{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T01:41:13Z","timestamp":1790041273793,"version":"4.0.1"},"reference-count":58,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2015,2,27]],"date-time":"2015-02-27T00:00:00Z","timestamp":1424995200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100002997","name":"Nierstichting","doi-asserted-by":"publisher","award":["NSN C08-2254 and IP13-114"],"award-info":[{"award-number":["NSN C08-2254 and IP13-114"]}],"id":[{"id":"10.13039\/501100002997","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2015,3]]},"abstract":"<jats:sec>\n                    <jats:title>Background and Purpose<\/jats:title>\n                    <jats:p>\n                      Hypertension is an important mediator of cardiac damage and remodelling. Hydrogen sulfide (\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:roman>\n                          H\n                          <jats:sub>2<\/jats:sub>\n                          S\n                        <\/jats:roman>\n                      <\/jats:styled-content>\n                      ) 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 (\n                      <jats:styled-content style=\"fixed-case\">STS<\/jats:styled-content>\n                      ), a clinically applicable\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:roman>\n                          H\n                          <jats:sub>2<\/jats:sub>\n                          S\n                        <\/jats:roman>\n                      <\/jats:styled-content>\n                      donor substance, in angiotensin\n                      <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n                      (\n                      <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                      ng\n                      <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n                      )\u2010induced hypertensive cardiac disease in rats.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>\n                      ale\n                      <jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>\n                      prague\n                      <jats:styled-content style=\"fixed-case\">D<\/jats:styled-content>\n                      awley rats were infused with\n                      <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                      ng\n                      <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n                      (435\u2009ng kg min\n                      <jats:sup>\u22121<\/jats:sup>\n                      ) or saline (control) for 3 weeks via s.c. placed osmotic minipumps. During these 3 weeks, rats received i.p. injections of either\n                      <jats:styled-content style=\"fixed-case\">STS<\/jats:styled-content>\n                      ,\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:roman>NaHS<\/jats:roman>\n                      <\/jats:styled-content>\n                      or vehicle (0.9%\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:roman>NaCl<\/jats:roman>\n                      <\/jats:styled-content>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      Compared with controls,\n                      <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                      ng\n                      <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n                      infusion caused an increase in systolic and diastolic\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      with associated cardiac damage as evidenced by cardiac hypertrophy, an increase in atrial natriuretic peptide (\n                      <jats:styled-content style=\"fixed-case\">ANP<\/jats:styled-content>\n                      ) m\n                      <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                      , cardiac fibrosis and increased oxidative stress. Treatment with\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:roman>NaHS<\/jats:roman>\n                      <\/jats:styled-content>\n                      and\n                      <jats:styled-content style=\"fixed-case\">STS<\/jats:styled-content>\n                      prevented the development of hypertension and the increase in\n                      <jats:styled-content style=\"fixed-case\">ANP<\/jats:styled-content>\n                      m\n                      <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                      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.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>\n                      <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                      ng\n                      <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>\n                      \u2010induced hypertensive cardiac disease can be attenuated by treatment with\n                      <jats:styled-content style=\"fixed-case\">STS<\/jats:styled-content>\n                      and\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:roman>NaHS<\/jats:roman>\n                      <\/jats:styled-content>\n                      . Although\n                      <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>\n                      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\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:roman>\n                          H\n                          <jats:sub>2<\/jats:sub>\n                          S\n                        <\/jats:roman>\n                      <\/jats:styled-content>\n                      might be a valuable addition to the already existing antihypertensive and cardioprotective therapies.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Linked Articles<\/jats:title>\n                    <jats:p>\n                      This article is part of a themed section on Pharmacology of the Gasotransmitters. To view the other articles in this section visit\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/dx.doi.org\/10.1111\/bph.2015.172.issue-6\">http:\/\/dx.doi.org\/10.1111\/bph.2015.172.issue\u20106<\/jats:ext-link>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.12825","type":"journal-article","created":{"date-parts":[[2014,6,24]],"date-time":"2014-06-24T16:57:36Z","timestamp":1403629056000},"page":"1494-1504","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":94,"title":["Exogenous administration of thiosulfate, a donor of hydrogen sulfide, attenuates angiotensin\n                    <scp>II<\/scp>\n                    \u2010induced hypertensive heart disease in rats"],"prefix":"10.1111","volume":"172","author":[{"given":"P M","family":"Snijder","sequence":"first","affiliation":[{"name":"Department of Pathology and Medical Biology 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