Steroid sulfatase inhibitor alters blood pressure and steroid profiles in hypertensive rats
Our hypothesis is that the steroid sulfatase gene ( Sts) may indirectly contribute to the modulation of blood pressure (BP) in rats with genetic hypertension. The steroid sulfatase enzyme (STS) catalyzes the conversion of estrone sulfate, dehydroepiandrosterone sulfate, cholesterol sulfate and gluco...
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| Veröffentlicht in: | The Journal of steroid biochemistry and molecular biology 2000-06, Vol.73 (3), p.113-122 |
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| container_title | The Journal of steroid biochemistry and molecular biology |
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| creator | Valigora, Shawna D. Li, Pui-Kai Dunphy, Gail Turner, Monte Ely, Daniel L. |
| description | Our hypothesis is that the steroid sulfatase gene (
Sts) may indirectly contribute to the modulation of blood pressure (BP) in rats with genetic hypertension. The steroid sulfatase enzyme (STS) catalyzes the conversion of estrone sulfate, dehydroepiandrosterone sulfate, cholesterol sulfate and glucocorticoid sulfates to their active nonconjugated forms. This causes the elevation of biologically active steroids, such as glucocorticoids, mineralcorticoids as well as testosterone, which may lead to increased BP. The main objective was to examine the effects of a steroid sulfatase inhibitor on blood pressure and steroid levels in rats with hypertensive genetic backgrounds. Three treatment groups, 5–15 weeks of age were used: controls, estrone and STS inhibitor (estrone-3-
O-sulfamate), (
n=8 per group). BP was taken weekly by tail cuff, and serum testosterone (T), estrogens (E), and plasma corticosterone (C) levels were measured by radioimmunoassay. BP was significantly reduced by the STS inhibitor in the strains with genetically elevated BP. Also the inhibitor alone significantly reduced plasma corticosterone in all strains compared to estrone treatment with a concomitant as well as significant rise in estrogens and reduction in testosterone and body weight. |
| doi_str_mv | 10.1016/S0960-0760(00)00062-5 |
| format | Article |
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Sts) may indirectly contribute to the modulation of blood pressure (BP) in rats with genetic hypertension. The steroid sulfatase enzyme (STS) catalyzes the conversion of estrone sulfate, dehydroepiandrosterone sulfate, cholesterol sulfate and glucocorticoid sulfates to their active nonconjugated forms. This causes the elevation of biologically active steroids, such as glucocorticoids, mineralcorticoids as well as testosterone, which may lead to increased BP. The main objective was to examine the effects of a steroid sulfatase inhibitor on blood pressure and steroid levels in rats with hypertensive genetic backgrounds. Three treatment groups, 5–15 weeks of age were used: controls, estrone and STS inhibitor (estrone-3-
O-sulfamate), (
n=8 per group). BP was taken weekly by tail cuff, and serum testosterone (T), estrogens (E), and plasma corticosterone (C) levels were measured by radioimmunoassay. BP was significantly reduced by the STS inhibitor in the strains with genetically elevated BP. Also the inhibitor alone significantly reduced plasma corticosterone in all strains compared to estrone treatment with a concomitant as well as significant rise in estrogens and reduction in testosterone and body weight.