Effects of prolonged high-altitude exposure on peripheral adrenergic receptors in young healthy volunteers View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2000-08

AUTHORS

Fabio Fischetti, Bruno Fabris, Marco Zaccaria, Annalisa Biagi, Mario Calci, Riccardo Candido, Monica Bortoletto, Renzo Carretta

ABSTRACT

The regulation of adrenergic receptors during hypoxia is complex, and the results of published reports have not been consistent. In the present study blood cell adrenoceptor characteristics at sea level (SL) before and after prolonged exposure to high altitude (HA) were measured in seven trained young male lowlanders. Sympathoadrenal activity and clinical haemodynamic parameters were also evaluated before departure (SLB), after 1 week (HA1) and 4 weeks (HA4) at HA and 1 week after return to sea level (SLA). As compared to pre-departure sea level values, urinary norepinephrine excretion increased significantly during altitude exposure [SLB: 10.26 (3.04) μg · 3 h−1; HA1: 23.2 (4.19) μg · 3 h−1; HA4: 20.3 (8.68) μg · 3 h−1] and fell to pre-ascent values 1 week after return to sea level [SLA: 9 (2.91) μg · 3 h−1]. In contrast, mean urinary epinephrine levels did not increase over time at HA. Both systolic and diastolic blood pressures, as well as heart rate, were increased during HA exposure. The circadian blood pressure and heart rate rhythms were preserved during all phases of altitude exposure. Mean maximal binding (Bmax) of the α2-adrenoceptor antagonist [3H]rauwolscine to platelet membranes was significantly reduced (P < 0.001) after exposure to chronic hypoxia [SLB: 172.6 (48.5) fmol · mg−1 protein versus SLA: 136.8 (56.1) fmol · mg−1 protein] without change in the dissociation constant (KD). Neither the lymphomonocyte β2-adrenoceptor Bmax [SLB: 38.5 (13.6) fmol · mg−1 protein, versus SLA: 32.4 (12.1) fmol · mg−1 protein] nor the KD for [3H]dihydroalprenolol was affected by chronic hypoxia. Cyclic AMP (adenosine 3′,5′-cyclic monophoshate) generation in lymphomonocytes by maximal isoproterenol stimulation was not modified after prolonged HA exposure. In conclusion, the down-regulation of α2-adrenoceptors appears to be an important component of the adrenergic system response to HA exposure. More... »

PAGES

439-445

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s004210000239

DOI

http://dx.doi.org/10.1007/s004210000239

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009204369

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10985598


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38 antagonist
39 binding
40 blood cell adrenoceptor characteristics
41 blood pressure
42 cell adrenoceptor characteristics
43 changes
44 characteristics
45 chronic hypoxia
46 circadian blood pressure
47 clinical haemodynamic parameters
48 components
49 conclusion
50 contrast
51 cyclic AMP generation
52 departure
53 diastolic blood pressure
54 dissociation
55 effect
56 epinephrine levels
57 excretion
58 exposure
59 generation
60 haemodynamic parameters
61 healthy volunteers
62 heart rate
63 heart rate rhythms
64 high altitude
65 high-altitude exposure
66 hypoxia
67 important component
68 isoproterenol stimulation
69 level values
70 levels
71 lowlanders
72 lymphomonocyte β2-adrenoceptor Bmax
73 lymphomonocytes
74 male lowlanders
75 maximal binding
76 maximal isoproterenol stimulation
77 membrane
78 norepinephrine excretion
79 parameters
80 peripheral adrenergic receptors
81 phase
82 pre-ascent values 1
83 pre-departure sea level values
84 present study blood cell adrenoceptor characteristics
85 pressure
86 prolonged HA exposure
87 prolonged exposure
88 rate
89 rate rhythm
90 receptors
91 regulation
92 report
93 response
94 results
95 return
96 rhythm
97 sea level
98 sea level values
99 stimulation
100 study blood cell adrenoceptor characteristics
101 sympathoadrenal activity
102 system response
103 time
104 urinary epinephrine levels
105 urinary norepinephrine excretion
106 value 1
107 values
108 volunteers
109 weeks
110 young healthy volunteers
111 young male lowlanders
112 α2-adrenoceptor antagonist
113 α2-adrenoceptors
114 β2-adrenoceptor Bmax
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