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L C Keil

Publications and source records attributed to L C Keil.

At least 145 records · Page 8Linked to original sources
PubMed1982

Apparent dissociation of adrenocorticotropin and corticosteroid responses to 15 ml/kg hemorrhage in conscious dogs.

The blood pressure, heart rate, ACTH, corticosteroid, vasopressin, and renin responses to rapid 15 ml/kg hemorrhage were measured in six conscious healthy dogs with chronically maintained femoral arterial catheters. The hemorrhage decreased the mean arterial blood pressure slightly (P less than 0.001), increased the heart rate (P less than 0.001), and increased arterial plasma levels of ACTH (P less than 0.01), corticosteroids (P less than 0.001), vasopressin (P less than 0.001), and renin activity (P less than 0.001). Overall and in the individual experiments, there appeared to be little correspondence between the ACTH and corticosteroid responses. In none of the experiments was there a clear rise in ACTH above control levels before the first rise in corticosteroids. To ascertain that adrenal secretion of corticosteroids was increased during 15 ml/kg hypovolemia, changes in the clearance and distribution volume of cortisol were estimated by counting tritium extracted from plasma of five dogs infused with [1,2-3H] cortisol to steady state levels before and during hypovolemia. The stimulus caused a 30% reduction from steady state levels of dichloromethane-extractable tritium counts (P less than 0.001). Combined with the observed increase in plasma corticosteroid levels, these results show that the increase in adrenal secretion of corticosteroids after hemorrhage was underestimated by measurement of changes in peripheral plasma levels. The hypothesis that hemorrhage results in an increase in adrenal sensitivity to ACTH is tested in the following paper.

Adrenal Cortex Hormones↗
PubMed1982

Lesions of the organum vasculosum of the lamina terminalis (OVLT) attenuate osmotically-induced drinking and vasopressin secretion in the dog.

Drinking and secretion of arginine vasopressin (AVP) in response to intravenous infusion of hypertonic NaCl were studied in dogs before and after destruction of the OVLT. The functional relationship between plasma osmolality and plasma AVP was eliminated following destruction of the OVLT. Furthermore, osmotically-induced drinking was significantly reduced in dogs with OVLT lesions. These data are compatible with the hypothesis that the OVLT contains osmoreceptors in the dog.

Animals↗
PubMed1981

Effects of centrally administered endogenous opioid peptides on drinking behavior, increased plasma vasopressin concentration and pressor response to hypertonic sodium chloride.

Intracerebroventricular (i.v.t.) administration of beta-endorphin or leucine5-enkephalin inhibited drinking behavior, the pressor response and increased plasma vasopressin concentration stimulated by an acute elevation in CSF sodium chloride concentration (10 microliter, 1 M NaCl i.v.t.). These effects of endogenous opioid peptides were prevented by naloxone, indicating opiate receptors were required for the biologic response. Drinking behavior associated with regulatory stimuli operant during dehydration was also inhibited by opioid peptides. beta-Endorphin (i.v.t.) delayed the onset and/or reduced the volume of water consumed in response to hypertonic sodium chloride (relative cellular dehydration), polyethylene glycol (hypovolemia) and food-associated drinking behavior. Inhibition of drinking did not appear related to sensory-motor dysfunction as another motivated behavior, eating (onset, amount consumed) was unaffected by beta-endorphin. It is concluded from these results that centrally administered endogenous opioid peptides inhibit sodium chloride-stimulated cerebral mechanisms affecting blood pressure and hydration.

Animals↗
PubMed1981

Satiety and inhibition of vasopressin secretion after drinking in dehydrated dogs.

The roles of oropharyngeal and gastric factors in satiation and arginine vasopressin (AVP) secretion were examined in water-deprived dogs. Dogs were prepared with chronic gastric fistulas and received six treatments after 24 h of water deprivation: rehydration with H2O or extracellular fluid (ECF) with the fistula closed; rehydration with H2O or ECF with the fistula open; gastric administration of H2O or ECF via the fistula. Drinking occurred immediately after presentation and was always completed by 6 min. At the end of the 60-min period of observation, water was offered in order to assess the degree of satiety. No differences were observed between the volumes of H2O or ECF consumed. However, only absorption of the water drunk produced complete satiety assessed 60 min later. Drinking H2O caused a fall in plasma AVP 6 min before a detectable decline in osmolality and reached water-replete levels by 15 min after drinking. Drinking H2O or ECF plus removal via the fistula and drinking ECF also brought about a rapid decline in plasma AVP without any change in plasma osmolality. Gastric administration of H2O caused a fall in plasma AVP that coincided with the fall in osmolality, and gastric administration of ECF had no effect on plasma AVP. We conclude that oropharyngeal factors account for temporary satiety and the rapid inhibition of vasopressin secretion.

