Angiotensin II inhibits both heat production and heat loss mechanisms in the rat

1980 ◽  
Vol 58 (8) ◽  
pp. 909-914 ◽  
Author(s):  
M. T. Lin ◽  
A. Chandra ◽  
J. J. Jou
Keyword(s):  
Angiotensin Ii ◽  
Heat Loss ◽  
Heat Production ◽  
Ambient Temperatures ◽  
Thermoregulatory Responses ◽  
Adrenergic Antagonist ◽  
Intracerebroventricular Injections ◽  
6 Hydroxydopamine ◽  
Dose Dependent ◽  
Loss Mechanisms

The effects of intracerebroventricular injections of angiotensin II on thermoregulatory responses of conscious rats to ambient temperatures (Ta) of 8, 22, and 30 °C were assessed. Administration of angiotensin II produced dose-dependent hypothermia in rats at both Ta 8 and 22 °C. The hypothermia in response to angiotensin II was due to decreased metabolic heat production. In addition, angiotensin II produced cutaneous vasoconstriction at Ta 8–22 °C. However, at Ta 30 °C angiotensin II produced no change in rectal temperature or other thermoregulatory responses. Furthermore, the hypothermia induced by angiotensin II was antagonized by pretreatment with 6-hydroxydopamine (a selective catecholamine neurotoxin) and propranolol (a selective β-adrenergic antagonist) but not by either 5,6-dihydroxytryptamine (a selective serotonin neurotoxin), atropine (a cholinergic antagonist), or phentolamine (a selective α-adrenergic antagonist). The data indicate that angiotensin II inhibits both heat production and heat loss mechanisms which lead to an alteration in body temperature, probably via the activation of central adrenergic receptors.

The catecholamine precursor L-3,4-dihydroxyphenylalanine inhibits both heat production and heat loss mechanisms in the rabbit

1980 ◽  
Vol 58 (8) ◽  
pp. 956-964 ◽  
Author(s):  
M. T. Lin
Keyword(s):  
Heat Loss ◽  
Intravenous Administration ◽  
Heat Production ◽  
Nerve Fibers ◽  
Evaporative Heat Loss ◽  
Intraventricular Administration ◽  
Ambient Temperatures ◽  
Behavioral Excitation ◽  
6 Hydroxydopamine ◽  
Loss Mechanisms

The effects of the catecholamine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) on the thermoregulatory responses of conscious rabbits to different ambient temperatures (Ta) (2, 22, and 32 °C) were assessed. Intravenous administration of L-DOPA alone, intravenous administration of L-DOPA plus R04-4602 (a peripheral decarboxylase inhibitor), and intraventricular administration of L-DOPA or norepinephrine all produced a hypothermia at Ta 2 °C. The hypothermia was due to a decrease in metabolic heat production (M). On the other hand, L-DOPA or norepinephrine produced both behavioral excitation and hyperthermia at both Ta 22 and 32 °C. At Ta 22 °C, the hyperthermia was due to decreased ear skin blood flow (EBF) and slightly increased M (due to behavioral excitation) whereas at Ta 32 °C the hyperthermia was due to decreased EBF, decreased respiratory evaporative heat loss, and slightly increased M (due to behavioral excitation). Further, the temperature effects induced by L-DOPA were antagonized by pretreatment with 6-hydroxydopamine (a relative depletor of catecholaminergic nerve fibers) but not with haloperidol (a relative blocker of dopaminergic receptors). The data indicate that activation of central adrenergic receptors via the endogenous release of norepinephrine with L-DOPA inhibits both heat production and heat loss mechanisms in the rabbit.

