Biomedical subjects

L C Keil

Publications and source records attributed to L C Keil.

At least 91 records · Page 5Linked to original sources

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↗

PubMed1986

Role of vasopressin in stimulation of ACTH secretion by angiotensin II in conscious dogs.

Three series of experiments were performed in conscious dogs to test the possibility that the stimulation of adrenocorticotropin (ACTH) release by angiotensin II (ANG II) is mediated by arginine vasopressin (AVP). In the first protocol, the effect of ANG II on ACTH release was studied in dogs in which endogenous AVP levels had been increased by water deprivation. Water deprivation for 24 h increased plasma AVP concentration from 3.0 +/- 0.5 to 7.7 +/- 0.5 pg/ml (P less than 0.01) and increased the AVP response to the highest dose of ANG II (20 ng X kg-1 X min-1). Despite these changes, water deprivation failed to increase the ACTH response to ANG II. Next, the contribution of endogenous AVP to the stimulation of ACTH release by ANG II was examined using the V1-receptor antagonist, d(CH2)5Tyr[Met]-AVP (10 micrograms/kg iv). The ACTH response to ANG II in the presence of the AVP antagonist (66.4 +/- 3.1 to 100.1 +/- 15.9 pg/ml) was not significantly less than that in its absence (53.0 +/- 4.8 to 72.2 +/- 11.1 pg/ml). Finally, ANG II and AVP were infused in combination to determine whether there is a synergism between these two peptides in the release of ACTH. In one protocol, AVP and ANG II were infused separately and in combination. The ACTH response to ANG II and AVP in combination (48.7 +/- 6.5 to 61.5 +/- 8.5 pg/ml) was not enhanced compared with the responses to ANG II (59.8 +/- 7.3 to 71.0 +/- 10.1 pg/ml) or AVP (48.8 +/- 5.7 to 55.6 +/- 6.5 pg/ml) alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1986

Effects of sodium depletion and angiotensin II on osmotic regulation of vasopressin.

After alterations in sodium balance, osmotic reactivity of vasopressin (AVP) release was evaluated in seven conscious dogs during bilateral intracarotid infusions of hypertonic saline. A low-sodium diet reduced plasma sodium concentration by 3%; deoxycorticosterone acetate (30 mg/day for 2 days) elevated the concentration by 1%. Neither treatment altered resting plasma AVP. Hypertonic intracarotid infusions increased jugular plasma osmolality by 20 +/- 2 mosmol/kg independent of manipulations. Plasma AVP values were significantly increased (P less than 0.05) in sodium-depleted dogs compared with values of the control animals. In addition, the osmotic reactivity of AVP release was evaluated during exogenous administration of angiotensin II (ANG II). Intravenous infusion of ANG II (5 ng . kg-1 . min-1) increased plasma concentration of ANG II but did not alter concentration of plasma AVP. The slope for the relationship of jugular plasma osmolality to plasma AVP during hypertonic intracarotid infusions was significantly increased with intravenous infusion of ANG II. Sodium depletion and intravenous ANG II potentiate the relationship of plasma osmolality and plasma AVP when evaluated with intracarotid hypertonic saline infusions in dogs.

Angiotensin II↗

PubMed1986

Endocrine mechanisms regulating sodium excretion during water deprivation in dogs.

The time course and mechanism of the natriuresis that accompanies 24 h of water, but not food, deprivation were studied in eight chronically catheterized dogs. Dogs were fed a controlled diet containing 35 meq of sodium, 110 meq of potassium, and 107 ml of water at 9:00 A.M. every day (time 0), and urine and blood samples were taken at 0, 2, 4, 6, 8, 10, 12, 16, 20, and 24 h after feeding on 3 consecutive days: the control, dehydration, and recovery days. Twenty-four hours of water deprivation decreased body weight by 880 g, increased plasma sodium by 7.2 meq, and increased plasma osmolality by 22.5 mosmol/kg. Cumulative daily sodium excretion increased from 30.4 +/- 2.8 meq on the control day to 50.7 +/- 5.7 meq on the dehydration day (P less than 0.01) and resulted in significant negative sodium balance that developed during the last half of the dehydration day. Cumulative sodium excretion during the first half of the dehydration day was not different from the corresponding period of the control day. Cumulative potassium excretion also increased from 91.9 +/- 4.5 meq during the control day to 123.0 +/- 6.7 meq during the dehydration day (P less than 0.01). Significant and progressive increases in plasma vasopressin concentration and renin activity were observed during water deprivation, but plasma aldosterone did not change from control levels. Furthermore, there was no correlation between the rate of sodium excretion and plasma vasopressin or aldosterone concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗

PubMed1986

Cardiac receptors, vasopressin, and corticosteroid release during arterial hypotension in dogs.

