Inhibition of oxytocin-induced but not angiotensin-induced rat uterine contractions following exposure to sodium sulfide

Hayden, Lawrence J.; Franklin, K. J.; Roth, Sheldon H.; Moore, Graham J.

doi:10.1016/0024-3205(89)90239-7

Cited by 27 publications

(21 citation statements)

References 4 publications

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“…H 2 S has potent relaxant effect in vascular and nonvascular smooth muscles (Hayden et al 1989;Hosoki et al 1997;Zhao et al 2001;Teague et al 2002). It has been shown that H 2 S produces relaxation response in isolated arteries and veins of rat in vitro and lowers rat blood pressure in vivo (Zhao et al 2001;Zhao and Wang 2002).…”

Section: Introductionmentioning

confidence: 98%

The vasorelaxant effect of hydrogen sulfide is enhanced in streptozotocin-induced diabetic rats

Denizalti

Bozkurt

Akpulat

et al. 2011

Naunyn-Schmiedeberg's Arch Pharmacol

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Hydrogen sulfide (H₂S) is an endogenous gas which has potent relaxant effect in vascular and nonvascular smooth muscles. In the present study, we have investigated how streptozotocin (STZ)-induced diabetes affected the relaxant effect of H₂S in rat isolated thoracic aorta and mesenteric and pulmonary arteries. Diabetes was induced by IV injection of STZ (35 mg/kg). Insulin treatment was applied by using insulin implants. At the end of 4 and 12 weeks, the thoracic aorta and mesenteric and pulmonary arteries were isolated, and the relaxation responses to sodium hydrogen sulfide (NaHS), diazoxide, and acetylcholine were evaluated. The mRNA and protein levels of H₂S-synthesizing enzymes were also examined by RT-PCR and Western Blot. The relaxation response to NaHS in the arteries isolated from both 4 and 12 week-diabetic rats was increased when compared with that obtained from the control group. Glibenclamide inhibited the relaxation response to NaHS in the arteries isolated from either diabetic or non-diabetic group of rats. Concurrent treatment of insulin to STZ-injected rats prevented the potentiation of the relaxant effect of NaHS in the arteries. However, acetylcholine and diazoxide-induced relaxation responses were not altered in diabetic group of rats. The mRNA and protein levels of H₂S-synthesizing enzymes were also not altered in diabetic rats. STZ-induced experimental diabetes in rats resulted in the potentiation of the relaxation response to H₂S in vascular tissues. The potentiated relaxation to H₂S in diabetic arteries may play a role in vascular complications frequently seen in severe diabetes.

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Section: Introductionmentioning

confidence: 98%

The vasorelaxant effect of hydrogen sulfide is enhanced in streptozotocin-induced diabetic rats

Denizalti

Bozkurt

Akpulat

et al. 2011

Naunyn-Schmiedeberg's Arch Pharmacol

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“…H 2 S is synthesized by, and has physiological actions in, a variety of mammalian tissues including brain (Abe and Kimura, 1996;Kimura, 2000;Kimura, 2002), vascular (Hosoki et al, 1997;Zhao et al, 2001;Zhao and Wang, 2002;Cheng et al, 2004), gastrointestinal (Hosoki et al, 1997;Teague et al, 2002), genitourinary (Patacchini et al, 2004;Patacchini et al, 2005) and reproductive (Hayden et al, 1989;Sidhu et al, 2001;Teague et al, 2002) tracts, pulmonary system (Shi et al, 2003;Zhang et al, 2003;Cheng et al, 2004), and heart (Zhang et al, 2003;Geng et al, 2004). H 2 S relaxes most mammalian smooth muscles including systemic vessels (Hosoki et al, 1997;Zhao et al, 2001;Zhao and Wang, 2002;Cheng et al, 2004), intestine (Hosoki et al, 1997;Teague et al, 2002), uterus (Sidhu et al, 2001) and vas deferens (Teague et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Hydrogen sulfide mediates hypoxia-induced relaxation of trout urinary bladder smooth muscle

Dombkowski

Doellman

Head

et al. 2006

Journal of Experimental Biology

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“…In particular, in the cardiovascular system, H 2 S relaxes isolated vessels and produces hypotension in vivo by opening ATPsensitive K þ channels (K ATP ) (Hosoki et al, 1997;Zhao et al, 2001). A smooth muscle relaxant activity of H 2 S has also been noted in gastrointestinal (Hosoki et al, 1997;Teague et al, 2002) and reproductive (Hayden et al, 1989;Teague et al, 2002) organs. However, unlike the inhibitory effects afforded by H 2 S in the rat aorta (Zhao et al, 2001), the relaxant effect produced by the gas in the guinea-pig ileum was unaffected by the K þ channel blocker glibenclamide, leading Teague et al (2002) to conclude that a still unidentified mechanismindependent of K ATP channels -is responsible for the intestinal effects of H 2 S. In the present study, we decided to investigate the effects produced by H 2 S in the detrusor muscle of the rat urinary bladder.…”

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confidence: 99%

Hydrogen sulfide (H₂S) stimulates capsaicin‐sensitive primary afferent neurons in the rat urinary bladder

Patacchini

Santicioli

Giuliani

et al. 2004

British J Pharmacology

119

103

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In the rat isolated urinary bladder, NaHS (30 mM-3 mM) and capsaicin (10 nM-3 mM) produced concentration-dependent contractile responses (pEC 50 ¼ 3.570.02 and 7.170.02, respectively) undergoing dramatic tachyphylaxis. In preparations in which sensory nerves were rendered desensitized (defunctionalized) by high-capsaicin (10 mM for 15 min) pretreatment, neither capsaicin itself nor NaHS produced any motor effect. NaHS-induced contractile effects were totally prevented by the simultaneous incubation with tachykinin NK 1 (GR 82334; 10 mM) and NK 2 (nepadutant; 0.3 mM) receptor-selective antagonists. Tetrodotoxin (1 mM) only partially reduced the response to NaHS. These results provide pharmacological evidence that H 2 S stimulates capsaicin-sensitive primary afferent nerve terminals, from which tachykinins are released to produce the observed contraction by activating NK 1 and NK 2 receptors. While the molecular site of action of H 2 S remains to be investigated, our discovery may have important physiological significance since H 2 S concentrations capable of stimulating sensory nerves overlap those occurring in mammalian tissues under normal conditions.

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Inhibition of oxytocin-induced but not angiotensin-induced rat uterine contractions following exposure to sodium sulfide

Cited by 27 publications

References 4 publications

The vasorelaxant effect of hydrogen sulfide is enhanced in streptozotocin-induced diabetic rats

The vasorelaxant effect of hydrogen sulfide is enhanced in streptozotocin-induced diabetic rats

Hydrogen sulfide mediates hypoxia-induced relaxation of trout urinary bladder smooth muscle

Hydrogen sulfide (H₂S) stimulates capsaicin‐sensitive primary afferent neurons in the rat urinary bladder

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Inhibition of oxytocin-induced but not angiotensin-induced rat uterine contractions following exposure to sodium sulfide

Cited by 27 publications

References 4 publications

The vasorelaxant effect of hydrogen sulfide is enhanced in streptozotocin-induced diabetic rats

The vasorelaxant effect of hydrogen sulfide is enhanced in streptozotocin-induced diabetic rats

Hydrogen sulfide mediates hypoxia-induced relaxation of trout urinary bladder smooth muscle

Hydrogen sulfide (H2S) stimulates capsaicin‐sensitive primary afferent neurons in the rat urinary bladder

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Product

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Hydrogen sulfide (H₂S) stimulates capsaicin‐sensitive primary afferent neurons in the rat urinary bladder