of centrally administered saralasin.

Uncertainty exists as to whether endogenous angiotensin activates brain mechanisms controlling vasopressin (AVP) secretion during dehydration. We injected various doses of saralasin into a lateral cerebroventricle (IVT) of conscious, male rats deprived of water for 48 h and killed them at different times. The concentration of AVP in the plasma (p[AVP]), measured by radioimmunoassay, was unaffected by saralasin. IVT pretreatment with 1-Sar-8-Ile-angiotensin II blocked maximal AVP release by IVT angiotensin, but this pretreatment did not reduce p[AVP] after 24, 48 or 72 h water deprivation. A 3-hour continuous IVT infusion of CSF or saralasin (10 micrograms/h) into 48-hour water-deprived rats revealed equivalent p[AVP] and urine volumes. When the infusions were continued for 3 h more with water available, control and saralasin-treated rats: (a) drank at similar rates, (b) excreted similar amounts of urine, and (c) reduced their p[AVP] levels to the same extent. IVT saralasin did not affect p[AVP] of rats dehydrated with hypertonic NaCl. Combined IVT saralasin and atropine reduced p[AVP] of 48-hour water deprived rats about 30% (p less than 0.05). We conclude that redundancy exists for sensing, integrating and releasing vasopressin in dehydrated rats.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1983

Eating, drinking and urine output after prolonged cerebroventricular vasopressin infusions in rats.

Prior studies suggested that centrally administered single doses of vasopressin (VP) do not affect consummatory behavior or peripheral hydration. To reduce uncertainties related to factors of unknown distribution, concentration and duration, we infused VP (0.5 or 50 ng/h) continuously for 5 h or 5 days into a lateral cerebroventricle of conscious male rats. Eating and drinking behavior, as well as urine volume and sodium and potassium output, were unaffected by these treatments. The results suggest that VP, at sites reached from cerebrospinal fluid, does not alter peripheral hydration of rats.

Animals↗
PubMed1982

Effect of CSF dilution on the blood pressure of rats with renal hypertension.

The concentration of many substances in cerebrospinal fluid (CSF) of hypertensive animals has been reported to be elevated but cause-effect relationships are unclear. Conscious adult male Sprague-Dawley rats were infused via a lateral cerebroventricle with artificial CSF or water (2 microliters/min) or were not infused. Three groups of rats were tested: rats with renal hypertension (bilateral renal artery stenosis), sham-operated controls and unoperated controls. Blood pressures of the normotensive or hypertensive animals were unaffected by a 5-hour infusion of artificial CSF or water. Urinary output of rats infused with water was increased, indicating that water infusion was efficacious in diluting CSF. Based on experiments in anesthetized rats, we estimate that water infusion diluted CSF 8-14%. These results support the opinion that altered sensitivity to, or concentration of, CSF constituents per se does not maintain hypertensive blood pressure. Furthermore, it is unlikely that CSF serves as a conduit to deliver active substances to periventricular brain sites regulating blood pressure and hydration. Excess concentration of CSF constituents in hypertension probably reflects overflow into CSF instead of a cause-effect phenomenon.

Animals↗