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10.1111/bph.12825 http://scihub22266oqcxt.onion/10.1111/bph.12825 C4369259!4369259 !24962324     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24962324 &cmd=llinks): Failed to open stream: HTTP request failed! 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Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats |pdf=|usr=}}{{24962324 }} gab.com Text Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats JO: Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=24962324 #FOAvip BACKGROUND AND PURPOSE: Hypertension is an important mediator of cardiac damage and remodelling. Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with cardioprotective properties. However, it is not yet in clinical use. We, therefore, investigated the protective effects of sodium thiosulfate (STS), a clinically applicable H2 S donor substance, in angiotensin II (Ang II)-induced hypertensive cardiac disease in rats. EXPERIMENTAL APPROACH: Male Sprague Dawley rats were infused with Ang II (435?ng kg min(-1)) or saline (control) for 3 weeks via s.c. placed osmotic minipumps. During these 3 weeks, rats received i.p. injections of either STS, NaHS or vehicle (0.9% NaCl). KEY RESULTS: Compared with controls, Ang II infusion caused an increase in systolic and diastolic BP with associated cardiac damage as evidenced by cardiac hypertrophy, an increase in atrial natriuretic peptide (ANP) mRNA, cardiac fibrosis and increased oxidative stress. Treatment with NaHS and STS prevented the development of hypertension and the increase in ANP mRNA levels. Furthermore, the degree of cardiac hypertrophy, the extent of histological fibrosis in combination with the expression of profibrotic genes and the levels of oxidative stress were all significantly decreased. CONCLUSIONS AND IMPLICATIONS: Ang II-induced hypertensive cardiac disease can be attenuated by treatment with STS and NaHS. Although BP regulation is the most plausible mechanism of cardiac protection, the antifibrotic and antioxidant properties of released sulfide may also contribute to their effects. Our data show that H2 S might be a valuable addition to the already existing antihypertensive and cardioprotective therapies. Twit Text FOAVip Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats ????Br J Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=24962324 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24962324 #FOAvip English Wikipedia <ref>{{Cite pmid|24962324 }}</ref> Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin II-induced hypertensive heart disease in rats #MMPMID24962324 Snijder PM ; Frenay AR ; de Boer RA ; Pasch A ; Hillebrands JL ; Leuvenink HG ; van Goor H Br J Pharmacol 2015[Mar]; 172 (6 ): 1494-504 PMID24962324 show ga BACKGROUND AND PURPOSE: Hypertension is an important mediator of cardiac damage and remodelling. Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with cardioprotective properties. However, it is not yet in clinical use. We, therefore, investigated the protective effects of sodium thiosulfate (STS), a clinically applicable H2 S donor substance, in angiotensin II (Ang II)-induced hypertensive cardiac disease in rats. EXPERIMENTAL APPROACH: Male Sprague Dawley rats were infused with Ang II (435?ng kg min(-1)) or saline (control) for 3 weeks via s.c. placed osmotic minipumps. During these 3 weeks, rats received i.p. injections of either STS, NaHS or vehicle (0.9% NaCl). KEY RESULTS: Compared with controls, Ang II infusion caused an increase in systolic and diastolic BP with associated cardiac damage as evidenced by cardiac hypertrophy, an increase in atrial natriuretic peptide (ANP) mRNA, cardiac fibrosis and increased oxidative stress. Treatment with NaHS and STS prevented the development of hypertension and the increase in ANP mRNA levels. Furthermore, the degree of cardiac hypertrophy, the extent of histological fibrosis in combination with the expression of profibrotic genes and the levels of oxidative stress were all significantly decreased. CONCLUSIONS AND IMPLICATIONS: Ang II-induced hypertensive cardiac disease can be attenuated by treatment with STS and NaHS. Although BP regulation is the most plausible mechanism of cardiac protection, the antifibrotic and antioxidant properties of released sulfide may also contribute to their effects. Our data show that H2 S might be a valuable addition to the already existing antihypertensive and cardioprotective therapies. |Angiotensin II/toxicity [MESH] |Animals [MESH] |Antihypertensive Agents/pharmacology [MESH] |Blood Pressure/drug effects [MESH] |Cardiomegaly/etiology/prevention & control [MESH] |Disease Models, Animal [MESH] |Hydrogen Sulfide/*metabolism [MESH] |Hypertension/complications/*drug therapy/physiopathology [MESH] |Male [MESH] |Oxidative Stress/drug effects [MESH] |Rats [MESH] |Rats, Sprague-Dawley [MESH] |Sulfides/*pharmacology [MESH]Exogenous administration of thiosulfate, a donor of hydrogen sulfide, (epmc).pdf DeepDyve Pubget Overpricing