The relative roles of cardiopulmonary and sinoaortic baroreceptors in the regulation of vasopressin and corticosteroid release were evaluated in conscious dogs. The dogs were prepared with inflatable cuffs around either the ascending aorta, proximal to the brachiocephalic trunk, or the pulmonary artery. Inflation of the cuffs was adjusted to cause a reduction of mean systemic arterial pressure (MAP) of 0, 5, 10, 20, or 30% of control for 1 h in separate experiments. In spite of the profound systemic hypotension caused by constriction of the ascending aorta, plasma vasopressin failed to increase and corticosteroids increased only in response to a 30% decrease in MAP. In contrast, a 5% reduction in MAP during pulmonary arterial constriction increased plasma vasopressin and corticosteroid concentrations significantly. The apparent paradox in these results is correlated with different effects of the two maneuvers on left atrial pressure. Left atrial pressure increased dose dependently during inflation of the ascending aortic cuff but decreased during inflation of the pulmonary arterial cuff. In contrast, graded inflation of the pulmonary arterial cuff caused dose-dependent increases in right atrial pressure, plasma vasopressin, and corticosteroids. Therefore, we conclude that powerful inhibitory signals, arising from the left heart, can inhibit vasopressin and hypotension release in response to systemic hypotension.

Adrenal Cortex Hormones↗

PubMed1986

Effect of antigravity suit inflation on cardiovascular, PRA, and PVP responses in humans.

Blood pressure, pulse rate (PR), serum osmolality and electrolytes, as well as plasma vasopressin (PVP) and plasma renin activity (PRA), were measured in five men and two women [mean age 38.6 +/- 3.9 (SE) yr] before, during, and after inflation of an antigravity suit that covered the legs and abdomen. After 24 h of fluid deprivation the subjects stood quietly for 3 h: the 1st h without inflation, the 2nd with inflation to 60 Torr, and the 3rd without inflation. A similar control noninflation experiment was conducted 10 mo after the inflation experiment using five of the seven subjects except that the suit was not inflated during the 3-h period. Mean arterial pressure increased by 14 +/- 4 (SE) Torr (P less than 0.05) with inflation and decreased by 15 +/- 5 Torr (P less than 0.05) after deflation. Pulse pressure (PP) increased by 7 +/- 2 Torr (P less than 0.05) with inflation and PR decreased by 11 +/- 5 beats/min (P less than 0.05); PP and PR returned to preinflation levels after deflation. Plasma volume decreased by 6.1 +/- 1.5% and 5.3 +/- 1.6% (P less than 0.05) during hours 1 and 3, respectively, and returned to base line during inflation. Inflation decreased PVP from 6.8 +/- 1.1 to 5.6 +/- 1.4 pg/ml (P less than 0.05) and abolished the significant rise in PRA during hour 1. Both PVP and PRA increased significantly after deflation: delta = 18.0 +/- 5.1 pg/ml and 4.34 +/- 1.71 ng angiotensin I X ml-1 X h-1, respectively. Serum osmolality and Na+ and K+ concentrations were unchanged during the 3 h of standing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986

Effect of hydration on plasma volume and endocrine responses to water immersion.

To determine the effect of hydration on the early osmotic and intravascular volume and endocrine responses to water immersion the hematocrit, hemoglobin, plasma renin activity (PRA), and plasma electrolyte, aldosterone (PA), and vasopressin (PVP) concentrations were measured during immersion following 24-h dehydration; these were compared with corresponding values following rapid rehydration. Six men and one woman (age 23-46 yr) underwent 45 min of standing immersion to the neck preceded by 45-min standing without immersion, first dehydrated, and then 105 min later after rehydration with water. Immersion caused an isotonic expansion of the plasma volume (P less than 0.001), which occurred independently of hydration status. Suppression of PRA (P less than 0.001) and PA (P less than 0.001) during both immersions also occurred independently of hydration status. Suppression of plasma vasopressin was observed during dehydrated immersion (P less than 0.001) but not during rehydrated immersion. It is concluded that plasma tonicity is not a factor influencing PVP suppression during water immersion.

