Analysis of erectile responses to H2S donors in the anesthetized rat.
Analysis of erectile responses to H2S donors in the anesthetized rat.
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分析麻醉大鼠对 H2S 供体的勃起反应。
DOI：
10.1152/ajpheart.00293.2015
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Kadowitz,PhilipJ
中科院分区：
文献类型：
--
作者：
Jupiter,RyanC;Yoo,Daniel;Pankey,EdwardA;Reddy,VishwaradhVG;Edward,JustinA;Polhemus,DavidJ;Peak,TaylorC;Katakam,Prasad;Kadowitz,PhilipJ
硫化氢（H2S）是阴茎组织中形成的具有生物活性的内源性气体递质，已被证明可松弛离体海绵体平滑肌。在本研究中，勃起反应的H2S供体硫化钠（Na 2S）和硫氢化钠（NaHS）在麻醉大鼠进行了研究。海绵体内注射0.03-1 mg/kg剂量的Na 2S可增加海绵体内压，并以剂量依赖性方式短暂降低平均动脉压。对Na 2S的血压反应起效快，持续时间短。在剂量高达0.3 mg/kg时，对Na 2S和NaHS的反应相似，之后对NaHS的勃起反应达到平台。四乙基铵（K+通道抑制剂）和伊比利亚毒素（大电导Ca 2+激活的K+通道抑制剂）可减弱Na 2S引起的海绵体内压增加，而格列本脲[ATP敏感性K+（KATP）通道抑制剂]和一氧化氮（NO）合酶、环氧合酶和细胞色素P-450环氧合酶抑制剂则无影响。这些数据表明，对Na 2S的勃起反应是由四乙铵和伊比利亚毒素敏感机制介导的，而KATP通道、NO或花生四烯酸代谢产物不参与其中。Na 2S没有改变对硝普钠（NO供体）或海绵体神经刺激的勃起反应，表明NO和cGMP代谢都没有改变。因此，Na 2S具有通过大电导Ca 2+激活的K+通道介导的勃起活性。这表明，增加阴茎组织中H2S形成的策略可能是有用的治疗勃起功能障碍时，NO的生物利用度，KATP通道功能，或PGE 1反应差。
Hydrogen sulfide (H2S) is a biologically active endogenous gasotransmitter formed in penile tissue that has been shown to relax isolated cavernosal smooth muscle. In the present study, erectile responses to the H2S donors sodium sulfide (Na2S) and sodium hydrosulfide (NaHS) were investigated in the anesthetized rat. Intracavernosal injections of Na2S in doses of 0.03–1 mg/kg increased intracavernosal pressure and transiently decreased mean arterial pressure in a dose-dependent manner. Blood pressure responses to Na2S were rapid in onset and short in duration. Responses to Na2S and NaHS were similar at doses up to 0.3 mg/kg, after which a plateau in the erectile response to NaHS was reached. Increases in intracavernosal pressure in response to Na2S were attenuated by tetraethylammonium (K+channel inhibitor) and iberiotoxin (large-conductance Ca2+-activated K+channel inhibitor), whereas glybenclamide [ATP-sensitive K+(KATP) channel inhibitor] and inhibitors of nitric oxide (NO) synthase, cyclooxygenase, and cytochromeP-450 epoxygenase had no effect. These data indicate that erectile responses to Na2S are mediated by a tetraethylammonium- and iberiotoxin-sensitive mechanism and that KATPchannels, NO, or arachidonic acid metabolites are not involved. Na2S did not alter erectile responses to sodium nitroprusside (NO donor) or cavernosal nerve stimulation, indicating that neither NO nor cGMP metabolism are altered. Thus, Na2S has erectile activity mediated by large-conductance Ca2+-activated K+channels. It is suggested that strategies that increase H2S formation in penile tissue may be useful in the treatment of erectile dysfunction when NO bioavailability, KATPchannel function, or poor responses to PGE1are present.
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