The effect of propranalol on the calorigenic response in brown adipose tissue of new‐born rabbits to catecholamines, glucagon, corticotrophin and cold exposure

Heim, T; Hull, D

doi:10.1113/jphysiol.1966.sp008088

Cited by 118 publications

(43 citation statements)

References 13 publications

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“…It is generally accepted that non-shivering thermogenesis is controlled by the sympathetic nervous system and that the fall in metabolic rate induced by adrenergic f-blockers is due to the blockade of non-shivering M. BANET AND H. HENSEL thermogenesis (Bruck & Wiinnenberg, 1965;Schdnbaum, Johnson, Sellers & Gill, 1966;Heim & Hull, 1966;Alexander & Williams, 1968;Blatteis, 1976;Horwitz & Hanes, 1976) rather than to interference with shivering (Bruck & Wunnenberg, 1965;Schonbaum et al 1966;Blatteis, 1976) or with the cardiovascular system (Bruck & Wunnenberg, 1965;Heim & Hull, 1966). Our own experiments also show that the fall in colonic temperature could not be due to cardiovascular depression because propanolol did not hinder the nearly maximum metabolic rate induced by 2,4-dinitrophenol.…”

Section: Discussionmentioning

confidence: 99%

The control of shivering and non‐shivering thermogenesis in the rat.

Banet¹,

Hensel²

1977

The Journal of Physiology

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SUMMARY1. The effect of intraperitoneal administration of propranolol (4, 8 and 12 mg/kg) on colonic temperature was studied in twelve rats during exposure to ambient temperatures of 30, 15 and 50 C.2. At 300 C, propranolol had no effect on colonic temperature; at 15 and 50 C, however, 4 mg propanolol/kg induced a fall in colonic temperature of about 0.80 C, whereas 8 and 12 mg propanolol/kg induced a fall of about 1.5-2-00 C.3. Assuming that the temperature regulation system of the rat has a proportional controller and that the effect of propranolol was due to the blockade of non-shivering thermogenesis, the results are interpreted as showing that shivering is activated only when heat loss exceeds the capacity for non-shivering thermogenesis.

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Section: Discussionmentioning

confidence: 99%

The control of shivering and non‐shivering thermogenesis in the rat.

Banet¹,

Hensel²

1977

The Journal of Physiology

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“…This result is consistent with a thermogenic regulatory role for adenosine in the perinatal period. However, a decline in fetal blood pressure, which averaged 12 mm Hg, occurred concurrently; this might itself be the cause of such an inhibition of thermogenesis because a substantial increase in blood flow through brown adipose tissue (19,20) normally accompanies nonshivering thermogenesis. Accordingly, we performed further experiments to separate the direct inhibitory effects of low doses of PIA on blood pressure and the consequent indirect alteration of thermogenesis.…”

Section: Discussionmentioning

confidence: 99%

A Potential Role for Adenosine in the Inhibition of Nonshivering Thermogenesis in the Fetal Sheep