Adult↗

PubMed1986

Role of dopamine in the inhibition of vasopressin secretion by L-dopa in carbidopa-treated dogs.

Elevation of brain catecholamine levels by systemic administration of L-dopa in dogs pretreated with the dopa decarboxylase inhibitor carbidopa inhibits the secretion of vasopressin and adrenocorticotropic hormone (ACTH) and decreases arterial blood pressure. The aim of the present study was to determine whether the inhibition of vasopressin secretion is mediated by dopamine or norepinephrine, both of which have been implicated in the control of vasopressin secretion, and whether the decrease in vasopressin secretion contributes to the suppression of ACTH secretion and fall in blood pressure produced by L-dopa. This was accomplished by comparing the effects of dopamine and alpha-adrenergic receptor antagonists on vasopressin, ACTH, and blood pressure responses to L-dopa. The effect of a specific antagonist of the vasoconstrictor action of vasopressin also was studied. Injection of L-dopa (20 mg/kg i.v.) in dogs pretreated with carbidopa (20 mg/kg i.v.) caused reductions in plasma vasopressin concentration (from 16.0 +/- 4.8 to 3.8 +/- 0.9 pg/ml; p less than 0.05), plasma ACTH concentration (from 96.0 +/- 20.4 to 49.2 +/- 10.0 pg/ml; p less than 0.05), and mean arterial pressure (from 121 +/- 6 to 78 +/- 5 mm Hg; p less than 0.05). Pretreatment with pimozide (1 mg/kg i.p.) completely blocked the inhibition of vasopressin secretion by L-dopa but failed to block the suppression of ACTH secretion (57.6 +/- 11.8 to 34.0 +/- 5.1 pg/ml; p less than 0.05) or the decrease in mean arterial pressure (126 +/- 5 to 93 +/- 7 mm Hg; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗

PubMed1986

Role of the renin-angiotensin system in the control of vasopressin secretion in conscious dogs.

The present studies were designed to evaluate the physiological significance of angiotensin II in the control of vasopressin secretion in conscious dogs. They demonstrated that exogenous angiotensin II (10 ng/kg per min) increased vasopressin secretion more when the pressor effect of angiotensin II was abolished. The fact that endogenous angiotensin II levels are normally increased without an increase in arterial pressure suggests that angiotensin II may play a greater role in the control of vasopressin secretion than was previously thought. The present study also evaluated the role of endogenous angiotensin II in the control of vasopressin secretion during sodium depletion, a state in which angiotensin II levels are elevated. Intracarotid infusion of a low dose of the angiotensin II antagonist, saralasin, decreased plasma vasopressin concentration, suggesting that endogenous angiotensin II acts in an area of the brain perfused by the carotid arteries to stimulate vasopressin secretion in sodium-deprived dogs. Finally, the present experiments evaluated the role of angiotensin II in baroreceptor reflex control of vasopressin secretion. Baroreflex function was assessed by examining the relationship between the change in blood pressure and the log of the change in vasopressin secretion over a range of blood pressure levels. Exogenous angiotensin II (10 ng/kg per min) altered baroreflex function by causing a shift of this relationship to a higher pressure level in sodium-replete dogs. In sodium-depleted dogs, inhibition of the renin-angiotensin system with saralasin or captopril produced an opposite shift. These results suggest that endogenous angiotensin II may be necessary for the maintenance of normal baroreflex control of vasopressin secretion during sodium depletion. Collectively, these results support the hypothesis that endogenous angiotensin II plays a role in the control of vasopressin secretion.

Angiotensin II↗

PubMed1986

Effect of hydration on plasma vasopressin, renin, and aldosterone responses to head-up tilt.

