Enhancement of the sympathoadrenal response to the cold-pressor test by naloxone in man

1985 ◽  
Vol 69 (3) ◽  
pp. 365-368 ◽  
Author(s):  
Pierre-Marc Bouloux ◽  
Ashley Grossman ◽  
Saad Al-Damluji ◽  
Timothy Bailey ◽  
Michael Besser

1. The effects of naloxone (8 mg) on the pressor and plasma catecholamine response to a standard cold-pressor test have been evaluated in six normal male subjects. Plasma catecholamines were estimated by high performance liquid chromatography coupled to electrochemical detection. 2. Cold stimulation induced significant elevations in plasma noradrenaline and adrenaline to reach mean peak levels 61% and 108% above their respective basal levels (P < 0.05). Systolic blood pressure increased by 23 ± 6.5 mmHg (P < 0.001), and heart rate increased by 7.5 ± 2.5 beats/min (P < 0.001). 3. Naloxone pretreatment significantly enhanced the plasma adrenaline response to the cold stimulus by 98% (P < 0.01) with concomitant changes in peak systolic blood pressure (peak increment 31 ± 6 mmHg) and pulse rate (12.5 ± 3.5 beats/min) responses (both P < 0.05). The mean plasma noradrenaline response to cold also increased after naloxone, but this failed to achieve significance. 4. Endogenous opioids are likely to be involved in the sympathoadrenal response to a mild acute stress in man.

2020 ◽  
Vol 87 (9) ◽  
pp. S352
Author(s):  
Olesia Muravizki ◽  
Faisal Akram ◽  
Melanie Daue ◽  
Kathleen A. Ryan ◽  
Soren Snitker ◽  
...  

1981 ◽  
Vol 61 (s7) ◽  
pp. 161s-164s ◽  
Author(s):  
P. Bolli ◽  
F. W. Amann ◽  
L. Hulthén ◽  
W. Kiowski ◽  
F. R. Bühler

1. Stressful sympathetic stimulation (cold pressor test) was applied to 18 patients with essential hypertension and 15 normotensive subjects. Intra-arterial blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations as well as forearm blood flow were measured before and during the cold pressor test; tests were repeated after regional postsynaptic α1-adrenoceptor blockade with prazosin. 2. Under basal conditions mean blood pressure (P &lt; 0.001), heart rate (P &lt; 0.01), forearm blood flow (P &lt; 0.001) as well as adrenaline concentration (P &lt; 0.01), but not noradrenaline, was higher in patients with essential hypertension. 3. During the cold pressor test, mean blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations increased and forearm flow decreased (all P &lt; 0.001). 4. Stress-stimulated plasma adrenaline was higher in essential hypertensive patients than in normotensive subjects (P &lt; 0.01). In the former the stress-induced increase in plasma adrenaline correlated with the increase in mean blood pressure (r = 0.514; P &lt; 0.05). 5. Prazosin increased forearm blood flow more in essential hypertension (P &lt; 0.001). This increase correlated with the resting plasma adrenaline in the hypertensive (r = 0.710; P &lt; 0.001), but not in normotensive, subjects. 6. When the cold pressor test was repeated during postsynaptic α1-adrenoceptor blockade forearm blood flow did not decrease; instead it increased further in both groups (P &lt; 0.05). 7. Thus in essential hypertension elevated plasma adrenaline concentration reflects sympathetic overactivity as also expressed by enhanced α-adrenoceptor-mediated vasoconstriction.


1989 ◽  
Vol 76 (6) ◽  
pp. 625-630 ◽  
Author(s):  
P. M. G. Bouloux ◽  
E. Newbould ◽  
R. Causon ◽  
L. Perry ◽  
L. H. Rees ◽  
...  