</description><identifier>ISSN: 0960-0760</identifier><identifier>EISSN: 1879-1220</identifier><identifier>DOI: 10.1016/S0960-0760(00)00062-5</identifier><identifier>PMID: 10925210</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Arterial hypertension. Arterial hypotension ; Arylsulfatases - antagonists & inhibitors ; Biological and medical sciences ; Blood and lymphatic vessels ; Body weight ; Cardiology. Vascular system ; Corticosterone ; Corticosterone - pharmacology ; Enzyme Inhibitors - pharmacology ; Estrogen ; Estrogens - pharmacology ; Estrone - analogs & derivatives ; Estrone - pharmacology ; Experimental diseases ; Female ; Male ; Medical sciences ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Steryl-Sulfatase ; Testosterone ; Testosterone - pharmacology ; Y chromosome</subject><ispartof>The Journal of steroid biochemistry and molecular biology, 2000-06, Vol.73 (3), p.113-122</ispartof><rights>2000 Elsevier Science Ltd</rights><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-a0cafcaa3515361587d9c307375fbc9d048378f1b7e4d3181eef9b53ac08318c3</citedby><cites>FETCH-LOGICAL-c389t-a0cafcaa3515361587d9c307375fbc9d048378f1b7e4d3181eef9b53ac08318c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0960076000000625$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=791351$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10925210$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Valigora, Shawna D.</creatorcontrib><creatorcontrib>Li, Pui-Kai</creatorcontrib><creatorcontrib>Dunphy, Gail</creatorcontrib><creatorcontrib>Turner, Monte</creatorcontrib><creatorcontrib>Ely, Daniel L.</creatorcontrib><title>Steroid sulfatase inhibitor alters blood pressure and steroid profiles in hypertensive rats</title><title>The Journal of steroid biochemistry and molecular biology</title><addtitle>J Steroid Biochem Mol Biol</addtitle><description>Our hypothesis is that the steroid sulfatase gene (
Sts) may indirectly contribute to the modulation of blood pressure (BP) in rats with genetic hypertension. The steroid sulfatase enzyme (STS) catalyzes the conversion of estrone sulfate, dehydroepiandrosterone sulfate, cholesterol sulfate and glucocorticoid sulfates to their active nonconjugated forms. This causes the elevation of biologically active steroids, such as glucocorticoids, mineralcorticoids as well as testosterone, which may lead to increased BP. The main objective was to examine the effects of a steroid sulfatase inhibitor on blood pressure and steroid levels in rats with hypertensive genetic backgrounds. Three treatment groups, 5–15 weeks of age were used: controls, estrone and STS inhibitor (estrone-3-
O-sulfamate), (
n=8 per group). BP was taken weekly by tail cuff, and serum testosterone (T), estrogens (E), and plasma corticosterone (C) levels were measured by radioimmunoassay. BP was significantly reduced by the STS inhibitor in the strains with genetically elevated BP. Also the inhibitor alone significantly reduced plasma corticosterone in all strains compared to estrone treatment with a concomitant as well as significant rise in estrogens and reduction in testosterone and body weight.</description><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Arylsulfatases - antagonists & inhibitors</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Body weight</subject><subject>Cardiology. Vascular system</subject><subject>Corticosterone</subject><subject>Corticosterone - pharmacology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Estrogen</subject><subject>Estrogens - pharmacology</subject><subject>Estrone - analogs & derivatives</subject><subject>Estrone - pharmacology</subject><subject>Experimental diseases</subject><subject>Female</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Steryl-Sulfatase</subject><subject>Testosterone</subject><subject>Testosterone - pharmacology</subject><subject>Y chromosome</subject><issn>0960-0760</issn><issn>1879-1220</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkF1L7DAQhoMc0fXjJ3goHBC9qM40m6a9OhzELxC8UK-8CGk6wRy67ZppBf-9WXcR74RACPO8mZlHiCOEMwQszx-gLiEHXcIJwCkAlEWutsQMK13nWBTwS8y-kF2xx_w_QVKi3hG7CHWhCoSZeH4YKQ6hzXjqvB0tUxb6l9CEcYiZ7VKRs6YbhjZbRmKeImW2T_QmtYyDDx1xCmUv70uKI_Uc3iiLduQDse1tx3S4uffF09Xl48VNfnd_fXvx7y53sqrH3IKz3lkrFSpZoqp0WzsJWmrlG1e3MK-krjw2muatxAqJfN0oaR1U6enkvjhe_5umeZ2IR7MI7KjrbE_DxEZjUeo5FglUa9DFgTmSN8sYFja-GwSzsmo-rZqVMgOrk6walXK_Nw2mZkHtt9RaYwL-bADLznY-2t4F_uJ0jWm5RP1dU5RkvAWKhl2g3lEbIrnRtEP4YZAP8hqUjg</recordid><startdate>20000601</startdate><enddate>20000601</enddate><creator>Valigora, Shawna D.</creator><creator>Li, Pui-Kai</creator><creator>Dunphy, Gail</creator><creator>Turner, Monte</creator><creator>Ely, Daniel L.