title: [Endogenous H2S is involved in the development of spontaneous hypertension].
abstract: Hydrogen sulfide (H2S) is recently found to be a new gaseous messenger playing an important role in many physiological and pathophysiological processes. The aim of this study was to explore the changes in endogenous H2S pathway and examine the effects of H2S on the development of spontaneous hypertensive rats (SHR). A controlled study on SHR and WKY rats at the age of 4 weeks showed that after 5 weeks of experiment, the blood pressure of SHR was markedly increased as compared with WKY rats (183.57 +/- 11.80 mm Hg vs 107.5 +/- 22.68 mm Hg, P < 0.05) and the ratio of left heart weight to whole heart weight of SHR was also increased as compared with WKY rats (0.85 +/- 0.02 vs 0.83 +/- 0.02, P < 0.05). While, the aortic H2S producing rate and H2S plasma level were decreased in SHR compared with WKY rats (15.63 +/- 2.89 nmol.min-1.g-1 vs 25.31 +/- 5.99 nmol.min-1.g-1, 20.35 +/- 9.20 mumol.L-1 vs 48.40 +/- 13.36 mumol.L-1, P < 0.05). NaHS, however, attenuated the high blood pressure and the ratio of left heart weight to whole heart weight of SHR (158.13 +/- 12.52 mm Hg vs 183.57 +/- 11.80 mm Hg and 0.83 +/- 0.03 vs 0.85 +/- 0.02), respectively. The above findings suggested that the reduced production of endogenous H2S was important in the development of spontaneous hypertension. The authors also observed that 5 weeks after the experiment the relaxing rate of aortic rings in response to acetylcholine in SHR was higher than that of WKY rats and NaHS enhanced the relaxing-response of aortic rings to acetylcholine in SHR significantly(P < 0.05). The aortic relaxing activities in both SHR and WKY rats displayed a dose-dependent response to different doses of NaHS. In conclusion, the reduced production of endogenous H2S in aorta is involved in the pathogenesis of spontaneous hypertension and is of great biological importance in modulating vasorelaxation.
authors.affiliation: Department of Pediatrics, Peking University First Hospital, Beijing 100034, China. junbaodu@ht.rol.cn.net
authors.forename: Junbao
authors.initials: J
authors.lastname: Du
authors.forename: Hui
authors.initials: H
authors.lastname: Yan
authors.forename: Chaoshu
authors.initials: C
authors.lastname: Tang
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000378:metabolism*; D006973:Hypertension / Q000209:etiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY
chemical_list: D006862:Hydrogen Sulfide