Sympathomimetic Amine-Induced Responses of Effector Organs Subserved by Alpha-, Beta1-, and Beta2-Adrenoceptors

Arnold, Aaron

doi:10.1007/978-3-642-67505-8_2

Cited by 5 publications

(2 citation statements)

References 150 publications

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“…Indeed, in our experiment, there was an increase in the level of subjectively rated anxiety in the THREAT condition, and it is known that anxiogenic stimuli can cause an acute increase in the concentrations of circulating adrenaline and noradrenaline (for review see Szabadi and Bradshaw, 1988). Furthermore, it is well documented that adrenaline, and to a lesser extent noradrenaline are potent mydriatics when injected into the blood stream (for review see Arnold, 1980). Thus, theoretically, it is possible that the increase in initial diameter in the THREAT condition was due to a direct effect of circulating catecholamines on the dilator muscle of the iris.…”

Section: Discussionmentioning

confidence: 94%

The inhibition of the pupillary light reflex by the threat of an electric shock: a potential laboratory model of human anxiety

1996

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It has been shown that the eye-blink response evoked by an abrupt loud white noise ('acoustic startle') is potentiated when the subjects anticipate an aversive stimulus, e.g. an electric shock ('fear-potentiated startle'). It has been proposed that this paradigm may be a useful laboratory model of human anxiety. We examined whether the threat of an electric shock, as used in the fear-potentiated startle paradigm, would affect the pupillary light reflex, in 12 healthy volunteers. Light stimuli (0.32 mW/cm(2), 200 msec) were generated by a light-emitting diode, and pupil diameter was monitored by computerized binocular infrared television pupillometry in the dark. The light reflex was recorded during either the anticipation of a shock ('threat' blocks) or periods in which no shocks were anticipated ('safe' blocks). The shock consisted of a single square wave current pulse (1.5 mA, 50 msec) applied to the median nerve. At the end of each 'threat' or 'safe' block, subjects rated their anxiety using visual analogue scales. Two-factor analysis of variance (condition x block) showed that in the 'threat' condition there was a consistent increase in initial pupil diameter, a decrease in light reflex amplitude and an increase in alertness and anxiety ratings. These effects were observable before the subjects received any shock (a single stimulation of the median nerve). These results show that the anticipation of an electric shock can modify not only the startle reflex response but also the pupillary light reflex, suggesting that the inhibition of the light reflex by threat may be another suitable laboratory model of human anxiety.

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Section: Discussionmentioning

confidence: 94%

The inhibition of the pupillary light reflex by the threat of an electric shock: a potential laboratory model of human anxiety

1996

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“…Through its action on skeletal muscle, Epi is known to increase energy expenditure, with a related increase in plasma lactate (2). These effects are attributable to ␤-AR stimulation, and Epi is much more potent than NE for muscle glycogenolysis (2). Thus the increased Epi-induced energy expenditure and plasma lactate concentrations during HDBR could also be attributable to an increased ␤-adrenergic responsiveness.…”

Section: Discussionmentioning

confidence: 99%

Increase in epinephrine-induced responsiveness during microgravity simulated by head-down bed rest in humans

Barbe

Galitzky

Thalamas

et al. 1999

Journal of Applied Physiology

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The epinephrine (Epi)-induced effects on the sympathetic nervous system (SNS) and metabolic functions were studied in men before and during a decrease in SNS activity achieved through simulated microgravity. Epi was infused at 3 graded rates (0.01, 0.02, and 0. 03 microg. kg(-1). min(-1) for 40 min each) before and on the fifth day of head-down bed rest (HDBR). The effects of Epi on the SNS (assessed by plasma norepinephrine levels and spectral analysis of systolic blood pressure and heart rate variability), on plasma levels of glycerol, nonesterified fatty acids (NEFA), glucose and insulin, and on energy expenditure were evaluated. HDBR decreased urinary norepinephrine excretion (28.1 +/- 4.2 vs. 51.5 +/- 9.1 microg/24 h) and spectral variability of systolic blood pressure in the midfrequency range (16.3 +/- 1.9 vs. 24.5 +/- 0.9 normalized units). Epi increased norepinephrine plasma levels (P < 0.01) and spectral variability of systolic blood pressure (P < 0.009) during, but not before, HDBR. No modification of Epi-induced changes in heart rate and systolic and diastolic blood pressures were observed during HDBR. Epi increased plasma glucose, insulin, and NEFA levels before and during HDBR. During HDBR, the Epi-induced increase in plasma glycerol and lactate levels was more pronounced than before HDBR (P < 0.005 and P < 0.001, respectively). Epi-induced energy expenditure was higher during HDBR (P < 0.02). Our data suggest that the increased effects of Epi during simulated microgravity could be related to both the increased SNS response to Epi infusion and/or to the beta-adrenergic receptor sensitization of end organs, particularly in adipose tissue and skeletal muscle.

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Potential Mechanisms for Repartitioning of Growth by β-Adrenergic Agonists

Mersmann¹

1989

Animal Growth Regulation

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Sympathomimetic Amine-Induced Responses of Effector Organs Subserved by Alpha-, Beta1-, and Beta2-Adrenoceptors

Cited by 5 publications

References 150 publications

The inhibition of the pupillary light reflex by the threat of an electric shock: a potential laboratory model of human anxiety

The inhibition of the pupillary light reflex by the threat of an electric shock: a potential laboratory model of human anxiety

Increase in epinephrine-induced responsiveness during microgravity simulated by head-down bed rest in humans

Potential Mechanisms for Repartitioning of Growth by β-Adrenergic Agonists

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