Changes in beta-adrenergic responsiveness of rats during chronic cold exposure

1980 ◽  
Vol 49 (6) ◽  
pp. 923-929 ◽  
Author(s):  
C. C. Barney ◽  
M. J. Katovich ◽  
M. J. Fregly ◽  
P. E. Tyler
Keyword(s):  
Heart Rate ◽  
Cold Exposure ◽  
Chronic Exposure ◽  
Cardiovascular Responses ◽  
Time Dependent ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Heart Rates ◽  
Beta Adrenergic Agonist

Administration of isoproterenol (50 micrograms/kg sc) to rats that had been exposed to cold (6 degrees C) for 10, 15, and 25 days was accompanied by a greater increase in tail skin and colonic temperatures than in controls kept at 25 degrees C. Administration of isoproterenol (8 micrograms/kg sc) to cold-treated rats (1, 3, 5, 7, 14, and 28 days) increased heart rates above that of controls. However, resting unstimulated heart rates of cold-treated rats were also increased above that of controls after 1, 3, 5, and 7 days of cold exposure but were not different from controls after 14 and 28 days. Cold exposure also led to time-dependent increases in the weights of heart, adrenals, and interscapular brown fat. Thus, chronic exposure of rats to cold is accompanied by an increase in responsiveness of both heart rate and tail skin and colonic temperatures to beta-adrenergic stimulation. The results also suggest that increases in responsiveness to a beta-adrenergic agonist may not occur at the same time for the different beta-adrenergic-mediated metabolic and cardiovascular responses in cold-treated rats.

Acclimatization of Scottish Blackface sheep to cold. 2. Skin temperature, heart rate, respiration rate, shivering intensity and skinfold thickness

1968 ◽  
Vol 10 (1) ◽  
pp. 17-35 ◽  
Author(s):  
A. R. Sykes ◽  
J. Slee
Keyword(s):  
Heart Rate ◽  
Skin Temperature ◽  
Cold Exposure ◽  
Chronic Exposure ◽  
Physiological Responses ◽  
Skinfold Thickness ◽  
Acute Exposure ◽  
Heart Rates ◽  
Ambient Temperatures ◽  
Acute Cold Exposure

Closely shorn Scottish Blackface female sheep aged 9–14 months, half on high plane and half on low plane nutrition, were subjected, in climate chambers, to two short acute cold exposures down to −20°C. The acute exposures were separated by two weeks chronic exposure to a moderately subcriticai temperature (+8°C) or to a thermoneutral temperature (+30°C). Most of the sheep showed a greater resistance to body cooling at the second acute exposure (Slee and Sykes, 1967). This increased resistance to hypothermia, defined as acclimatization, was apparently influenced more by acute than by chronic cold exposure. The present paper deals with changes in skin temperature, heart rate, shivering intensity and skinfold thickness which also resulted from cold exposure, and accompanied acclimatization.After acute cold exposure followed by chronic exposure to +8°C the following changes in these parameters were observed:1. Extremity skin temperatures and heart rates were consistently increased at thermoneutral ambient temperatures.2. Vasoconstriction of the extremities and increased heart rate, both of which normally occur during the early stages of cold exposure, were delayed.3. Heart rates at sub-zero ambient temperatures were increased.4. Cold-induced vasodilatation at sub-zero ambient temperatures was increased.After acute cold treatment alone the intensity of shivering during the second acute exposure was reduced. Also the onset of foot vasoconstriction was slightly delayed.A highly significant relationship was observed between shivering intensity and heart rate during cold exposure.Plane of nutrition had less effect on the physiological responses to cooling than did previous cold experience.It was suggested in discussion that the physiological responses associated with acclimatization were: elevated basal metabolic rate, delayed onset of vasoconstriction and delayed metabolic response to cold, and consequent lowering of the critical temperature. Summit metabolism was also increased and shivering intensity reduced during acute cold exposure. Some of these responses could have resulted from either acute or chronic moderate cold exposure. However their persistence, once induced, appeared to depend upon continued exposure to moderate cold.

