RT Journal Article
SR Electronic
T1 Modulated vasodilator responses to natriuretic peptides in rats exposed to chronic hypoxia
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 400
OP 406
DO 10.1034/j.1399-3003.2000.15b29.x
VO 15
IS 2
A1 Y Mitani
A1 J Maruyama
A1 A Yokochi
A1 K Maruyama
A1 T Yoshimoto
A1 M Naruse
A1 M Sakurai
YR 2000
UL http://erj.ersjournals.com/content/15/2/400.abstract
AB Natriuretic peptides (NPs), such as atrial natriuretic peptide (ANP), C-type natriuretic peptide (CNP), and adrenomedullin (ADM), are endogenous vasodilators acting via specific receptors. This study addressed the question of how pulmonary artery (PA) responses to these peptides and the gene expression of their receptors are modulated in pulmonary hypertension rat models exposed to chronic hypoxia. In this study, isometric tension was measured in PA rings exposed to these NPs and 8-bromoguanosine 3', 5'-cyclic monophosphate (8-bromo-cGMP). It was compared with messenger ribonucleic acid (mRNA) levels of NP-A and -B receptors, which bind to ANP and CNP, respectively, as determined by ribonuclease (RNase) protection assay. Chronic hypoxia increased the maximal relaxation elicited by ANP, but the responses to CNP and 8-bromo-cGMP were unchanged. Chronic hypoxia did not change NP-A and -B receptor mRNA levels. The results showed that pulmonary artery response to atrial natriuretic peptide is selectively enhanced, possibly via a post-transcriptional modulation of its receptor in chronically hypoxia rats. These pharmacological characteristics of atrial natriuretic peptide are consistent with the hypothesis that the atrial natriuretic peptide system is protective against the progression of pulmonary hypertension.