</creator><general>Elsevier Ltd</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20000601</creationdate><title>Steroid sulfatase inhibitor alters blood pressure and steroid profiles in hypertensive rats</title><author>Valigora, Shawna D. ; Li, Pui-Kai ; Dunphy, Gail ; Turner, Monte ; Ely, Daniel L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-a0cafcaa3515361587d9c307375fbc9d048378f1b7e4d3181eef9b53ac08318c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Arylsulfatases - antagonists & inhibitors</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Body weight</topic><topic>Cardiology. Vascular system</topic><topic>Corticosterone</topic><topic>Corticosterone - pharmacology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Estrogen</topic><topic>Estrogens - pharmacology</topic><topic>Estrone - analogs & derivatives</topic><topic>Estrone - pharmacology</topic><topic>Experimental diseases</topic><topic>Female</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Steryl-Sulfatase</topic><topic>Testosterone</topic><topic>Testosterone - pharmacology</topic><topic>Y chromosome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Valigora, Shawna D.</creatorcontrib><creatorcontrib>Li, Pui-Kai</creatorcontrib><creatorcontrib>Dunphy, Gail</creatorcontrib><creatorcontrib>Turner, Monte</creatorcontrib><creatorcontrib>Ely, Daniel L.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Valigora, Shawna D.</au><au>Li, Pui-Kai</au><au>Dunphy, Gail</au><au>Turner, Monte</au><au>Ely, Daniel L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Steroid sulfatase inhibitor alters blood pressure and steroid profiles in hypertensive rats</atitle><jtitle>The Journal of steroid biochemistry and molecular biology</jtitle><addtitle>J Steroid Biochem Mol Biol</addtitle><date>2000-06-01</date><risdate>2000</risdate><volume>73</volume><issue>3</issue><spage>113</spage><epage>122</epage><pages>113-122</pages><issn>0960-0760</issn><eissn>1879-1220</eissn><abstract>Our hypothesis is that the steroid sulfatase gene (
Sts) may indirectly contribute to the modulation of blood pressure (BP) in rats with genetic hypertension. The steroid sulfatase enzyme (STS) catalyzes the conversion of estrone sulfate, dehydroepiandrosterone sulfate, cholesterol sulfate and glucocorticoid sulfates to their active nonconjugated forms. This causes the elevation of biologically active steroids, such as glucocorticoids, mineralcorticoids as well as testosterone, which may lead to increased BP. The main objective was to examine the effects of a steroid sulfatase inhibitor on blood pressure and steroid levels in rats with hypertensive genetic backgrounds. Three treatment groups, 5–15 weeks of age were used: controls, estrone and STS inhibitor (estrone-3-
O-sulfamate), (
n=8 per group). BP was taken weekly by tail cuff, and serum testosterone (T), estrogens (E), and plasma corticosterone (C) levels were measured by radioimmunoassay. BP was significantly reduced by the STS inhibitor in the strains with genetically elevated BP. Also the inhibitor alone significantly reduced plasma corticosterone in all strains compared to estrone treatment with a concomitant as well as significant rise in estrogens and reduction in testosterone and body weight.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>10925210</pmid><doi>10.1016/S0960-0760(00)00062-5</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals Arterial hypertension. Arterial hypotension Arylsulfatases - antagonists & inhibitors Biological and medical sciences Blood and lymphatic vessels Body weight Cardiology. Vascular system Corticosterone Corticosterone - pharmacology Enzyme Inhibitors - pharmacology Estrogen Estrogens - pharmacology Estrone - analogs & derivatives Estrone - pharmacology Experimental diseases Female Male Medical sciences Rats Rats, Inbred SHR Rats, Inbred WKY Steryl-Sulfatase Testosterone Testosterone - pharmacology Y chromosome |
| title | Steroid sulfatase inhibitor alters blood pressure and steroid profiles in hypertensive rats |
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