If plasma vasopressin (PVP), plasma renin (PRA), and plasma aldosterone (PA) responses to change in posture are mediated only by alterations in intrathoracic baroreceptor activity, hydration status should have minimal influence on these responses. To test this hypothesis, six male subjects underwent 45 min of 70 degree head-up tilt (HUT) following 26 h dehydration, and again, 105 min later, following rehydration. Compared with preceding supine hydrated control values, PVP, PRA, and PA increased (p less than 0.001) during dehydrated HUT, but only PVP and PRA increased during rehydrated HUT (p less than 0.001). The dissociation during rehydrated HUT of PRA and PA may have been related more to the reduction (p less than 0.001) in plasma potassium concentration than to the accompanying decrease (p less than 0.001) in plasma osmolality and sodium concentration. Although increases in PVP and PRA during HUT were attenuated (p less than 0.01) following rehydration, this attenuation was associated with the absence of symptoms of overt hypotension following rehydration. However, since rehydration did not abolish the increases in PVP and PRA induced by HUT, it is concluded that the present observations support the concept of intrathoracic baroreceptor involvement in the regulation of vasopressin secretion and renin release.

Adult↗

PubMed1985

Differential effects of naloxone on the release of neurohypophysial hormones in normotensive and spontaneously hypertensive rats.

The hypothalamo-neurohypophysial system is altered in the spontaneously hypertensive rat (SHR). We hypothesized that an aberrant regulation of vasopressin (VP) and oxytocin (OT) release by endogenous opioid peptides alters this neuroendocrine system in the SHR. Concentrations of the neurohypophysial hormones in plasma and the pituitary were measured in 17-week-old SHRs and two strains of normotensive controls. Wistar Kyoto (WKY) and Sprague-Dawley rats. Animals were decapitated 20 min after s.c. injection of saline (1 ml/kg) or naloxone hydrochloride (1 or 10 mg/kg). In addition, neurohypophysial hormones excreted during the day (08.00-17.30 h) and night (17.30-08.00 h) were determined in urine from 16-week-old animals kept in metabolic cages for 5 days. VP at extrahypothalamic sites was also measured as [VP] in acid extracts of the subfornical organ area, hippocampal commissure-fornix and choroid plexus. Hormones were quantified by radioimmunoassay. The pituitary content, plasma concentration, and urinary excretion of OT were reduced (P less than 0.05) in SHRs, whereas VP content was increased (P less than 0.05) in the pituitary and plasma, but unchanged in urine, of hypertensive animals. In extrahypothalamic tissues, [VP] in the hippocampal commissure-fornix was increased in the SHR. Naloxone elevated (P less than 0.05) the plasma concentration of OT in WKY animals and VP in SHRs. Neither [VP] nor [OT] in plasma was changed by naloxone in Sprague-Dawley rats. Pituitary stores of the neurohypophysial hormones were not altered by naloxone in either hypertensive or normotensive rats. In conclusion, endogenous opioid peptides tonically inhibit OT release in WKY rats, whereas VP release is decreased by opioid peptides in SHRs, 16-17 weeks of age. The neuromodulatory role of opioid peptides in the release of neurohypophysial hormones appears to be altered in the SHR such that VP release is suppressed and OT release is augmented.

Animals↗

PubMed1985

Acute volume expansion decreases adrenocortical sensitivity to ACTH and angiotensin II.

This study examined the plasma aldosterone and corticosteroid responses to a 60-min infusion of adrenocorticotropin (ACTH) or angiotensin (ANG) II started immediately after an acute isotonic saline volume expansion (0.5 ml . kg-1 . min-1 for 30 min). Five conscious dogs of either sex with exteriorized carotid loops were used in this repeated-design study. Volume expansion per se caused a 10% decrease in hematocrit, a 12.5% decrease in plasma protein, and a 2.7-mmHg increase in central venous pressure with no change in mean arterial pressure, heart rate, or plasma sodium. Volume expansion per se also resulted in significant reductions in vasopressin, plasma renin activity, ACTH, aldosterone, and corticosteroid levels. The aldosterone responses to ACTH and ANG II were significantly inhibited (46-71%) by acute volume expansion. The corticosteroid response to ACTH was 19-29% inhibited by volume expansion. We conclude that acute volume expansion significantly inhibits the adrenocortical sensitivity to its tropic hormones probably via alterations of synergistic factors.