Animals↗
PubMed1981

Plasma volume, osmolality, vasopressin, and renin activity during graded exercise in man.

Plasma volume (PV), renin activity (PRA), and osmotic (Osm), sodium (Na+), and arginine vasopressin (AVP) concentrations were measured in venous blood samples taken before and after three levels of cycle ergometer exercise (100, 175, and 225 W) in 15 young male volunteers. Plasma volume and solute concentrations changed significantly (P less than 0.05, denoted by *) with work intensity. The % delta PV was -3.7%* at 100 W, -8.8%* at 175 W, and -12.4%* at 225 W. Plasma Na+ concentration, Osm, and AVP increase were curvilinear with graded exercise and were significant only when work intensity exceeded 40% VO2max. PRA increase was linear and significant at all work levels. The % delta PV was significantly correlated with delta Osm (r = 0.99*) and delta Na+ (r = 0.89*) but had low correlations with delta AVP (r = 0.22, NS) and delta PRA (r = 0.12, NS). However, delta AVP was significantly correlated with delta Na+ (r = 0.86*) and delta Osm (r = 0.83*), whereas delta PRA had low correlations with delta Na+ (r = 0.33, NS), delta Osm (r = 0.29, NS), and delta AVP (r = 0.43, NS). The data support the hypothesis that a) with exercise, AVP release is a primary factor for fluid and electrolyte regulation as it is highly correlated with the plasma hyperosmolality produced by a net hypotonic plasma efflux; b) an exercise intensity greater than 40% VO2max is required to change plasma osmolality and, thus, stimulate significant AVP release; and c) the stimulation of the renin-angiotensin system is a more general stress response, which responds to increasing sympathetic nervous activity.

Adult↗
PubMed1981

Exercise training hypotension: implications for plasma volume, renin, and vasopressin.

To determine the function of changes in plasma volume (PV), plasma renin activity (PRA), and arginine vasopressin (AVP) in the mechanism of the reduction of resting blood pressure during exercise training, resting supine, sitting, and standing systolic (SBP) and 5th-phase diastolic (DBP) blood pressures were measured in 10 men (19-24 yr) before and after an 8-day (2 h/day) training period on a cycle ergometer. The control group (5 men) exercised at 1.4 1/min [44% peak O2 uptake (VO2 max)] at 23.8 degrees C Tdb and 50% rh, and the acclimation group at 1.5 1/min (46% VO2 max) at 39.8 degrees C Tdb and 50% rh. After acclimation, resting supine and sitting DPB decreased (P less than 0.05) by 6 and 9 mmHg, respectively. There were no significant changes in DBP in the controls or in SBP in either group. After training, PV increased by 12.2% in controls and by 17.6% after acclimation. The resting hypotension could not be attributed to changes in resting levels of PV, AVP, or PRA. However, large decreases in PV and large increases in AVP and especially PRA during acclimation exposures suggest these responses may play a role in the chronic hypotensive response.

Acclimatization↗
PubMed1981

Orthostatic fluid-electrolyte and endocrine responses in fainters and nonfainters.

A tilt-table test was administered to five young men before (test 1) and after (test 2) 8 days of heat acclimation (2-h daily exercise at 50% VO2max at 40 degrees db, 30 degrees C wb) and to five other young men before and after the same exercise at 24 degrees C to determine fluid-electrolyte and endocrine responses in orthostasis in fainters and nonfainters. Half of the 10 subjects showed improved orthostatic reactions from test 1 to test 2 (disappearance of nausea and dizziness and improved heart rate and blood pressure), and the other 5 subjects showed no improvement. The improvement, especially in the nonfainters, was related to increases in posttilt plasma volume (PV) and plasma concentration of potassium. During test 1, plasma renin activity (PRA) increased five times from supine to orthostatis, with a corresponding increase in plasma vasopressin (ADH) of 50 times. The corresponding increases in test 2 were lower by 50 and 75% compared with those occurring in test 1 for PRA and ADH, respectively. PRA was five times higher in nonfainters than in fainters in test 1, whereas ADH showed an opposite trend. The orthostatic-induced increase in ADH seems to be related to volume control independent of PRA. This increase is reduced with improvement in orthostatic reactions, probably because of an increase in PV.

Adult↗
PubMed1981

Urethane anesthesia in rats. Altered ability to regulate hydration.

Anesthesia in rats produced by urethane administered intraperitoneally caused (1) peritoneal fluid accumulation; (2) inability to undergo a renal response to NaCl or water loading, and (3) pronounced hyperosmolality of body fluids without affecting plasma [Na+]. The impairment of the renal function appears not to be due to anesthesia per se, angiotensin, aldosterone, vasopressin or renal nerves. It probably is attributable to osmotoxicity of the mesenteric vasculature. By contrast, urethane administered intravenously evokes a brisk osmotic diuresis without fluid leakage into the peritoneum. Plasma osmolality is still increased. The osmotic toxicity to the mesenteric vasculature, poor renal function and altered composition of body fluids that occur after intraperitoneal urethane may complicate the interpretation of data obtained in rats anesthetized in this manner.