Development of autonomic control of fetal circulation

1975 ◽  
Vol 228 (2) ◽  
pp. 337-344 ◽  
Author(s):  
B Nuwayhid ◽  
Brinkman CR ◽  
C Su ◽  
JA Bevan ◽  
NS Assali
Keyword(s):  
Heart Rate ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Peripheral Circulation ◽  
Fetal Life ◽  
Resting Heart Rate ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Significant Control ◽  
Parasympathetic System

Development of parasympathetic and sympathetic reflexes controlling heart rate, vascular pressures, and blood flows was investigated in fetal lambs weighing 300-5,800 g (65-165 days' gestation). Cardiovascular responses to veratridine injections, atrial stretching, bilateral cervical vagotomy, and cholinergic blockade with atropine were used to test parasympathetic activities. Responses to propranolol and phenoxybenzamine were used to test beta- and alpha-adrenergic activities. Autonomic ganglionic blockade and stimulation provided additional information on both cholinergic and adrenergic systems. Fetal responses to various tests were compared to those of the mother. Results show: a) little parasympathetic tone on resting heart rate and other circulatory functions exists prior to fetal maturity; b) despite the feeble resting tone, the parasympathetic system is capable of exerting significant control when stimulated in both premature and mature fetuses, the capability increases as fetus approaches term; c) alpha- and beta-adrenergic tone in control of resting heart rate and peripheral circulation exists in early fetal life and increases as the fetus reaches maturity, and both adrenergic receptors respond strongly to stimuli in immature, premature, and mature fetuses; d) in immature fetuses, veratridine does not elicit a vagally mediated reflex; instead, it produces a centrally mediated alpha- and beta-adrenergic stimulation; e) the fetal cardiovascular response to any given test is dampened by the existence of the various vascular shunts, the umbilicoplacental circulation and, possibly, by incomplete maturation of vasomotor tone.

scholarly journals The effects of forced activity on circulating catecholamines and pH and water content of erythrocytes in the toad

1987 ◽  
Vol 128 (1) ◽  
pp. 411-418
Author(s):  
B. L. Tufts ◽  
D. C. Mense ◽  
D. J. Randall
Keyword(s):  
Water Content ◽  
Adrenergic Stimulation ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
In Vivo Experiments ◽  
Beta Adrenergic Agonist ◽  
Toad Bufo ◽  
Adrenergic Effects

In vivo experiments were carried out to determine the effect of forced activity on circulating catecholamine levels, haematocrit, and the pH and water content of erythrocytes in the toad, Bufo marinus. In addition, the effect of the beta-adrenergic agonist isoproterenol on erythrocyte pH and water content was examined in vitro. Forced activity caused a significant decrease in both whole blood and erythrocyte pH, while haematocrit and circulating adrenaline and noradrenaline levels increased. Erythrocyte water content did not change following forced activity. Addition of isoproterenol to toad blood in vitro had no effect on either erythrocyte pH or water content. The apparent absence of beta-adrenergic effects on erythrocyte pH and water content in the toad is in sharp contrast to the response of teleost fish erythrocytes to beta-adrenergic stimulation. The significance of these differences is discussed.

Chemoreflex and endocrine components of cardiovascular responses to acute hypoxemia in the llama fetus

1996 ◽  
Vol 271 (1) ◽  
pp. R73-R83 ◽  
Author(s):  
D. A. Giussani ◽  
R. A. Riquelme ◽  
F. A. Moraga ◽  
H. H. McGarrigle ◽  
C. R. Gaete ◽  
...  
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
High Altitude ◽  
Chronic Exposure ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Cardiovascular Responses ◽  
Pronounced Increase ◽  
Plasma Vasopressin ◽  
Plasma Angiotensin

