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Involvement of calcitonin gene-related peptide (CGRP) receptors in insulin-induced vasodilatation in mesenteric resistance blood vessels of rats.
Br J Pharmacol. 1998 Apr; 123(8):1684-90.BJ

Abstract

1. The vascular effect of insulin in the mesenteric resistance blood vessel and the role of calcitonin generelated peptide (CGRP)-receptor in insulin-induced vascular responsiveness were investigated in rats. 2. The mesenteric vascular beds isolated from Wistar rats were perfused with Krebs solution, and perfusion pressure was measured with a pressure transducer. In preparations contracted by perfusion with Krebs solution containing methoxamine in the presence of guanethidine, the perfusion of insulin (from 0.1 to 3000 nM) caused a concentration-dependent decrease in perfusion pressure due to vasodilatation. The pD2 value and maximum relaxation (%) were 6.94+/-0.22 and 43.9+/-5.2, respectively. 3. This vasodilator response to insulin was unaffected by 100 nM propranolol (beta-adrenoceptor antagonist) plus 100 nM atropine (muscarinic cholinoceptor antagonist), 100 microM L-NG-nitroarginine (nitric oxide synthase inhibitor), 1 microM ouabain (Na+-K+ ATPase inhibitor), or 1 microM glibenclamide (ATP sensitive K+-channel inhibitor). 4. In preparations without endothelium, perfusion of insulin produced a marked vasodilatation. The pD2 value and maximum relaxation (%) were 7.62+/-0.21 and 81.0+/-4.6, respectively, significantly greater than in preparations with intact endothelium. 5. The vasodilator responses to insulin in the preparations without endothelium were significantly inhibited by CGRP[8 37], a CGRP receptor antagonist, whereas pretreatment with capsaisin, a toxin for CGRP-containing nerves, did not affect insulin-induced vasodilatation. 6. These results suggest that insulin induces non-adrenergic, non-cholinergic and endothelium-independent vasodilatation, which is partially mediated by CGRP receptors.

Authors+Show Affiliations

Department of Hospital Pharmacy, Okayama University Medical School, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

9605576

Citation

Mimaki, Y, et al. "Involvement of Calcitonin Gene-related Peptide (CGRP) Receptors in Insulin-induced Vasodilatation in Mesenteric Resistance Blood Vessels of Rats." British Journal of Pharmacology, vol. 123, no. 8, 1998, pp. 1684-90.
Mimaki Y, Kawasaki H, Okazaki M, et al. Involvement of calcitonin gene-related peptide (CGRP) receptors in insulin-induced vasodilatation in mesenteric resistance blood vessels of rats. Br J Pharmacol. 1998;123(8):1684-90.
Mimaki, Y., Kawasaki, H., Okazaki, M., Nakatsuma, A., Araki, H., & Gomita, Y. (1998). Involvement of calcitonin gene-related peptide (CGRP) receptors in insulin-induced vasodilatation in mesenteric resistance blood vessels of rats. British Journal of Pharmacology, 123(8), 1684-90.
Mimaki Y, et al. Involvement of Calcitonin Gene-related Peptide (CGRP) Receptors in Insulin-induced Vasodilatation in Mesenteric Resistance Blood Vessels of Rats. Br J Pharmacol. 1998;123(8):1684-90. PubMed PMID: 9605576.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of calcitonin gene-related peptide (CGRP) receptors in insulin-induced vasodilatation in mesenteric resistance blood vessels of rats. AU - Mimaki,Y, AU - Kawasaki,H, AU - Okazaki,M, AU - Nakatsuma,A, AU - Araki,H, AU - Gomita,Y, PY - 1998/5/30/pubmed PY - 1998/5/30/medline PY - 1998/5/30/entrez SP - 1684 EP - 90 JF - British journal of pharmacology JO - Br J Pharmacol VL - 123 IS - 8 N2 - 1. The vascular effect of insulin in the mesenteric resistance blood vessel and the role of calcitonin generelated peptide (CGRP)-receptor in insulin-induced vascular responsiveness were investigated in rats. 2. The mesenteric vascular beds isolated from Wistar rats were perfused with Krebs solution, and perfusion pressure was measured with a pressure transducer. In preparations contracted by perfusion with Krebs solution containing methoxamine in the presence of guanethidine, the perfusion of insulin (from 0.1 to 3000 nM) caused a concentration-dependent decrease in perfusion pressure due to vasodilatation. The pD2 value and maximum relaxation (%) were 6.94+/-0.22 and 43.9+/-5.2, respectively. 3. This vasodilator response to insulin was unaffected by 100 nM propranolol (beta-adrenoceptor antagonist) plus 100 nM atropine (muscarinic cholinoceptor antagonist), 100 microM L-NG-nitroarginine (nitric oxide synthase inhibitor), 1 microM ouabain (Na+-K+ ATPase inhibitor), or 1 microM glibenclamide (ATP sensitive K+-channel inhibitor). 4. In preparations without endothelium, perfusion of insulin produced a marked vasodilatation. The pD2 value and maximum relaxation (%) were 7.62+/-0.21 and 81.0+/-4.6, respectively, significantly greater than in preparations with intact endothelium. 5. The vasodilator responses to insulin in the preparations without endothelium were significantly inhibited by CGRP[8 37], a CGRP receptor antagonist, whereas pretreatment with capsaisin, a toxin for CGRP-containing nerves, did not affect insulin-induced vasodilatation. 6. These results suggest that insulin induces non-adrenergic, non-cholinergic and endothelium-independent vasodilatation, which is partially mediated by CGRP receptors. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/9605576/Involvement_of_calcitonin_gene_related_peptide__CGRP__receptors_in_insulin_induced_vasodilatation_in_mesenteric_resistance_blood_vessels_of_rats_ L2 - https://doi.org/10.1038/sj.bjp.0701779 DB - PRIME DP - Unbound Medicine ER -