Aldosterone↗
PubMed1981

Insulin-induced hypoglycemia in conscious dogs. I. Dose-related pituitary and adrenal responses.

We have measured changes in plasma glucose, ACTH, corticosteroids, and vasopressin and hematocrit after five doses of insulin in six conscious dogs. We found insulin dose-related changes for each of these responses (P less than 0.01, by two-way analysis of variance). The increases in plasma ACTH and hematocrit correlated to the decrease in plasma glucose; the increase in plasma vasopressin was more strongly correlated with the increases in plasma Na+ than with the decreases in plasma glucose. Each dog appeared to have a characteristic ACTH response curve; therefore, the relationship between plasma glucose and plasma ACTH responses varied among dogs, but was significant in five of six dogs studied. Maximal plasma corticosteroid responses occurred with submaximal plasma ACTH responses (200-600 pg/ml). A single dose of insulin produced reproducible changes in plasma ACTH when given to five dogs in three separate experiments over a 2- to 6-month period. In these experiments, the measurement of ACTH allowed us to distinguish three levels of response to insulin, whereas measurement of the corticosteroid response allowed us to distinguish only two levels of response.

11-Hydroxycorticosteroids↗
PubMed1981

Endogenous opioid peptide inhibition of the central actions of angiotensin.

Effects of endogenous opioid peptides (leucine5-enkephalin; methionine5-enkephalin; and beta-endorphin) and morphine on isoleucine5-angiotensin II (All)-stimulated increase in plasma vasopressin concentration, blood pressure and drinking behavior were characterized in conscious rats. Plasma vasopressin concentration, drinking frequency and latency were measured 90 sec after intracerebroventricular (i.v.t.) All in animals pretreated with enkephalins, beta-endorphin or morphine, i.v.t. Vasopressin was measured by radioimmunoassay. A consistent dose-related, naloxone-sensitive inhibition of the All-stimulated increase in plasma vasopressin concentration and drinking behavior (frequency) occurred after enkephalins, beta-endorphin or morphine. beta-Endorphin and morphine were longer acting and more potent than enkephalins. In other experiments, All (i.v.t.) pressor activity, drinking volume and latency were measured at hourly intervals after opiates, i.v.t. The All-stimulated increase in mean blood pressure and drinking volume were inhibited by endogenous opioid peptides and morphine, i.v.t. Naloxone prevented opiate inhibition of the All pressor response. Endogenously synthesized opiates may modulate All activity as naloxone potentiated the pressor response and decreased water consumption after All, i.v.t. Continuous i.v. infusion of leucine-enkephalin did not affect All drinking or pressor activity, indicating a central nervous system site of inhibition. Opiate inhibition of the central actions of All appeared independent of sedation; head shakes or wet dog shakes occurred at effective doses of enkephalins. Naloxone did not affect basal blood pressure or plasma vasopressin concentration. Endogenous opioid peptides may modulate the central actions of angiotensin II affecting blood pressure and hydration.

Angiotensin II↗
PubMed1981

Opiate regulation of angiotensin-induced drinking and vasopressin release.

In rats, intracerebroventricular (i.v.t.) administration of endogenous opioid peptides inhibited angiotensin II-stimulated increase in plasma vasopressin concentration and drinking behavior. Naloxone and naltrexone were used to evaluate the effect of opiate receptor blockade on angiotensin drinking behavior. Both antagonists reduced the amount of water consumed and number of animals drinking in response to angiotensin II (i.v.t.). The time to onset of drinking was unaffected. Leucine5-enkephalin inhibition of angiotensin-stimulated release of vasopressin was also studied. Changes in plasma vasopressin concentration with time (5, 45, 90, 150 and 300 sec) were measured after a single i.v.t. injection of angiotensin II (50 ng), with and without pretreatment with leucine5-enkephalin (100 microgram i.v.t.). Vasopressin was measured by radioimmunoassay. The onset of vasopressin release occurred 5 to 45 sec after angiotensin, reaching peak response between 45 to 90 sec. Leucine5-enkephalin did not affect the onset but reduced the peak response to angiotensin (P less than .05). Saralasin, i.v.t., abolished angiotensin-stimulated increase in plasma vasopressin concentration and prevented the residual, but significant, increase in plasma vasopressin concentration in angiotensin-treated rats given enkephalin. It is concluded that angiotensin stimulates release of vasopressin by interaction with specific, saralasin-sensitive, receptors; leucine5-enkephalin inhibits angiotensin release of vasopressin; and an endogenously synthesized opiate ligand(s) may affect angiotensin drinking behavior.

