Adrenergic and non-adrenergic mechanisms in sympathetic vascular control of the nasal mucosa.
1. Co-existence of NA and NPY-LI was observed in the dense network of sympathetic nerves around both resistance and capacitance vessels in the nasal mucosa from most species including man. NPY-LI seems also to be present together with VIP-LI and PHI-LI in periglandular and some perivascular parasympathetic fibres in some species. 2. A new in vivo model was developed in the pig which allowed parallel recordings of arterial blood flow (BF), capacitance function (V) and superficial movement of blood cells (LDF signal) of the nasal mucosa upon SNS and/or local intra-arterial injection of various pharmacological agents. SNS reduced both BF and V. The V response was maximal already at low frequency. The LDF signal was increased when the SNS-evoked BF reduction was under 40% but was reduced upon larger BF response. After pretreatment with the alpha-adrenoceptor antagonist PBZ, the vascular responses to SNS were significantly attenuated but clear-cut reductions of BF, V and LDF responses remained even to a single impulse. Exogenous NA induced dose-dependent reductions of the BF, V and LDF signal, which were abolished by PBZ treatment. ATP caused biphasic vascular effects with short-lasting vasoconstriction followed by vasodilatation. NPY and mATP caused reduction of the vascular parameters via non-adrenergic mechanisms. 3. A frequency-dependent increase of NA overflow was observed in the nasal venous effluent upon SNS in control pigs, whereas detectable release of NPY-LI occurred only at high frequency. Pretreatment with PBZ significantly increased the SNS-evoked NA and NPY-LI overflow, while DMI enhanced both the functional response and NA release but reduced the NPY-LI overflow. These data suggest that NA and NPY release in the pig nasal mucosa is regulated by prejunctional alpha-adrenoceptor mechanisms. During tachyphylaxis to mATP, the NA and NPY-LI overflow and the vasoconstrictor responses to SNS were unmodified in controls. 4. Reserpine pretreatment induced a marked depletion of both NA and NPY-LI in the pig nasal mucosa. The reduction of NA was not influenced by preganglionic denervation while the depletion of NPY then was prevented. Slowly developing, frequency-dependent and long-lasting vascular responses remained (up to 80% of control) upon SNS in reserpinized and decentralized animals. In these animals, the NA overflow was abolished while release of NPY-LI was enhanced. Stimulation with irregular bursts, caused both larger vascular responses and more NPY-LI overflow in comparison with continuous stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)
Lacroix
J S
JS
Department of Pharmacology, Karolinska Institutet, Stockholm, Sweden.
D000255:Adenosine Triphosphate / Q000008:administration & dosage / Q000378:metabolism; D000320:Adrenergic Fibers / Q000378:metabolism / Q000502:physiology*; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D007269:Injections, Intra-Arterial; D009297:Nasal Mucosa / Q000098:blood supply* / Q000294:innervation / Q000378:metabolism; D009478:Neuropeptide Y / Q000008:administration & dosage / Q000378:metabolism; D009638:Norepinephrine / Q000008:administration & dosage / Q000378:metabolism; D013552:Swine; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D014655:Vascular Resistance / Q000187:drug effects
D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D009478:Neuropeptide Y; D000255:Adenosine Triphosphate; D009638:Norepinephrine