Intracerebroventricular injection of sympathomimetic drugs inhibits both heat production and heat loss mechanisms in the rat

1980 ◽  
Vol 58 (8) ◽  
pp. 896-902 ◽  
Author(s):  
M. T. Lin ◽  
A. Chandra ◽  
Y. F. Chern ◽  
B. L. Tsay
Keyword(s):  
Heat Loss ◽  
Heat Production ◽  
Intracerebroventricular Injection ◽  
Ambient Temperatures ◽  
Adrenoceptor Antagonist ◽  
Sympathomimetic Drugs ◽  
Cutaneous Temperature ◽  
Behavioral Excitation ◽  
Cutaneous Vasoconstriction ◽  
Loss Mechanisms

The effects of intracerebroventricular (i.c.v.) injections of sympathomimetic drugs on thermoregulatory functions in conscious rats maintained at low (8 °C), moderate (22 °C), and high (30 °C) ambient temperatures were assessed. Norepinephrine, tyramine, and ephedrine each produced hypothermia at ambient temperature (Ta) 8 °C and hyperthermia at Ta 22 and 30 °C. At Ta 8 °C, the hypothermia in response to norepinephrine, tyramine, and ephedrine was due to decreased metabolic rate (M) whereas at Ta 22 °C the hyperthermia was due to cutaneous vasoconstriction. At Ta 22 °C, the hyperthermia in response to norepinephrine and tyramine was due to cutaneous vasoconstriction whereas the hyperthermia in response to ephedrine was brought about by increased M (due to behavioral excitation). Intracerebroventricular injection of epinephrine produced hypothermia followed by hyperthermia at Ta 8 and 22 °C. The hypothermia was due to decreased M whereas the hyperthermia was due to cutaneous vasoconstriction and increased M. At Ta 30 °C, epinephrine led to a reduction in cutaneous temperature and hyperthermia. Furthermore, i.c.v. administration of phenylephrine produced a decreased M and hypothermia at Ta, 8 °C and an increased M (due to behavioral excitation) and hyperthermia at Ta 30 °C. At Ta 22 °C, phenylephrine produced hyperthermia (due to cutaneous vasoconstriction and increased M) preceded by hypothermia (due to decreased M). Moreover, the temperature effects induced by norepinephrine were antagonized by pretreatment with the adrenoceptor antagonist phentolamine. In general, the data indicate that activation of central adrenoceptors with sympathomimetic drugs inhibits both heat production and heat loss mechanisms in the rat.

The role of the cholinergic systems in the central control of thermoregulation in rats

1979 ◽  
Vol 57 (11) ◽  
pp. 1205-1212 ◽  
Author(s):  
M. T. Lin ◽  
F. F. Chen ◽  
Y. F. Chern ◽  
T. C. Fung
Keyword(s):  
Heat Loss ◽  
Heat Production ◽  
Nerve Fibers ◽  
Cholinergic Receptors ◽  
Evaporative Heat Loss ◽  
Central Administration ◽  
Ambient Temperatures ◽  
Dose Dependent ◽  
Selective Blocker

Systemic and central administration of methacholine (a synthetic choline derivative) both produced dose-dependent decreases in rectal temperature in rats at all the ambient temperatures studied. Both at room temperature (22 °C) and in the cold (8 °C), the hypothermia in response to methacholine application was brought about by both a decrease in metabolic heat production and an increase in cutaneous circulation. In the heat (29 °C), the hypothermia was due solely to an increase in respiratory evaporative heat loss. Furthermore, the methacholine-induced hypothermia was antagonized by central pretreatment of atropine (a selective blocker of cholinergic receptors), but not by the central administration of either 6-hydroxy-dopamine (a relative depletor of catecholaminergic nerve fibers) or 5,6-dihydroxytryptamine (predominately a serotonin depletor). The data indicate that activation of the cholinergic receptors within brain with methacholine decreases heat production and (or) increases heat loss which leads to hypothermia in rats.

Thermoregulatory effects of methoxamine and isoprenaline following injections into the cerebral ventricles of conscious rabbits

1977 ◽  
Vol 55 (4) ◽  
pp. 821-827 ◽  
Author(s):  
D. L. Jones ◽  
W. L. Veale ◽  
K. E. Cooper
Keyword(s):  
Body Temperature ◽  
Ambient Temperature ◽  
Heat Loss ◽  
Heat Production ◽  
Adrenergic Receptors ◽  
Cerebral Ventricles ◽  
Inhibitory Neurotransmitter ◽  
Ambient Temperatures ◽  
Hypothalamic Preoptic Area ◽  
Dose Dependent

