Adrenergic-purinergic interactions on vasoconstrictor responses to periarterial electric nerve stimulation in canine splenic arteries.
1. Periarterial nerve electrical stimulation caused a double peaked vasoconstriction in isolated perfused canine splenic arterial preparations. At low frequencies (1-3 Hz), the 1st peak responses were significantly inhibited by alpha,beta-methylene ATP. On the other hand, at high frequencies (8-10 Hz), the responses were not completely inhibited by alpha,beta-methylene ATP but the remaining response was abolished by an additional treatment of prazosin. 2. Concerning the 2nd peak responses, at low frequencies (1-3 Hz), the response was mostly suppressed by alpha,beta-methylene ATP, but at high frequencies (6-10 Hz), the response was not significantly modified by it, although the remaining responses were completely blocked by prazosin. Thus, at high frequencies an adrenergic and purinergic interaction may exist presynaptically, to prevent the inhibition by alpha,beta-methylene ATP. 3. At 1 Hz, rauwolscine, an alpha2-adrenoceptor antagonist, caused a potentiation of electrical stimulation-induced responses (both 1st and 2nd peaked responses) which were inhibited by prazosin, and the remaining ones were abolished by alpha,beta-methylene ATP. On the other hand, at 10 Hz, rauwolscine did not cause any potentiation of the double peaked responses. 4. The biphasic responses at 1 Hz were strongly inhibited by exogenously applied ATP, and its inhibition was reversed in part by a P1 receptor antagonist 8-phenyltheophylline (8-PT). On the other hand, the biphasic vasoconstrictions at 10 Hz were only slightly depressed by ATP, and a subsequent administration of 8-PT produced a partial recovery of the 1st phase response but not that of the 2nd one. 5. From these results, it is concluded that (1) at low frequencies the double peaked responses are mostly mediated via P2X receptor, presynaptic P1 receptors may also modulate the release of ATP, and presynaptic alpha2-adrenergic mechanism may tonically participate in the release of noradrenaline (2) at high frequencies the responses are mostly mediated via alpha1-adrenoceptors and presynaptic P2 receptors may exert its action to inhibit the release of noradrenaline from adrenergic nerve terminals.
Yang
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Department of Pharmacology, Shinshu University School of Medicine, Matsumoto, Japan.
Chiba
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D000255:Adenosine Triphosphate / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009424:Nervous System Physiological Phenomena; D010477:Perfusion; D011224:Prazosin / Q000494:pharmacology*; D011941:Receptors, Adrenergic / Q000502:physiology; D011983:Receptors, Purinergic / Q000502:physiology; D013157:Splenic Artery / Q000502:physiology*; D013565:Sympatholytics / Q000494:pharmacology; D013806:Theophylline / Q000031:analogs & derivatives / Q000494:pharmacology; D015016:Yohimbine / Q000494:pharmacology
D011941:Receptors, Adrenergic; D011983:Receptors, Purinergic; D013565:Sympatholytics; D015016:Yohimbine; D000255:Adenosine Triphosphate; D013806:Theophylline; C028322:8-phenyltheophylline; C002630:alpha,beta-methyleneadenosine 5'-triphosphate; D011224:Prazosin