maxadilan-protein--insect and icatibant

Experiments were designed to determine if salivary gland homogenates (SGH) of the sand fly Lutzomyia longipalpis, the vasodilatory peptides maxadilan and pituitary adenylate cyclase-activating peptide (PACAP-38) may cause plasma leakage and to what extent these effects could be due to PAC1 receptor stimulation.. Using FITC-dextran as a plasma marker, intravital microscopy of the hamster cheek pouch (HCP) and a digital camera were used to assess arteriolar diameter and fluorescence of a selected area (5 mm(2)) representative of the HCP microcirculation.. Cheek pouches prepared for intravital microscopy and exposed to topical application of SGH, maxadilan or PACAP-38 developed maximal dilation of arterioles in the range of 20-60 mum within 10 min, and this effect lasted for 30-90 min. The increase in fluorescence intensity induced by each of these compounds was due to plasma leakage from postcapillary venules. The mutant peptide of maxadilan (M-65), a PAC1 receptor antagonist, inhibited both dilation and plasma leakage induced by SGH or maxadilan. Plasma leakage induced by SGH was modestly inhibited by the bradykinin B(2) receptor antagonist HOE-140, but not by the antihistamine mepyramine or the nitric oxide synthase inhibitor L-NA.. SGH of L. longipalpis and its vasodilatory peptide maxadilan caused long-lasting arteriolar dilation and plasma leakage in the cheek pouch via PAC1 receptor activation.

Topics: Adrenergic beta-Antagonists; Animals; Arterioles; Bradykinin; Cricetinae; Enzyme Inhibitors; Female; Histamine H1 Antagonists; Insect Proteins; Male; Microscopy, Fluorescence; Nitroarginine; Pituitary Adenylate Cyclase-Activating Polypeptide; Plasma; Psychodidae; Pyrilamine; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I; Salivary Glands; Vasodilation; Vasodilator Agents; Venules