C-type natriuretic peptide inhibits upregulation of alpha1-adrenoceptor and inositol 1,4,5-trisphosphate receptor in rat vascular smooth muscle after vascular endothelial injury.

OBJECTIVE: In a model of balloon injury of rat aortic endothelium, the effects of C-type natriuretic peptide (CNP) on alpha1-adrenoreceptor and inositol 1,4,5-triphosphate (IP3) receptor were studied. METHODS: Aortic injuries were produced by vascular endothelium-denudation. Alpha1-adrenoreceptor in smooth muscle sarcolemma and IP3 receptor in smooth muscle sarcoplasmic reticulum in the rat aorta were assayed by radioactive analysis method. RESULTS: It was found that neointima was formed and the contents of DNA, collagen and elastin of each intima-media were sigificantly increased in 7 days and 21 days after balloon injury of rat aorta. Alpha1-adrenoreceptor in smooth muscle sarcolemma and IF3 receptor in sarcoplasmic reticulum were also upregulated. Results also showed that the administration of CNP i.p. significantly decreased the contents of DNA, collagen and elastin of each intima-media, and inhibited the up-regulation of alpha1-adrenoreceptor and IP3 receptor. CONCLUSION: The inhibition of the up-regulation of alpha1-adrenoreceptor and IP3 receptor by CNP might be one of the mechanisms of its suppressive action on intimal proliferation.

Endogenous heme oxygenase/carbon monoxide system mediates lipopolysaccharide-induced intussusception in rats.

OBJECTIVES: To investigate the role of endogenous heme oxygenase (HO)/carbon monoxide (CO) system in regulating the process of intussusception (IN) induced by administration of lipopolysaccharide (LPS) in rats. METHODS: IN model of rats were induced by lipopolysaccharide. HO activity was determined by the amount of bilirubin formation which was measured with a double-beam spectrophotometer, and HbCO formation was measured by CO-oximeter. RESULTS: The results showed that LPS (10 mg/kg) caused IN in up to 40% of the rats at 6 h after each treatment of LPS. The incidence of IN were significantly increased by 50% (P < 0.05) and by 83.2% (P < 0.01) in HO substrate (heme-L-lysinate)-treated rats and in exogenous CO-treated rats, respectively; but it was sigificantly decreased by 41.8% (P < 0.05) after administration of ZnDPBG, an inhibitor of heme oxygense (HO) activity. Furthermore, LPS increased HO activity, HbCO formation cGMP content within colic smooth muscle and the plasma level of cGMP, and these parameters were significantly elevated by 62.6% (P < 0.01), 40.0% (P < 0.01), 49.3% (P < 0.05) and 38.9% (P<0.05), respectively, compared with LPS-non-IN rats. CONCLUSION: It is suggested that endogenous HO/CO system plays an important role in the process of IN induced by LPS, and inhibition of HO activity may decrease the formation of IN.