L-NAME enhances responses to atrial natriuretic peptide in the pulmonary vascular bed of the cat

Hyman A. L., De Witt B. J., Gumusel B., Hao Q., Kadowitz P. J., Lippton H. L.

Journal of Applied Physiology, cilt.90, sa.6, ss.2101-2108, 2001 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 90 Sayı: 6
  • Basım Tarihi: 2001
  • Doi Numarası: 10.1152/jappl.2001.90.6.2101
  • Dergi Adı: Journal of Applied Physiology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.2101-2108
  • Anahtar Kelimeler: lung, guanosine 3 ', 5 '-cyclic monophosphate, methylene blue, atrial natriuretic peptide receptors, N omega-monomethyl-L-arginine, NONPEPTIDE ANP ANTAGONIST, CYCLIC-GMP, VASODILATOR RESPONSES, RELAXING FACTOR, NITRIC-OXIDE, HS-142-1, INHIBITION, RECEPTOR, CIRCULATION, BRADYKININ
  • Lokman Hekim Üniversitesi Adresli: Hayır

Özet

This study investigated the hypothesis that atrial natriuretic peptide (ANP) responses are mediated by particulate guanylate cyclase in the pulmonary vascular bed of the cat. When tone in the pulmonary vascular bed was raised to a high steady level with thethromboxane mimic U-46619, injections of ANP caused dose-related decreases in lobar arterial pressure. After administration of HS-142-1, an ANP-A- and ANP-B-receptor antagonist, vasodilator responses to ANP were reduced. The nitric oxide (NO) synthase inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) enhanced ANP vasodilator responses, suggesting that inhibition of NO modulates ANP responses. L-NAME administration with constant 8-bromo-cGMP infusion attenuated the increased vasodilator response to ANP, suggesting that supersensitivity to ANP occurs upstream to activation of a cGMP-dependent protein kinase. In pulmonary arterial rings, ANP produced concentration-related vasorelaxant responses with and without endothelium. Methylene blue, L-NAME, or Nω-monomethyl-L-arginine did not alter ANP vasorelaxant responses. These data show that ANP supersensitivity observed in the intact pulmonary vascular bed is not seen in isolated pulmonary arterial segments, suggesting that it may only occur in resistance vessel elements. These results suggest that ANP responses occur through activation of ANP-A and/or -B receptors in an endothelium-independent manner and are modulated by NO in resistance vessel elements in the pulmonary vascular bed of the cat.