We tested the hypothesis that the llama fetus has a blunted cardiovascular chemoreflex response to hypoxemia by investigating the effects of acute hypoxemia on perfusion pressure, heart rate, and the distribution of the combined ventricular output in 10 chronically instrumented fetal llamas at 0.6-0.7 gestation. Four llama fetuses had the carotid sinus nerves sectioned. In the intact fetuses, there was a marked bradycardia, an increase in perfusion pressure, and a pronounced peripheral vasoconstriction during hypoxemia. These cardiovascular responses during hypoxemia in intact fetuses were accompanied by a pronounced increase in plasma vasopressin, but not in plasma angiotensin II concentrations. Carotid denervation prevented the bradycardia at the onset of hypoxemia, but it did not affect the intense vasoconstriction during hypoxemia. Plasma vasopressin and angiotensin II levels were not measured in carotid-denervated fetuses. Our results do not support the hypothesis that the carotid chemoreflex during hypoxemia is blunted in the llama fetus. However, they emphasize that other mechanisms, such as increased vasopressin concentrations, operate to produce an intense vasoconstriction in hypoxemia. This intense vasoconstriction in the llama fetus during hypoxemia may reflect the influence of chronic exposure to the hypoxia of high altitude on the magnitude and gain of fetal cardiovascular responses to a superimposed acute episode of hypoxemia.

Glibenclamide attenuates adenosine-induced bradycardia and coronary vasodilatation

1991 ◽  
Vol 261 (3) ◽  
pp. H720-H727 ◽  
Author(s):  
F. L. Belloni ◽  
T. H. Hintze
Keyword(s):  
Heart Rate ◽  
Cardiovascular Responses ◽  
K Channel ◽  
Receptor Blockade ◽  
Beta Adrenergic ◽  
Coronary Vasodilatation ◽  
Cervical Vagotomy ◽  
Adenosine Antagonism ◽  
Anesthetized Dogs ◽  
Control State

The effects of the ATP-sensitive K(+)-channel blocker glibenclamide on the cardiovascular responses to adenosine in dogs were determined. Adenosine (0.01-20 mumol/kg iv) caused coronary vasodilatation, arterial hypotension, and bradycardia in dogs with either combined beta-adrenergic and muscarinic receptor blockade or with bilateral cervical vagotomy plus beta-adrenergic receptor blockade. The 50% effective dose for adenosine-induced coronary dilatation was increased from 0.13 +/- 0.04 mumol/kg in the control state to 1.1 +/- 0.5 mumol/kg after 2 mg/kg of glibenclamide (P less than 0.001). Adenosine at 5 mumol/kg reduced heart rate by 19 +/- 5% from a baseline of 158 +/- 6 beats/min in five anesthetized dogs. After glibenclamide (10 mg/kg), this dose of adenosine failed to cause a significant change in heart rate. The arterial hypotensive effects of adenosine were also attenuated by glibenclamide. Thus glibenclamide inhibited adenosine-induced bradycardia, hypotension, and coronary dilatation. On the other hand, glibenclamide did not affect the reductions in heart rate caused by vagus nerve stimulation. The mechanism of this adenosine antagonism is not known but, in the case of bradycardia, it does not appear to involve any of the steps shared in common by both adenosine-induced and vagal responses of the sinoatrial node.

Effect of adrenergic agonists on big and small renin

1980 ◽  
Vol 238 (5) ◽  
pp. E416-E420
Author(s):  
H. Iwao ◽  
C. S. Lin ◽  
A. M. Michelakis
Keyword(s):  
Submaxillary Gland ◽  
Plasma Renin ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Molecular Weights ◽  
Submaxillary Glands ◽  
Beta Adrenergic Agonists ◽  
Beta Adrenergic Agonist ◽  
Alpha Adrenergic Agonist

The effect of alpha- and beta-adrenergic agonists on renal and submaxillary renin of different molecular weights was studied using male albino mice as experimental animals. Phenylephrine or isoproterenol was administered intravenously after removal of the submaxillary glands and/or kidneys. Renin was isolated from plasma by column chromatography and then measured by a direct radioimmunoassay. Phenylephrine increased both 68,500-dalton renin (big renin) and 38,000-dalton renin (small renin) in the plasma of nephrectomized mice. Isoproterenol increased big and small renin in the plasma of mice whose submaxillary glands were removed. In both cases, the increase of small renin was significantly greater than that of big renin. The results suggest that the alpha-adrenergic agonist phenylephrine affects the submaxillary gland, leading to the increase of both big and small plasma renin. In contrast, the beta-adrenergic agonist isoproterenol affects the kidney, leading to the increase of both big and small plasma renin.

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