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Biomedical subjects

L C Keil

Publications and source records attributed to L C Keil.

At least 127 records · Page 7Linked to original sources
PubMed1983

Hypervolemia and plasma vasopressin response during water immersion in men.

To investigate changes in plasma volume (PV) and osmolality as stimuli for plasma vasopressin (PVP) suppression and diuresis, seven normal healthy men (22-48 yr) were immersed to the neck for 4 h in a sitting position in tap water (34.5 degrees C) after overnight food and fluid restriction. Mean +/- SE urine volume was 823 +/- 123 ml/4 h; fluid intake was 400 ml/4 h, and mean negative water balance was 944 ml/4 h. Urinary sodium excretion increased from 0.77 to 1.25 mosmol/min (P less than 0.05) and UNaV from 0.14 to 0.37 meq/min (P less than 0.05). During immersion, PV (T-1824) increased by 8.8% (P less than 0.05) during the first 30 min and declined linearly thereafter. Mean +/- SD serum osmolality (294 +/- 1.2 mosmol/kg H2O) and sodium (143.2 +/- 0.4 meq/l) were constant throughout immersion; PVP (2.3 +/- 0.5 pg/ml) and plasma renin activity [0.3 +/- 0.2 ng ANG I/(ml X h]) were not significantly changed. Thus, the composition of the fluid entering the vascular space maintained constant serum osmolality and PVP throughout immersion. These findings do not support the hypothesis that acute expansion of central volume and PV cause suppression of PVP. The results suggest a mechanism other than or in addition to PVP suppression as a contributory cause of the immersion diuresis.

Adult↗
PubMed1983

Deficits in drinking and vasopressin secretion after lesions of the nucleus medianus.

The effects of ablation of the nucleus medianus on drinking and vasopressin secretion were studied in male Long-Evans rats. The amount of water drunk in 1 h was assessed after subcutaneous injection of 5.8% NaCl (13.34 mosm/kg) or of angiotensin II (1.5 mg/kg). In a separate test with no water available, plasma vasopressin was measured 15 min after the above dose hypertonic saline. Ablation of the nucleus medianus, or the dorsal and anterior portions of the nucleus medianus, blocked drinking to hypertonic saline or angiotensin II and attenuated the vasopressin response to hyperosmolality. Animals with septal or diagonal band lesions showed responses comparable to sham-operated rats. These results indicate that a neural pathway important for fluid balance passes through, or terminates in, the nucleus medianus.

Angiotensin II↗
PubMed1983

Role of volume and osmolality in the control of plasma vasopressin in dehydrated dogs.

Plasma vasopressin concentrations (pAVP) are elevated during dehydration due to alterations in extracellular fluid (ECF) volume and tonicity. The contributions of the reduction in volume and increase in plasma osmolality to the rise in pAVP were assessed in 6 dogs with bilateral carotid loops following 24 h of fluid, but not food, deprivation. Dehydration significantly (p less than 0.05) increased plasma osmolality from 297 +/- 1 to 315 +/- 2 mosm/kg), decreased body weight from 20.8 +/- 1.2 to 20.3 +/- 1.2 kg, and elevated pAVP from 1.4 +/- 0.2 to 5.3 +/- 0.6 pg/ml. The effect of extracellular fluid volume reduction was tested by reexpanding this compartment in dehydrated dogs with 0.15 M NaCl. Plasma vasopressin concentration was significantly reduced by 1.3 +/- 0.2 pg/ml (33 +/- 4%) and plasma osmolality unchanged following volume replacement. The contribution of the increase in plasma osmolality was assessed by bilateral intracarotid infusions of water at 0.6 ml/min/artery which lowered jugular venous plasma osmolality to euhydrated values (296 +/- 4 mosm/kg), but did not significantly reduce systemic plasma osmolality. Plasma vasopressin levels were significantly reduced 3.2 +/- 1.1 pg/ml (70 +/- 5%). Thus, following 24 h of fluid deprivation in dogs, the rise in pAVP is due to changes in both ECF volume and tonicity. The increase in tonicity plays a greater role in the elevation of pAVP, than the reduction in volume.

Animals↗
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↗
PubMed1983

Role of vasopressin in blood pressure regulation during adrenal insufficiency.

