Characteristics of body temperature, vasopressin, and oxytocin responses to endotoxin in the rat

1986 ◽  
Vol 64 (12) ◽  
pp. 1575-1578 ◽  
Author(s):  
N. W. Kasting
Keyword(s):  
Body Temperature ◽  
Temperature Response ◽  
Base Line ◽  
Subsequent Increase ◽  
Temperature Plasma ◽  
Strong Negative Correlation ◽  
Vasopressin Release ◽  
Endotoxin Administration ◽  
Physiological Variables ◽  
Plasma Vasopressin

Several physiological variables were measured after endotoxin administration in the rat to examine the relationship between these variables. Rats responded to endotoxin with a biphasic body temperature response, an initial decrease and a subsequent increase in body temperature. Plasma vasopressin and oxytocin levels increased markedly after endotoxin administration. Diarrhea occurred in some animals. There was a strong negative correlation between increase in body temperature and base-line body temperature, and weak correlations between body weight and plasma vasopressin release and between base-line body temperature and minimum body temperature reached. Plasma vasopressin and oxytocin levels were correlated if samples from all time points were analyzed together, whereas they were not correlated if data from each time point were analyzed separately or if total peptide release for each rat was evaluated. These data suggest similar regulation for the release of vasopressin and oxytocin, that is, release by a common stimulus, but the magnitude of release of vasopressin and oxytocin appears to be independent, probably reflecting differences in synthesis and storage of these two peptides.

Hypothalamic thermal stimulation modulates vasopressin release in hyperosmotically stimulated rabbits

1994 ◽  
Vol 267 (4) ◽  
pp. R1089-R1097 ◽  
Author(s):  
R. Keil ◽  
R. Gerstberger ◽  
E. Simon
Keyword(s):  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Significant Rise ◽  
Hypertonic Solution ◽  
Temperature Plasma ◽  
Evaporative Water ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Hypothalamic Control ◽  
Hypertonic Stimulation

Under thermoneutral conditions conscious rabbits received systemic infusions of NaCl as hypertonic solution (90 mueq.min-1.kg body wt-1), which raised their plasma osmolality from 283 to 312 mosmol/kgH2O. Rabbits receiving isotonic saline served as controls. Hypertonic stimulation induced a 60% reduction of both respiratory frequency and evaporative water loss. Rectal temperature rose by 0.4 degrees C despite enhanced peripheral vasodilation as indicated by increased ear skin temperature. Plasma vasopressin (AVP), aldosterone (ALDO), and corticosterone (COR) were significantly elevated from 6 to 16 pg/ml, 90 to 180 pg/ml, and 17 to 40 ng/ml, respectively. To elucidate the importance of central temperature for AVP and adrenal corticosteroid release, hypothalamic thermal stimulations (20 min) were superimposed during established iso- and hyperosmotic steady-state conditions. Different from isosmotic controls, hyperosmotic animals responded to hypothalamic cooling (37 degrees C) with a significant decrease in plasma AVP from 16 to 13 pg/ml and to hypothalamic warming (41 degrees C) with a significant rise from 16 to 19 pg/ml. A weak temperature effect on COR release was also disclosed, especially of hypothalamic cooling, which significantly lowered plasma COR from 42 to 34 ng/ml. These results provide evidence for positive local temperature coefficients of hypothalamic control of AVP release and suggest a similar property also for the control of COR release by the hypothalamo-adenohypophysial axis.

Vasopressin in plasma and ventricular cerebrospinal fluid during dehydration, postural changes, and nausea

1985 ◽  
Vol 248 (1) ◽  
pp. R78-R83 ◽  
Author(s):  
P. S. Sorensen ◽  
M. Hammer
Keyword(s):  
Cerebrospinal Fluid ◽  
Plasma Concentration ◽  
Plasma Osmolality ◽  
High Plasma ◽  
Base Line ◽  
Vasopressin Release ◽  
Modest Increase ◽  
Plasma Vasopressin ◽  
Postural Changes ◽  
Head Up Tilt