Angiotensin II↗
PubMed1981

Hemodilution, vasopressin suppression, and diuresis during water immersion in man.

We hypothesize that hemodilution in the early stages of water immersion plays an important role in vasopressin (AVP) suppression and subsequent diuresis. Ten men (19-24 years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem years) were immersed to the neck in a semireclining position for 8 h in 34.6 degree C tap water. After 8 h of immersion there were decreases (p less than 0.05) in plasma volume (PV) of 15.6%, extracellular volume (ECV) of 18.8%, interstitial volume (ISV) of 19.6%, and red cell volume of 10.7%. Hemodilution (hyposmotem of 4 mosmol/kg H2O) and near maximal suppression of AVP (to 0.5 pg/ml) and plasma renin activity (to 0.4 ng Ang 1 .ml-1.h-1) were evident by hour 2 of immersion. The early hemodilution (2-2 h) was due to a slight increase in PV with no change in plasma Na+ or osmotic content, even though urine volume and UosmV increased significantly. The hyposmotemia and PRA suppression continued throughout immersion in spite of the progressively increasing diuresis and decreasing PV. These findings suggest the transfer of hypotonic fluid into the vascular system; this fluid does not appear to come from the intracellular volume. We conclude that hyposmotemia is an important part of the mechanism contributing to AVP suppression during water immersion.

Adult↗
PubMed1980

Arginine vasopressin and prolactin after hemorrhage in the fetal lamb.

Chronically prepared fetal lambs had basal plasma arginine vasopressin (AVP) levels of 1.6 +/- 0.23 pg/ml throughout the final third of gestation. Fetal AVP levels measured by radioimmunoassay were increased significantly to 5.8 +/- 0.92, 9.95 +/- 0.95, and 10.0 +/- 5 pg/ml in association with surgical stress, acute exteriorization, and acidosis or hypoxia, respectively. At 59-65 days gestation three lamb fetuses had a 50-fold increase in plasma AVP levels after acute exteriorization and hemorrhage indicating that the 0.4 gestation lamb fetus is capable of secreting pituitary AVP stores after intravascular volume change, temperature stress, and tactile stimulation. In six chronically catheterized third trimester fetuses, a 10-min, 20% hemorrhage caused a significant fall in fetal blood pressure, heart rate, and hematocrit. Plasma AVP increased significantly to 24.3 +/- 5.8 ng/ml without change in arterial blood gases or pH. Basal plasma prolactin concentration of 9.0 +/- 2.0 ng/ml was unchanged after hemorrhage in five fetuses.

Animals↗
PubMed1980

Thirst and vasopressin release in the dog: an osmoreceptor or sodium receptor mechanism?

The effects of intravenous infusion of hypertonic NaCl, sucrose, glucose, urea, or isotonic NaCl solution on thirst and plasma arginine vasopressin concentration (AVP) were studied in five conscious dogs. The changes in osmolality and sodium concentration of plasma and cerebrospinal fluid (CSF) were measured at the threshold of drinking, or after 45 min if no drinking occurred. Hypertonic NaCl and sucrose stimulated drinking in all dogs and significantly elevated plasma AVP. Equally hypertonic glucose, urea, or isotonic NaCl failed to stimulate any drinking or vasopressin secretion. All hypertonic solutions caused significant and similar increases in the osmolality and sodium concentration of CSF. Plasma osmolality was increased by the hypertonic solutions. Plasma sodium was increased by hypertonic NaCl, decreased by sucrose and glucose, and not changed by urea. Isotonic NaCl had no effect on either plasma or CSF composition. These data are not consistent with either a sodium or an osmoreceptor mechanism located within the blood-brain barrier (BBB) or with a peripheral sodium receptor mechanism. An intracranial osmoreceptor located on the blood side of the BBB is proposed to explain these results.

Animals↗
PubMed1980

Drinking and vasopressin release during ventricular infusions of hypertonic solutions.

Six dogs were administered third ventricular infusions of artificial cerebrospinal fluid (CSF) (292 mosmol/l) alone or artificial CSF to which neither NaCl, sucrose, glucose, or urea was added to yield a final osmolar concentration of 500 mosmol/l. The volume of water drunk during 45 min of infusion was measured and blood was sampled for determination of plasma vasopressin concentration at 15-min intervals. Artificial CSF made hypertonic by addition of NaCl or sucrose stimulated water intakes of 9.0 +/- 3.2 ml/kg (mean +/- SE) and 7.3 +/- 3.7 ml/kg, respectively. There was no statistical difference in the amounts drunk and the latencies. In contrast, artificial CSF containing glucose, urea, or artificial CSF alone were without effect. Plasma vasopressin concentration increased significantly in response to intraventricular NaCl and sucrose but was not affected by glucose, urea, or artificial CSF alone. These data are compatible with an osmoreceptor mechanism mediating drinking and vasopressin release.

Animals↗