There is evidence to suggest that within the hypothalamus noradrenaline (NA) is an inhibitory neurotransmitter acting on both the heat production and heat loss pathways in the rabbit. Further, it has been proposed that the inhibition of the heat loss pathway which results in hyperthermia is mediated primarily through α-adrenergic receptors within the anterior hypothalamic–preoptic area. We have investigated the effects of the α-receptor agonist methoxamine, administered directly into the cerebral ventricles, on body temperature at various ambient temperatures in both the shorn and unshorn rabbit. At all ambient temperatures tested, administration of methoxamine into a lateral cerebral ventricle produced a gradual dose-dependent hyperthermia. The magnitude of the hyperthermic response diminished with decreasing ambient temperatures. It is already known that the β-adrenergic agonist isoprenaline produces little or no effect on body temperature following intracranial application at ambient temperatures above 18 °C. In our experiments conducted at the lower ambient temperature, it produced a pronounced dose-dependent fall in body temperature in the shorn rabbit. The results of this work support the suggestion that NA can act as an inhibitory substance on the heat production or heat loss pathway in the rabbit. Which pathway is inhibited at any one time is dependent on the ambient temperature. Further, it would appear that inhibition of the heat loss pathway is largely mediated through α-adrenergic receptors, whilst the inhibition of the heat production pathway is mediated to a large extent through β-adrenergic receptors.

Effects of bombesin on thermoregulatory responses and hypothalamic neuronal activities in the rat

1986 ◽  
Vol 251 (2) ◽  
pp. R303-R309
Author(s):  
K. S. Lin ◽  
M. T. Lin
Keyword(s):  
Heat Loss ◽  
Rectal Temperature ◽  
Heat Production ◽  
The Other ◽  
Single Neurons ◽  
Hypothalamic Area ◽  
Ambient Temperatures ◽  
Thermoregulatory Responses ◽  
Cutaneous Temperature ◽  
Direct Administration

Direct administration of bombesin (1, 10, and 100 ng/microliter) into the preoptic anterior hypothalamic area caused a dose-related fall in rectal temperature at ambient temperatures (Ta) of 8 and 22 degrees C. The hypothermia in response to bombesin was brought about by a decrease in metabolism at Ta 8 degrees C, whereas at Ta 22 degrees C the hypothermia was brought about by both a decrease in metabolism and an increase in cutaneous temperature. However, at Ta 30 degrees C, intrahypothalamic administration of bombesin caused an insignificant change in thermoregulatory responses. On the other hand, 51 single neurons in the preoptic anterior hypothalamic area were examined in 20 rats under urethan anesthesia. Each animal was subjected to scrotal warming or cooling and to the administration of bombesin. Microiontophoretic application of bombesin resulted in inhibition of the majority (62.5%) of cold-responsive neurons as well as excitation of the majority (50%) of warm-responsive neurons recorded in the preoptic anterior hypothalamic area. However, the majority (74%) of thermally unresponsive neurons were not affected by bombesin application. The data indicate that bombesin, when administered intrahypothalamically, excites warm-responsive neurons and inhibits cold-responsive neurons within the preoptic anterior hypothalamic area to induce hypothermia by promoting an increase in heat loss and a decrease in heat production.

Effects of brain monoamine depletion on chlorpromazine-induced hypothermia in rabbits

1979 ◽  
Vol 57 (1) ◽  
pp. 16-23 ◽  
Author(s):  
M. T. Lin
Keyword(s):  
Blood Flow ◽  
Heat Production ◽  
Intraperitoneal Administration ◽  
Induced Hypothermia ◽  
Evaporative Heat Loss ◽  
Ambient Temperatures ◽  
Normal Limits ◽  
Wide Range ◽  
Monoamine Depletion ◽  
6 Hydroxydopamine