The effect of adrenal insufficiency on the plasma concentrations of two vasoactive hormones, vasopressin and angiotensin II, was studied in conscious dogs. In addition the role of vasopressin in the maintenance of blood pressure during adrenal insufficiency was studied using [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin, a specific antagonist of the vasoconstrictor action of vasopressin. Dogs were bilaterally adrenalectomized and maintained on daily cortisol and deoxycorticosterone acetate injections. Withdrawal of steroids for 4 days resulted in a 4-fold increase in plasma vasopressin concentration (P less than 0.05) and a 3-fold increase in plasma angiotensin II concentration (P less than 0.001); mean arterial pressure did not change significantly. Administration of the vasopressin antagonist in adrenalectomized dogs maintained on steroids had no effect on blood pressure. In marked contrast, vasopressin blockade in dogs with adrenal insufficiency decreased mean arterial pressure by 22 +/- 5 mm Hg (P less than 0.001). These results demonstrate the plasma angiotensin II and vasopressin concentrations increase during adrenal insufficiency in conscious dogs, and that vasopressin plays an important role in blood pressure regulation in this hypovolemic state.

Adrenal Insufficiency↗
PubMed1982

Hormonal and hemodynamic responses to vena caval obstruction in fetal sheep.

To test the hypothesis that ACTH and vasopressin responses are quantifiable as functions of induced changes in central venous or arterial pressures, we produced various degrees of vena caval obstruction in fetal sheep (118--134 days gestation). In seven experiments, vena caval obstruction increased heart rate 18 +/- 7 beats/min and carotid arterial oxygen saturation 8.4 +/- 2.1%, but did not alter any measured vascular pressure or hormones. More severe vena caval obstruction (n = 10) decreased mean arterial pressure 13 +/- 2 mmHg, central venous pressure 1.3 +/- 0.3 mmHg, and heart rate 47 +/- 12 beats/min, and increased fetal plasma ACTH 1,047 +/- 448 pg/ml, cortisol 4.4 +/- 2.2 ng/ml, and vasopressin 47.9 +/- 24.2 pg/ml, but did not alter 11-deoxycortisol. The stimulus increased plasma cortisol (radioimmunoassay after chromatography) 100% and "corticosteroids" (radiotransinassay without chromatography) 20%, demonstrating the nonlinear relationship between these two variables. End-inflation plasma ACTH and vasopressin concentrations were significantly related to the induced decreases in mean arterial and central venous pressures, suggesting that the hormonal responses to vena caval obstruction were mediated by cardiovascular mechanoreceptors. Plasma vasopressin concentrations were linearly related to plasma ACTH concentrations (4 = 0.94; P less than 0.001), suggesting parallel release of the two hormones.

Adrenal Cortex Hormones↗
PubMed1982

Osmotic control of plasma vasopressin in the dog.

Seven dogs prepared with carotid loops were used to evaluate the responsiveness of the cerebral osmoreceptors regulating plasma vasopressin concentration (pAVP). Intracarotid and intravenous infusions of hypo- and hypertonic solutions were used to alter cerebral plasma osmolality. Bilateral intracarotid infusion of hypertonic saline (0.90 mmol NaCl kg-1 . min-1 . artery-1) significantly elevated jugular vein plasma osmolality (pOsm) in the first minute (P less than 0.05). Systemic values, determined from saphenous vein samples, were increased after 6 min. After 4 min of infusion, systemic pAVP was significantly increased, attaining a constant level at 6 min. Subsequent experiments with infusions 6 min in duration demonstrated that hypertonic saline infused intracarotidly significantly increased pAVP in a dose-related fashion, whereas similar solutions administered intravenously did not alter pAVP. Hypotonic infusions (intravenous or intracarotid) did not change pAVP consistently. The lack of a depression in pAVP during hypotonic infusions is consistent with the argument that jugular pOsm must be elevated above a threshold to stimulate the release of vasopressin. Linear relationships were demonstrated for jugular pNa+ and pOsm to pAVP employing the threshold model. Cerebral osmoreceptors that regulate plasma vasopressin concentration respond linearly to increasing tonicity above a threshold stimulating the release of vasopressin.

Animals↗
PubMed1982

Effect of hypertonic intracarotid infusions on plasma vasopressin concentration.

