title: Feeble bronchomotor responses in diabetic rats in association with decreased sensory neuropeptide release.
abstract: Type I diabetes is associated with a low incidence of asthma. We tested whether a decrease in sensory neuropeptide release is associated with an attenuated bronchoconstrictive response to field stimulation (FS; 100 stimuli, 20 V, 0.1 ms, 20 Hz) in streptozotocin (STZ)-induced diabetes. The organ fluid of the preparations were also tested for substance P, calcitonin gene-related peptide (CGRP), and somatostatin concentrations by RIA. Preparations were from either normal rats or those pretreated with 50 mg/kg STZ iv 8 wk before experiment. A group of STZ-treated animals was supplied with insulin delivery (4 IU/day sc) implants between 4 and 8 wk. A subgroup was formed to study the effect of capsaicin desensitization. The atropine-resistant contraction was attenuated by diabetes without capsaicin-sensitive relaxation response. Exogenous CGRP and substance P potentiated, whereas somatostatin inhibited (1 nM-10 microM) the FS-induced contractions in rings from either group. FS released somatostatin, CGRP, and substance P from 0.17 +/- 0.024, 0.15 +/- 0.022, and 1.65 +/- 0.093 to 0.58 +/- 0.032, 0.74 +/- 0.122, and 5.34 +/- 0.295 in preparations from normal, and from 0.19 +/- 0.016, 0.11 +/- 0.019, and 0.98 +/- 0.116 to 0.22 +/- 0.076, 0.34 +/- 0.099, and 1.84 +/- 0.316 fmol/mg wet wt in preparations from diabetic rats. Insulin supplementation restored neuropeptide release in rings from STZ-treated rats. The results show that the decreased FS-induced contractions occurred with a decrease in sensory neuropeptide release in STZ-diabetic rats.
authors.affiliation: Department of Oto-rhino-laryngology, Medical University of Debrecen, H-4032 Debrecen, Hungary. szj@jaguar.dote.hu
authors.forename: Judith
authors.initials: J
authors.lastname: Szilvássy
authors.forename: István
authors.initials: I
authors.lastname: Sziklai
authors.forename: Peter
authors.initials: P
authors.lastname: Horvath
authors.forename: Maria
authors.initials: M
authors.lastname: Szilasi
authors.forename: József
authors.initials: J
authors.lastname: Németh
authors.forename: Péter
authors.initials: P
authors.lastname: Kovács
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Szilvássy
mesh_terms: D000818:Animals; D001786:Blood Glucose; D001835:Body Weight; D016535:Bronchial Hyperreactivity / Q000503:physiopathology; D016084:Bronchoconstriction / Q000187:drug effects / Q000502:physiology*; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism*; D002211:Capsaicin / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D006168:Guinea Pigs; D007328:Insulin / Q000097:blood; D008297:Male; D009431:Neural Conduction; D009475:Neurons, Afferent / Q000378:metabolism*; D010047:Ovalbumin / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013004:Somatostatin / Q000097:blood; D013373:Substance P / Q000378:metabolism*; D014132:Trachea / Q000294:innervation / Q000503:physiopathology
chemical_list: D001786:Blood Glucose; D007328:Insulin; D013373:Substance P; D013004:Somatostatin; D010047:Ovalbumin; D015740:Calcitonin Gene-Related Peptide; D002211:Capsaicin