The responses of plasma and ventricular cerebrospinal fluid (CSF) vasopressin concentration to dehydration, postural changes, and induction of nausea were studied in 21 patients with hydrocephalus of various etiology. The 24-h dehydration test evoked a significant increase in plasma osmolality and vasopressin concentration, whereas the concentration of vasopressin in CSF was unchanged. Head-up tilt to 50 degrees for 45 min with a tilt bed resulted in a modest increase of plasma vasopressin in patients who did not develop presyncopal symptoms, but no changes were seen in CSF vasopressin. Induction of nausea by subcutaneously injected apomorphine provoked a marked (20- to 50-fold) rise in plasma vasopressin concentration within 15 min, and the plasma concentration was significantly increased above base-line values for 60-120 min. Despite the prolonged period of high plasma vasopressin concentration CSF vasopressin was not influenced by the apomorphine injection. The findings suggest that the concentration of vasopressin in the CSF is controlled by mechanisms other than the well-known osmotic and nonosmotic stimuli of vasopressin release into the blood.

Effects of water immersion on arginine vasopressin release in humans

1988 ◽  
Vol 64 (1) ◽  
pp. 1-10 ◽  
Author(s):  
P. Norsk ◽  
M. Epstein
Keyword(s):  
Water Intake ◽  
Arginine Vasopressin ◽  
Critical Review ◽  
Water Immersion ◽  
Base Line ◽  
Vasopressin Release ◽  
Arterial Baroreceptors ◽  
Lower Base

Since suppression of arginine vasopressin (AVP) appears to be a determinant of the diuresis of water immersion (WI) in humans, a further understanding of its responsiveness has important implications for normal physiology, pathophysiology, and space physiology. In recent years, discrepant measurements of AVP in plasma during WI have led to conflicting conclusions. In studies in which the subjects ingested water before or during WI, plasma AVP was reported to be unchanged or even increased. In contrast, plasma AVP was suppressed in studies in which the subjects remained hydropenic. A critical review discloses that water intake before and/or during the experiments introduces several new stimuli for AVP release. Furthermore the lower base-line levels of AVP in hydrated subjects complicate detection of small changes in plasma AVP. Although the mechanisms of AVP suppression during WI are incompletely defined, it appears that not only cardiopulmonary mechanoreceptors but also arterial baroreceptors mediate the response. Additional studies are proposed to delineate further the mechanisms governing AVP release during WI.

Osmoregulation of thirst and vasopressin during normal menstrual cycle

1988 ◽  
Vol 254 (4) ◽  
pp. R641-R647 ◽  
Author(s):  
T. J. Vokes ◽  
N. M. Weiss ◽  
J. Schreiber ◽  
M. B. Gaskill ◽  
G. L. Robertson
Keyword(s):  
Menstrual Cycle ◽  
Luteal Phase ◽  
Plasma Osmolality ◽  
Free Water ◽  
Urine Osmolality ◽  
Free Water Clearance ◽  
Vasopressin Release ◽  
Plasma Vasopressin ◽  
Normal Menstrual Cycle ◽  
Basal Plasma

Changes in osmoregulation during normal menstrual cycle were examined in 15 healthy women. In 10 women, studied repetitively during two consecutive menstrual cycles, basal plasma osmolality, sodium, and urea decreased by 4 mosmol/kg, 2 meq/l, and 0.5 mM, respectively (all P less than 0.02) from the follicular to luteal phase. Plasma vasopressin, protein, hematocrit, mean arterial pressure, and body weight did not change. In five other women, diluting capacity and osmotic control of thirst and vasopressin release were assessed in follicular, ovulatory, and luteal phases. Responses of thirst and/or plasma vasopressin, urine osmolality, osmolal and free water clearance to water loading, and infusion of hypertonic saline were normal and similar in the three phases. However, the plasma osmolality at which plasma vasopressin and urine osmolality were maximally suppressed as well as calculated osmotic thresholds for thirst and vasopressin release were lower by 5 mosmol/kg in the luteal than in the follicular phase. This lowering of osmotic thresholds for thirst and vasopressin release, which occurs in the luteal phase, is qualitatively similar to that observed in pregnancy and should be taken into account when studying water balance and regulation of vasopressin secretion in healthy cycling women.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Effect of salicylates on elevation of body temperature during exercise

1962 ◽  
Vol 17 (2) ◽  
pp. 323-325 ◽  
Author(s):  
John A. Downey ◽  
Robert C. Darling
Keyword(s):  
Body Temperature ◽  
Acetylsalicylic Acid ◽  
Rectal Temperature ◽  
Temperature Response ◽  
Young Men ◽  
Work Load ◽  
Conclusive Evidence ◽  
Blood Levels ◽  
Total Proteins ◽  
Before And After