The effect of short-term bilateral intracarotid infusions of hypertonic saline on plasma vasopressin concentration (pAVP) was evaluated in five dogs. Intracarotid infusion of saline at 90 mumol . kg-1 . min-1 . artery-1 significantly (P less than 0.05) increased jugular vein osmolality (pOsm) and sodium concentration (pNa+) within 2 min. Saphenous vein pOsm was not altered during the 6 min of infusion, whereas pNa+ was increased (P less than 0.05) from 0.8 +/- 0.1 to 2.3 +/- 0.3 pg/ml. Subsequent experiments using hypertonic saline infusions of 90 and 180 mumol . kg-1 . min-1 administered intracarotidly and intravenously for 6 min were performed. Intracarotid isotonic infusions and intravenous hypertonic infusions did not significantly alter pAVP. Hypertonic intracarotid saline increased jugular vein pOsm and pNa+ in a dose-related fashion, whereas saphenous vein pOsm and pNa+ were not significantly changed after 6 min of infusion. Plasma vasopressin, compared with the isotonic intracarotid infusion (1.5 +/- 0.3 pg/ml), was increased (P less than 0.05) after hypertonic saline to 3.2 +/- 0.6 and 4.8 +/- 0.2 pg/ml for the 90 and 180 mumol . kg-1 . min-1 infusions, respectively. The cerebral osmolality indicated by jugular vein pOsm was therefore increased in the absence of changes in systemic pOsm during intracarotid hypertonic infusions. The increase in pAVP in response to these changes in pOsm supports the presence of central osmoreceptors regulating vasopressin release in the area of distribution of the common carotid arteries.

Adrenocorticotropic Hormone↗
PubMed1982

Analysis of the actions of angiotensin on the central nervous system of conscious dogs.

Angiotensin II (ANG II) acts on the brain to elevate blood pressure (BP), stimulate drinking, increase the secretion of vasopressin and corticotropin (ACTH), and inhibit the secretion of renin. The present studies were designed to evaluate the possible physiological significance of these effects. The experiments were performed in conscious dogs with small catheters chronically implanted in both carotid and both vertebral arteries. ANG II was infused into both carotid or both vertebral arteries in doses of 0.1, 0.33, 1.0, and 2.5 ng.kg-1.min-1. Intravertebral ANG II produced dose-related increases in BP that were generally accompanied by increases in heart rate. Intracarotid angiotensin also increased BP but did not change heart rate. Intracarotid ANG II stimulated drinking and, at the highest dose only, increased the secretion of vasopressin, ACTH, and corticosteroids. Intravertebral and intracarotid ANG II suppressed plasma renin activity (PRA). In a parallel series of experiments, the effects of intravenous ANG II, in doses of 2, 5, 10, and 20 ng.kg-1.min-1, were studied. These infusions produced dose-related increases in BP and water intake and suppressed PRA. Only the highest dose of ANG II increased vasopressin or corticosteroid secretion. Analysis of these results in terms of calculated or measured changes in plasma ANG II concentration indicate that the central cardiovascular and dipsogenic actions of angiotensin, as well as the suppression of PRA, can be elicited by concentrations of the peptide that are within the physiological range. On the other hand high, probably supraphysiological, levels of ANG II are required to increase vasopressin or ACTH secretion.

Adrenal Cortex Hormones↗
PubMed1982

Hemodynamic, hormonal, and drinking responses to reduced venous return in the dog.

The effect of an acute reduction in venous return, caused by reversible constriction of the thoracic vena cava, on drinking and secretion or arginine vasopressin (AVP) was examined in the dog. Plasma AVP levels rose immediately from a control level of 1.4 +/- 0.1 pg/ml (mean +/- SE) to a plateau ranging between 36 and 42 pg/ml during the first 30 min after constriction but declined to 12.6 +/- 4.2 pg/ml 2 h after constriction even though systemic arterial hypotension was maintained. Drinking occurred with a latency of 22 +/- 6 min and 13.2 +/- 1.8 ml H2O/kg was consumed during 2 h of vena caval constriction. Water intake was significantly correlated with the average reduction in blood pressure (r = 0.86; n = 8; P less than 0.01) but not with plasma renin activity. The role of angiotensin II (ANG II) in the drinking and secretion of AVP in response to decreased venous return was evaluated using the ANG II receptor blocker, saralasin, infused intravenously (iv) or intracerebroventricularly (icv). Intravenous, but not icv, infusion of saralasin during vena caval constriction reduced the ability of the dogs to maintain arterial blood pressure (P less than 0.05). However, neither iv nor icv saralasin significantly affected water intake or the rise in plasma AVP in response to vena caval constriction when compared to their respective controls. Taken together, these data show that angiotensin is important in the maintenance of systemic arterial blood pressure but is not essential for the rise in plasma AVP or drinking in response to an acute reduction in venous return. It is suggested that either arterial baroreceptors or "low-pressure" volume receptors or both mediate the drinking and AVP responses in the presence of central blockade of the effects of circulating angiotensin.

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↗