The thermal responses of three groups of control, 6-hydroxydopamine (6-OHDA) treated and 5,7-dihydroxytryptamine (5,7-DHT) treated rabbits to the administration of chlorpromazine (CPZ) were assessed at three different ambient temperatures (Ta: 2, 22, and 32 °C). Depleting catecholamines (CA) in brain with 6-OHDA produced a decrease in metabolic rate, in respiratory evaporative heat loss, and in ear blood flow at both Ta's of 2 and 22 °C, while depleting 5-hydroxytryptamine (5-HT) contents in brain with 5,7-DHT produced the opposite responses at the same Ta's. However, these amine-depleted animals maintained their rectal temperatures within normal limits over a wide range of Ta's tested. Furthermore, intraperitoneal administration of CPZ produced hypothermia at both Ta's of 2 and 22 °C. The major cause of the CPZ-induced hypothermia was an inhibition of metabolic heat production at Ta of 2 °C. At Ta of 22 °C, the CPZ-induced hypothermia was due to both a decrease in heat production and an increase in ear blood flow. However, CPZ hypothermia was attenuated in the CA-depleted animals, but was potentiated in the 5-HT-depleted animals. The data indicate that brain monoamines are involved in the central mechanisms of CPZ-induced hypothermia.

Effects of phentolamine on thermoregulatory functions of rats to different ambient temperatures

1979 ◽  
Vol 57 (12) ◽  
pp. 1401-1406 ◽  
Author(s):  
M. T. Lin ◽  
Andi Chandra ◽  
T. C. Fung
Keyword(s):  
Heat Loss ◽  
Rectal Temperature ◽  
Heat Production ◽  
Room Temperature ◽  
Metabolic Heat Production ◽  
Central Component ◽  
Evaporative Heat Loss ◽  
Central Administration ◽  
Ambient Temperatures ◽  
Metabolic Heat

The effects of both systemic and central administration of phentolamine on the thermoregulatory functions of conscious rats to various ambient temperatures were assessed. Injection of phentolamine intraperitoneally or into a lateral cerebral ventricle both produced a dose-dependent fall in rectal temperature at room temperature and below it. At a cold environmental temperature (8 °C) the hypothermia in response to phentolamine was due to a decrease in metabolic heat production, but at room temperature (22 °C) the hypothermia was due to cutaneous vasodilatation (as indicated by an increase in foot and tail skin temperatures) and decreased metabolic heat production. There were no changes in respiratory evaporative heat loss. However, in the hot environment (30 °C), phentolamine administration produced no changes in rectal temperature or other thermoregulatory responses. A central component of action is indicated by the fact that a much smaller intraventricular dose of phentolamine was required to exert the same effect as intraperitoneal injection. The data indicate that phentolamine decreases heat production and (or) increases heat loss which leads to hypothermia, probably via central nervous system actions.

Persistence of febrile response to pyrogens after PO/AH lesions in squirrel monkeys

1976 ◽  
Vol 231 (6) ◽  
pp. 1638-1648 ◽  
Author(s):  
JM Lipton ◽  
GP Trzcinka
Keyword(s):  
Oxygen Consumption ◽  
Heat Production ◽  
Prostaglandin E1 ◽  
Squirrel Monkeys ◽  
Febrile Response ◽  
Intravenous Injections ◽  
Central Representation ◽  
Intracerebroventricular Injections ◽  
6 Hydroxydopamine ◽  
Skin Temperatures

Observation of a patient who developed fever in spite of severe CNS sarcoidosis led us to test the idea that febrile responses require mediation by neurons in the preoptic/anterior hypothalamic (PO/AH) region. Changes in rectal and skin temperatures and oxygen consumption were recorded after intravenous and intracerebroventricular injections of endotoxin, after intracerebroventricular prostaglandin E1 (PGE1), and after intravenous injections of leukocyte pyrogens in animals in which the PO/AH region had been destroyed. The capacity to develop fever persisted after PO/AH destruction, and the patterns of heat production and heat loss were unchanged. Pyrogens were still effective after intracerebroventricular 6-hydroxydopamine and intraperitoneal reserpine given to reduce brain amines in monkeys with PO/AH lesions. It is unlikely that a secondary control in the medulla oblongata is responsible for the persisting sensitivity to pyrogens, since multiple injections of endotoxin into this region did not cause fever either before or after the PO/AH region was destroyed. The results do not support the idea that control of fever is localized in the PO/AH region alone. Rather, it appears that in the brains of primates there is either multiple central representation of fever control or an inherent capacity to develop sensitivity to pyrogens and to produce coordinated febrile responses.

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