An attempt was made to determine the effect of orally ingested acetylsalicylic acid (ASA) in moderate amounts for varying periods of time, on temperature response of ten healthy young men walking on a power-driven treadmill with a work load of approximately 6 mets. Three experiments were conducted, ranging from one dose of 1.8–2.4 g ASA to 3.6–4.8 g/day in divided doses for 48 hr, and the same amount in divided doses for 5–7 days, the dose in the first experiment and the last dose in those following being given 1frac12–2 hr before exercise. Rectal temperature was measured at rest, during exercise, and for 20–45 min of recovery. Blood levels of salicylate were determined, hematocrits were recorded, and total proteins were determined; each subject was weighed before and after exercise. It was found that rise in body temperature was not modified by ASA in any of the various dosages, nor was significant hemodilution of the blood caused. Suggestive, but not conclusive, evidence emerged indicating that salicylates accelerate the early stages of the fall in body temperature after exercise. Submitted on October 5, 1961

Vasopressin release within the ventral septal area of the rat brain during drug-induced antipyresis

1993 ◽  
Vol 264 (6) ◽  
pp. R1133-R1138 ◽  
Author(s):  
M. F. Wilkinson ◽  
N. W. Kasting
Keyword(s):  
Body Temperature ◽  
Rat Brain ◽  
Extracellular Fluid ◽  
Subsequent Treatment ◽  
Septal Area ◽  
Nerve Terminals ◽  
Perfusion Fluid ◽  
Drug Induced ◽  
Vasopressin Release ◽  
Neuronal Mechanisms

The techniques of push-pull perfusion and radioimmunoassay were used to determine concentrations of arginine vasopressin (AVP) in extracellular fluid derived from the ventral septal area (VSA) of the rat brain following antipyresis elicited by acetaminophen or indomethacin in conscious and unrestrained rats. Reduction of bacterial lipopolysaccharide (LPS)-induced fever by intraperitoneal indomethacin resulted in significant increases in AVP levels in VSA perfusion fluid (P < 0.05). In contrast, antipyresis after acetaminophen treatment was without significant effect on AVP output from VSA nerve terminals. In control animals (non-pyrogen treated), body temperature rose in apparent response to the perfusion procedure. Despite this elevation in core temperature, subsequent treatment with acetaminophen or indomethacin did not result in significant changes in AVP release from VSA perfusates. We conclude that AVP release into VSA extracellular fluids following intraperitoneal indomethacin is dependent upon the neuronal sequelae inherent to pyrogen-evoked fever and not nonspecific rises in body temperature. These results support the hypothesis that endogenous AVP, acting within the VSA, participates in the neuronal mechanisms mediating indomethacin-induced antipyresis.

Thermal responses of unclothed men exposed to both cold temperatures and high altitudes

1975 ◽  
Vol 39 (5) ◽  
pp. 796-800 ◽  
Author(s):  
L. F. Cipriano ◽  
R. F. Goldman
Keyword(s):  
Body Temperature ◽  
Ambient Temperature ◽  
Sea Level ◽  
Initial Rate ◽  
Base Line ◽  
High Altitudes ◽  
Level Control ◽  
Cold Temperatures ◽  
Skin Temperatures

Six resting men were exposed to three temperatures (15.5, 21, 26.5 degrees C) for 120 min at three altitudes (sea level, 2,500 m, 5,000 m). A 60-min sea-level control at the scheduled temperature preceded the nine altitude episodes. Comparison of the base-line results at any one temperature showed no differences between rectal temperatures (Tre) or mean weighted skin temperatures (Tsk). After 120 min, Tre and Tsk not only depended on ambient temperature but also altitude. The initial rate of fall in Tre increased with altitude and equilibrium occurred earlier. At 15.5 degrees C, Tre was 0.3 degrees C lower at 5,000 m and 0.2 degrees C lower at 2,500 m than at sea level. Tsk was almost 2 degrees C higher at 15.5 degrees C at 5,000 m and 1 degrees C higher at 2,500 m than at sea level. Similar, smaller differences were observed at 21 degrees C. Mean weighted body temperature showed no change with altitude, but, since the gradient between core and shell was reduced, a shift of blood toward the periphery is implied.

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