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Attenuation of Hydrogen Sulfide‐Induced Relaxation of Aorta from Diabetic Rats
Author(s) -
Zangeneh Shiva,
Oyekan Adebayo O,
Yakubu Momoh A
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1148.22
Subject(s) - aorta , streptozotocin , chemistry , cystathionine beta synthase , hydrogen sulfide , medicine , endocrinology , contraction (grammar) , diabetes mellitus , relaxation (psychology) , cysteine , enzyme , biochemistry , sulfur , organic chemistry
Hydrogen Sulfide (H 2 S) is the new gasotransmitter produced from L‐Cysteine by cystathionine‐β‐synthase, and cystathionine‐γ‐lyase causing vasorelaxation via activation of K (ATP) ‐channel. Information on the regulation of the H 2 S vascular function in disease conditions is limited. We studied the effects of diabetes on H 2 S relaxation of aorta from rats treated with 70 mg/kg, i.p. streptozotocin (STZ) or vehicle. Vascular responses to H 2 S (10 −6 −10 −2 M) was determined in control and diabetic aorta following contraction with PE (10 −7 ) or 5‐Hydroxytryptamine (5‐HT, 10 −6 M). Tension generated by PE or 5‐HT were dose‐dependently relaxed by application of H 2 S with the highest concentration of H 2 S 10 −2 M producing 66% of the 5‐HT and 40% of the PE induced tension. In the STZ, relaxation by H 2 S was attenuated to 41 and 32% respectively for 5‐HT and PE tensions. In this study, both 5‐HT and PE‐induced tensions were significantly enhanced in the STZ compared to the control. The enhancement was significantly higher for 5‐HT at 2.03 ± 0.03 gm compared to PE at 1.47 ± 0.025 gm. In conclusion: H 2 S‐induced relaxation was selectively higher in the 5‐HT than in the PE pre‐contracted aortic rings and relaxations of aorta from STZ‐induced diabetic rats was selectively attenuated for 5‐HT‐ but not for PE‐induced tension. Thus, these selective effects could be due to the several mechanisms involved in the H 2 S‐induced vascular relaxation. This work was supported by grants from NHLBI: HL03674 and HL70669.