1. Although the opiate antagonist naloxone has been shown to affect sympathoadrenomedullary function in some studies, this has not been a uniform finding in all investigations, using different doses of naloxone. We have therefore investigated the actions of saline placebo and increasing bolus doses of intravenous naloxone (25, 100 and 250 μg/kg) on the plasma noradrenaline, adrenaline, adrenocorticotrophin (ACTH) and cortisol responses to a cold-pressor test in six males and two females in a double-blind randomized study. 2. Basal levels of adrenaline did not differ on any of the study occasions: the cold-pressor stimulus produced a significant rise in mean plasma adrenaline to a peak of 0.16 nmol/l, with a peak incremental rise of 0.08 nmol/l. In the presence of the two higher doses of naloxone, the incremental rise in the mean adrenaline level was significantly enhanced, reaching 0.30 nmol/l at 100 μg of naloxone/kg and 0.29 nmol/l at 250 μg of naloxone/kg, with no significant enhancement observed at the lowest dose of naloxone. The rise in plasma noradrenaline, systolic and diastolic blood pressure and pulse rate during the cold-pressor test was not consistently altered by any dose of naloxone, but there was a significant trend for the degree of discomfort to increase with the dose of naloxone. 3. Neither plasma ACTH nor serum cortisol rose in response to the cold-pressor stimulus. Analysis of variance demonstrated a significant naloxone-treatment effect for both ACTH and cortisol, with the 100 μg/kg and 250 μg/kg doses of naloxone leading to a significant rise in mean plasma ACTH not seen at the lowest dose of 25 μg/kg. 4. In a separate study of the effect of naloxone on the clearance of plasma adrenaline, adrenaline was infused on two occasions into eight normal male subjects to a maximum dose of 5 μg/min for 15 min, and blood was sampled at regular intervals during and after termination of the infusion, preceded by 8 mg of naloxone or placebo. After termination of the adrenaline infusion, there was a rapid fall in plasma adrenaline (Λ = −1.9 ± 0.3 min), which was not altered by naloxone (Λ = −1.8 ± 0.3 min). 5. We conclude that the potentiation of the adrenaline response to a cold-pressor test by naloxone is mediated by increased secretion of adrenaline and not by a reduction in its clearance rate, and that this response is of low naloxone sensitivity.


1985 ◽  
Vol 69 (5) ◽  
pp. 533-540 ◽  
Author(s):  
Gianfranco Parati ◽  
Guido Pomidossi ◽  
Agustin Ramirez ◽  
Bruno Cesana ◽  
Giuseppe Mancia

1. In man evaluation of neural cardiovascular regulation makes use of a variety of tests which address the excitatory and reflex inhibitory neural influences that control circulation. Because interpretation of these tests is largely based on the magnitude of the elicited haemodynamic responses, their reproducibility in any given subject is critical. 2. In 39 subjects with continuous blood pressure (intra-arterial catheter) and heart rate monitoring we measured (i) the blood pressure and heart rate rises during hand-grip and cold-pressor test, (ii) the heart rate changes occurring during baroreceptor stimulation and deactivation by injection of phenylephrine and trinitroglycerine, and (iii) the heart rate and blood pressure changes occurring with alteration in carotid baroreceptor activity by a neck chamber. Each test was carefully standardized and performed at 30 min intervals for a total of six times in each subject. 3. The results showed that the responses to any test were clearly different from one another and that this occurred in all subjects studied. For the group as a whole the average response variability (coefficient of variation) ranged from 10.2% for the blood pressure response to carotid baroreceptor stimulation to 44.2% for the heart rate response to cold-pressor test. The variability of the responses was not related to basal blood pressure or heart rate, nor to the temporal sequence of the test performance. 4. Thus tests employed for studying neural cardiovascular control in man produce responses whose reproducibility is limited. This phenomenon may make it more difficult to define the response magnitude typical of each subject, as well as its comparison in different conditions and diseases.


JAMA ◽  
1963 ◽  
Vol 183 (10) ◽  
Author(s):  
Paul H. Barnett ◽  
Edgar A. Hines ◽  
Alexander Schirger ◽  
Robert P. Gage

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