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.

Central vasopressin V1-blockade prevents salicylate but not acetaminophen antipyresis

1990 ◽  
Vol 68 (5) ◽  
pp. 1793-1798 ◽  
Author(s):  
M. F. Wilkinson ◽  
N. W. Kasting
Keyword(s):  
Rat Brain ◽  
Core Temperature ◽  
Mechanism Of Action ◽  
Arginine Vasopressin ◽  
Sodium Salicylate ◽  
Septal Area ◽  
Receptor Blockade ◽  
Drug Induced ◽  
Normal Core ◽  
The Brain

Recent evidence has suggested that the endogenous antipyretic arginine vasopressin (AVP) may participate in drug-induced antipyresis. This study sought to further those investigations by comparing the effects of two other antipyretic drugs, sodium salicylate and acetaminophen, administered intraperitoneally, during AVP V1-receptor blockade within the ventral septal area (VSA) of the rat brain. During endotoxin-evoked fever, V1-receptor blockade within the VSA of the conscious unrestrained rat significantly antagonized the antipyretic effects of salicylate. The effects of the V1-antagonist on salicylate-induced antipyresis were dose related. In contrast, the antipyresis elicited by acetaminophen was unaffected by VSA V1-antagonist pretreatment. Neither saline nor the V1-antagonist microinjected into the VSA of febrile or nonfebrile rats had any significant effects on the normal progression of endotoxin fever or normal core temperature, respectively. These data suggest that the mechanism of action of salicylate-induced antipyresis includes activation of AVP V1-type receptors within the VSA, as has been shown for indomethacin. However, the lack of effect of the V1-antagonist on antipyresis induced by acetaminophen indicates that not all antipyretic drugs act through the same mechanism in the brain.

Vasopressin and oxytocin in rat brain in response to prostaglandin fever

1990 ◽  
Vol 259 (5) ◽  
pp. R1056-R1062 ◽  
Author(s):  
R. Landgraf ◽  
T. J. Malkinson ◽  
W. L. Veale ◽  
K. Lederis ◽  
Q. J. Pittman
Keyword(s):  
Body Temperature ◽  
Rat Brain ◽  
Arginine Vasopressin ◽  
Prostaglandin E1 ◽  
Dorsal Hippocampus ◽  
Significant Rise ◽  
Septal Area ◽  
Intracerebroventricular Injection ◽  
Body Temperatures ◽  
The Brain

Urethan-anesthetized rats were used to identify effective stimuli for the release of the peptides arginine vasopressin (AVP) and oxytocin into the ventral septal area (VSA) of the brain. Febrile responses to intracerebroventricular injection of prostaglandin E1 (PGE1) were observed in rats whose body temperatures were maintained at 35, 37, or 39 degrees C. Microinjection of the AVP antagonist d(CH2)5Tyr(Me)AVP into the VSA enhanced fever only when PGE1 administration was associated with a significant rise in body temperature. Passive elevation (“artificial fever”) or reduction of body temperature in the absence of a PGE1 stimulus was not affected by the antagonist. Push-pull perfusion of the VSA and the dorsal hippocampus, followed by radioimmunoassay of perfusates for AVP and oxytocin, revealed enhanced release into the VSA of AVP only when PGE1 administration was followed by a rise in body temperature. Oxytocin was released whenever body temperature was raised. Peptide concentrations in simultaneous perfusates of dorsal hippocampus did not change in response to PGE1 administration or to passive elevation of body temperature. We conclude that AVP is released into the VSA, but not the dorsal hippocampus, of the rat during a fever induced by PGE1. Oxytocin is released into the VSA, but not the hippocampus, when temperature is elevated.

scholarly journals Vasopressin at Central Levels and Consequences of Dehydration

2016 ◽  
Vol 68 (Suppl. 2) ◽  
pp. 19-23 ◽  
Author(s):  
Daniel G. Bichet
Keyword(s):  
Animal Studies ◽  
Transient Receptor Potential ◽  
Animal Experiments ◽  
Extracellular Fluid ◽  
Receptor Potential ◽  
Circumventricular Organ ◽  
Thermal Perception ◽  
Trpv1 Channel ◽  
Vasopressin Release ◽  
Transient Receptor

Disorders of water balance are a common feature of clinical practice. An understanding of the physiology and pathophysiology of central vasopressin release and perception of thirst is the key to diagnosis and management of these disorders. Mammals are osmoregulators; they have evolved mechanisms that maintain extracellular fluid osmolality near a stable value, and, in animal studies, osmoregulatory neurons express a truncated delta-N variant of the transient receptor potential vannilloid (TRPV1) channel involved in hypertonicity and thermal perception while systemic hypotonicity might be perceived by TRPV4 channels. Recent cellular and optogenetic animal experiments demonstrate that, in addition to the multifactorial process of excretion, circumventricular organ sensors reacting to osmotic pressure and angiotensin II, subserve genesis of thirst, volume regulation and behavioral effects of thirst avoidance.

Drug-induced alterations of 3-methoxy-4-hydroxyphenylethanol (MHPE) in rat brain

1973 ◽  
Vol 8 (1) ◽  
pp. 61-71 ◽  
Author(s):  
L.D. Waterbury ◽  
O.T. Wendel ◽  
L.A. Pearce
Keyword(s):  
Rat Brain ◽  
Drug Induced

Extracellular and intracellular carbon dioxide concentration as a function of temperature in the toad Bufo marinus.

1994 ◽  
Vol 195 (1) ◽  
pp. 345-360 ◽  
Author(s):  
J N Stinner ◽  
D L Newlon ◽  
N Heisler
Keyword(s):  
Body Temperature ◽  
Extracellular Fluid ◽  
Carbon Dioxide Concentration ◽  
The Body ◽  
Whole Body ◽  
Mean Values ◽  
Temperature Changes ◽  
Fluid Compartment ◽  
Average Change ◽  
Higher Temperature

Previous studies of reptiles and amphibians have shown that changing the body temperature consistently produces transient changes in the respiratory exchange ratio (RE) and, hence, changes in whole-body CO2 stores, and that the extracellular fluid compartment contributes to the temperature-related changes in CO2 stores. The purpose of this study was to determine whether the intracellular fluid compartment contributes to the changes in CO2 stores in undisturbed resting cane toads. Increasing body temperature from 10 to 30 degrees C temporarily elevated RE, and returning body temperature to 10 degrees C temporarily lowered RE. The estimated average change in whole-body CO2 stores associated with the transient changes in RE was 1.0 +/- 0.8 mmol kg-1 (+/- S.D., N = 6). Plasma [CO2] and, thus, extracellular fluid [CO2], were unaffected by the temperature change. Plasma calcium levels were also unaffected, so that bone CO2 stores did not contribute to changes in whole-body CO2 stores. Intracellular [CO2] was determined for the lung, oesophagus, stomach, small intestine, liver, ventricle, red blood cells, skin and 14 skeletal muscles. [CO2] was significantly lower (P &lt; 0.05) at higher temperature in 10 of these, and seven others, although not statistically significant (P &gt; 0.05), had mean values at least 0.5 mmol kg-1 lower at the higher temperature. The average change in intracellular [CO2] for all tissues examined was -0.165 mmol kg-1 degrees C-1. We conclude that, in cane toads, the temperature-related transients in RE result from intracellular CO2 adjustments, that different tissues have unique intracellular CO2/temperature relationships, and that a combination of respiratory and ion-exchange mechanisms is used to adjust pH as temperature changes.

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