Enhancement of ATP release in hindlimb sympathetic perivascular nerve of the golden hamster during hibernation.
The present study investigated the effects of hibernation and hibernating body temperature (10 degrees C) on the relative changes that may occur in adrenergic and purinergic perivascular neurotransmission of the golden hamster. The hindlimb resistance vessels and the tibial artery of age-matched controls, cold exposed controls and hibernated hamsters were examined by pharmacological and electrophysiological techniques. At 34 degrees C, electrical field stimulation (EFS; supramaximal voltage, 0.5 ms; for 10 s) in all three groups evoked only twitch responses at 1-5 Hz, which were inhibited by piridoxal phosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), a 2PX receptor antagonist. At 10-50 Hz the twitch responses were followed by sustained contractile responses, which were inhibited by prazosin, an alpha1-adrenoceptor antagonist. These responses were markedly enhanced at higher frequencies in hibernated tissues. At 10 degrees C, EFS evoked only the PPADS-sensitive transient responses in all the three groups, and this was markedly enhanced in hibernated tissues. At 34 degrees C, a single stimulus evoked a PPADS-sensitive excitatory junction potential (EJP) in all three groups but a train of pulses (e.g. approximately 0.5) evoked EJPs and prazosin-sensitive sustained depolarizations. These responses were markedly enhanced in hibernated cells. At 10 degrees C, either a single stimulus or a train of stimuli evoked only transient PPADS-sensitive EJPs, which were markedly enhanced in hibernated cells. The contractile responses and electrical membrane responses to exogenous ATP (1-1000 microM) and noradrenaline (0.1-100 microM) were unchanged in the three groups at 34 and at 10 degrees C. These results suggest that during hibernation enhancement of ATP release from the sympathetic perivascular nerves may occur, leading to an efficient means for maintenance of vascular tone and peripheral resistance.
Department of Pathogenetic Veterinary Science, United Graduate School, Gifu University, Yanagido 1-1, Gifu city, 501-1193, Japan.
H
H
Saito
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S
Thapaliya
H
H
Matsuyama
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M
Nishimura
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T
Takewaki
D000255:Adenosine Triphosphate / Q000378:metabolism* / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001808:Blood Vessels / Q000187:drug effects / Q000502:physiology; D006224:Cricetinae; D004558:Electric Stimulation; D004594:Electrophysiology; D005260:Female; D017629:Gap Junctions / Q000187:drug effects / Q000502:physiology; D006605:Hibernation / Q000502:physiology*; D006614:Hindlimb / Q000098:blood supply* / Q000294:innervation*; D008297:Male; D008647:Mesocricetus; D009638:Norepinephrine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives* / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000378:metabolism*; D013696:Temperature; D014661:Vasoconstriction / Q000502:physiology
D000317:Adrenergic alpha-Antagonists; C077792:pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid; D011732:Pyridoxal Phosphate; D000255:Adenosine Triphosphate; D009638:Norepinephrine; D011224:Prazosin