Adrenal Cortex↗

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

Enkephalin inhibition of angiotensin-stimulated release of oxytocin and vasopressin.

The effect of leucine5 -enkephalin on angiotensin II (AII)-stimulated release of oxytocin and vasopressin (VP) was investigated in the conscious male rat. Changes in the plasma concentration ([]) of both oxytocin and VP were measured in animals: (1) 60 s after intracerebroventricular (i.v.t.) administration of either artificial cerebrospinal fluid (CSF) or CSF with AII (10, 50, 100 ng/5 microliter); (2) 30, 60, 90 and 300 s after single injection of AII (50 ng/5 microliter; i.v.t.) or CSF and (3) 60 s after AII (50 ng/5 microliter) or CSF in animals pretreated with leucine5 -enkephalin (100 ng/5 microliter; i.v.t.) or CSF (5 microliter). Oxytocin and VP were quantified by radioimmunoassay and values corrected for 100% recovery. The development of a sensitive radioimmunoassay for oxytocin is described. The antiserum for oxytocin enabled detection of greater than or equal to 0.8 pg/ml oxytocin with cross-reactivity of 0.01% with arginine vasopressin and 0.10% with arginine vasotocin. The inter- and intra-assay coefficients of variation were 3-9% and 3.2%, respectively. The hypotheses being tested were that i.v.t. injection of AII stimulates release of both neurohypophysial hormones non-selectively and that leucine5 -enkephalin inhibits both AII-stimulated oxytocin and VP release. Angiotensin II at doses ranging from 10 to 100 ng/5 microliter, i.v.t. increased the plasma concentration of both oxytocin and VP. Plasma levels of both neurohypophysial hormones were elevated 30 s after AII administration i.v.t. and remained elevated 300 sec later.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

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↗

PubMed1984

Role for the subfornical organ in vasopressin release.

The effect of subfornical organ (SFO) lesions on plasma vasopressin and drinking was tested in rats given either of two stimuli: subcutaneous injection of hypertonic saline or injection of a single dose of angiotensin II (AII) into the dorsal third cerebral ventricle. Drinking in response to hypertonicity was significantly attenuated, whereas AII-induced drinking was unaffected by the lesions. In contrast, SFO lesions were associated with significantly reduced vasopressin responses following either of these potent stimuli to vasopressin secretion. Partial lesions that damaged structures adjoining the SFO (fornix or septum) had no significant effects. These results demonstrate that, in rats, the SFO is in some way necessary for vasopressin responses to both AII and hypertonicity.

Angiotensin II↗

PubMed1984

Sodium balance and aldosterone during dehydration and rehydration in the dog.

The regulation of sodium metabolism and the renin-angiotensin-aldosterone system was evaluated during 24 h of water, but not food, deprivation and during rehydration in the dog. Dehydration caused increases in plasma concentrations of sodium (6.0 +/- 0.7 meq/l), protein (0.8 +/- 0.1 g/dl), vasopressin (5.3 +/- 0.9 pg/ml), and renin activity (3.5 +/- 1.1 ng AI X ml-1 X 3 h-1). Plasma aldosterone was unchanged and plasma potassium fell slightly (0.2 +/- 0.1 meq/l). During dehydration, food, and thus sodium intake fell by more than 10% in 12 of 19 dogs, but urinary sodium excretion increased significantly, leading to a negative sodium balance (1.9 +/- 0.2 meq/kg). Sodium retention was observed after rehydration and sodium balance; plasma electrolytes, vasopressin, and plasma renin activity (PRA) returned turned to control levels after the 1st day of recovery. However, plasma aldosterone was slightly elevated at this time, returning to control after the 2nd day of recovery. The dehydration-induced natriuresis could not be accounted for by a fall in plasma aldosterone. However, sodium retention following rehydration could be aldosterone dependent, because additional studies showed a threefold rise in plasma levels of the hormone 1 h after drinking. The acute rise in aldosterone correlated closely (r = 0.82) with the fall in plasma sodium after drinking but not with changes in adrenocorticotrophic hormone, PRA, or plasma potassium. It is concluded that natriuresis is a homeostatic response to dehydration as a means of ameliorating the rise in body fluid osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