et al. 1995

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Adenosine is released by the placenta into the fetal circulation and has potent antilipolytic properties in vitro. Nonshivering thermogenesis cannot be demonstrated by cooling fetal sheep in utero but can be induced by supplemental oxygenation and umbilical cord occlusion; this suggests the presence of inhibitor(~) of placental origin. To test whether circulating adenosine could be such an inhibitor, a series of experiments was carried out in nine fetal sheep at 136-145 d gestation. Birth was simulated in utero by sequentially cooling the fetus 2.49 ? 0.23"C with no change in the low levels of plasma FFA or glycerol; ventilating with 0, via an exteriorized tracheostomy tube and umbilical cord occlusion. Thermogenic indices rose markedly, and plasma FFA and glycerol concentrations peaked at 725 + 88 pEq/L ( p < 0.01) and 771 -C 154 pmoVL, ( p < 0.001), respectively, 0, consumption rose to 20 + 2 mUminkg, and temperature increased 1.99 ? 0.35"C. The long-acting adenosine analog N6-(L-2-phenylisopropy1)-adenosine (PIA) was then infused (90 p@g bolus, then 300 p@gh for 30 min); plasma FFA and glycerol decreased to 265 + 56 pEq/L (p < When a fetal sheep is cooled in utero, nonshivering thermogenesis is not initiated, as evidenced by the failure of plasma FFA and glycerol concentrations to increase and the lack of additional heat production by brown adipose tissue (1). The failure of this thermogenic response is observed despite the capability of ovine brown fat cells to respond to thermogenic stimuli in vitro (2) and despite the ability of prematurely delivered and term-delivered lambs to thermoregulate (3). These findings indicate that brown adipose tissue is competent but unresponsive before birth.The stimulus or combination of stimuli that may account for the initiation of nonshivering thermogenesis within minutes of birth is unknown. Although a number of potential stimuli have been tested and found to be necessary, none has proved sufficient. For example, cooling and increased oxygenation of the fetal sheep (1, 4-7) and an intact sympathetic nervous -------system (8) are necessary for thermogenesis, but they fail to evoke responses comparable to those seen after birth. Only after the umbilical cord has been occluded do the thermogenic responses increase appreciably (1, 4-7). Such observations suggest that the onset of nonshivering thermogenesis in the fetal lamb is dependent on the removal of an inhibitor of placental origin. The removal of the inhibitor after interruption of the umbilical circulation at birth would enable thermogenesis to increase appreciably. Adenosine is a compound released by the placenta (9, lo), is present in high concentrations in fetal plasma (11, 12), has a short half-life in circulating blood (13), and inhibits catecholamine-stimulated lipolysis in brown adipose tissue in vitro (14,15). Thus, we hypothesized that the high circulating levels of adenosine in the fetus would inhibit nonshivering thermogenesis in utero, and then the declining levels upon removal of the umbilical circulation...

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“…In four experiments the KCl response was suppressed by lowering the calcium concentration to 10-5 M, without changing the magnesium concentration, although in this case the effects of the KCl stimulation disappeared more slowly. (4) Effects of (-)-and (+ )-propranolol on the KCI response Propranolol has been shown to efficiently prevent the fl-effects of catecholamines in many tissues including brown adipose tissue (Heim & Hull, 1966). Specificity of a /3-adrenergic block can be assessed by using the criteria of both low dose and stereospecificity (Nickerson, 1970).…”

Section: Resultsmentioning

confidence: 99%

Potassium‐induced increase in oxygen consumption of brown adipose tissue from the rat.

Barde¹,

Chinet²,

Girardier³

1975

The Journal of Physiology

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SUMMARY1. In brown adipose tissue, noradrenaline induces an increase in respiration and a depolarization of the cells. The effect of an increase in potassium concentration in a range known to depolarize the brown adipocytes was tested on the 02 consumption.2. Isolated interscapular brown adipose tissue from the rat was incubated in chambers that allowed 02 consumption to be measured over prolonged periods.3. 45-50 mM-KCl were found to induce a more than fourfold increase in 02 consumption, which was stable, reversible and dependent upon the presence of calcium in the medium. 4. When rats were pre-treated with reserpine or 6-hydroxydopamine the KCl-induced increase in 02 consumption was sharply reduced or entirely absent.5. The effect of KCI was greatly inhibited by (-)-propranolol, but not by (+ )-propranolol.6. Moderate increases in 02 consumption induced by low concentrations of potassium were potentiated by desipramine, a drug which is known to block the uptake of catecholamines by adrenergic nerve endings.7. Surgical denervation caused a decrease in the catecholamine content of the tissue, but had no effect on the KCl response.8. It is concluded that in brown adipose tissue, potassium stimulates 02 consumption by causing a release of noradrenaline from nerve endings. This implies that surgical denervation as it is commonly performed on this tissue does not denervate the brown adipocytes but probably only the blood vessels.

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The effect of propranalol on the calorigenic response in brown adipose tissue of new‐born rabbits to catecholamines, glucagon, corticotrophin and cold exposure

Cited by 118 publications

References 13 publications

The control of shivering and non‐shivering thermogenesis in the rat.

The control of shivering and non‐shivering thermogenesis in the rat.

A Potential Role for Adenosine in the Inhibition of Nonshivering Thermogenesis in the Fetal Sheep

Potassium‐induced increase in oxygen consumption of brown adipose tissue from the rat.

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