{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T21:19:44Z","timestamp":1778275184595,"version":"3.51.4"},"reference-count":47,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1995,2,15]]},"abstract":"<jats:p>\n            <jats:italic>Background<\/jats:italic>\n            Stimulation of endothelin subtype B (ET\n            <jats:sub>B<\/jats:sub>\n            ) receptors has been proposed to induce release of endothelium-derived nitric oxide (EDNO).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods and Results<\/jats:italic>\n            To obtain direct evidence of its release and its alteration in deoxycorticosterone acetate (DOCA)-salt hypertension, EDNO released from renal vessels by ET stimulation was assayed by a highly sensitive chemiluminescence method. Kidneys were isolated from DOCA-salt and control rats, and renal perfusion pressure (RPP) and EDNO (by hydrogen peroxide\u2013luminol chemiluminescence) in the perfusate were monitored simultaneously during perfusion of ET-1, ET-3, an ET\n            <jats:sub>A<\/jats:sub>\n            receptor antagonist (BQ-123), and an ET\n            <jats:sub>B<\/jats:sub>\n            receptor agonist (BQ-3020). In control rats, ET-1 and ET-3 dose-dependently increased both RPP and NO release. Although the vasoconstricting effects of ET-1 were greater, their NO-releasing effects were comparable. The increase in NO release by ETs was inhibited by\n            <jats:italic>N<\/jats:italic>\n            <jats:sup>G<\/jats:sup>\n            -monomethyl-\n            <jats:sc>l<\/jats:sc>\n            -arginine. After 10\n            <jats:sup>\u22126<\/jats:sup>\n            mol\/L BQ-123 treatment, ET-1 decreased RPP and increased NO release in control kidneys. DOCA-salt rats responded to these agents with much less NO release. BQ-3020 at up to 10\n            <jats:sup>\u221210<\/jats:sup>\n            mol\/L caused vasodilation (RPP, 10\n            <jats:sup>\u221211<\/jats:sup>\n            mol\/L, \u22125.4\u00b11.7%,\n            <jats:italic>P<\/jats:italic>\n            &lt;.01) associated with increased NO release in control kidneys (+9.0\u00b12.7 fmol \u00b7 min\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 g\n            <jats:sup>\u22121<\/jats:sup>\n            kidney wt,\n            <jats:italic>P<\/jats:italic>\n            &lt;.01). However, in DOCA-salt kidneys, BQ-3020 caused renal vasoconstriction (RPP, +5.4\u00b12.4%,\n            <jats:italic>P<\/jats:italic>\n            &lt;.01 versus control) and a much smaller NO release (+1.1\u00b10.4 fmol \u00b7 min\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 g\n            <jats:sup>\u22121<\/jats:sup>\n            kidney wt,\n            <jats:italic>P<\/jats:italic>\n            &lt;.01 versus control). Northern blot analysis revealed that renal ET\n            <jats:sub>B<\/jats:sub>\n            mRNA was significantly decreased in DOCA-salt rat kidneys compared with controls (0.36\u00b10.13 versus 1.00\u00b10.23,\n            <jats:italic>P<\/jats:italic>\n            &lt;.05).\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            These results suggest that ET-1 and ET-3 release EDNO via ET\n            <jats:sub>B<\/jats:sub>\n            receptors in renal vessels. ET\n            <jats:sub>B<\/jats:sub>\n            -mediated NO release was reduced in DOCA-salt rats, which may modulate renal function and thus blood pressure regulation in DOCA-salt hypertensive rats.\n          <\/jats:p>","DOI":"10.1161\/01.cir.91.4.1229","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:34:42Z","timestamp":1339461282000},"page":"1229-1235","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":64,"title":["Direct Measurements of Endothelium-Derived Nitric Oxide Release by Stimulation of Endothelin Receptors in Rat Kidney and Its Alteration in Salt-Induced Hypertension"],"prefix":"10.1161","volume":"91","author":[{"given":"Yasunobu","family":"Hirata","sequence":"first","affiliation":[{"name":"From the Second Department of Internal Medicine (Y.H., H.H., E.S., K. Kimura, M.O.) and Faculty of Pharmaceutical Sciences (K. Kikuchi, T.N., M.H.), University of Tokyo, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroshi","family":"Hayakawa","sequence":"additional","affiliation":[{"name":"From the Second Department of Internal Medicine (Y.H., H.H., E.S., K. Kimura, M.O.) and Faculty of Pharmaceutical Sciences (K. Kikuchi, T.N., M.H.), University of Tokyo, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Etsu","family":"Suzuki","sequence":"additional","affiliation":[{"name":"From the Second Department of Internal Medicine (Y.H., H.H., E.S., K. Kimura, M.O.) and Faculty of Pharmaceutical Sciences (K. Kikuchi, T.N., M.H.), University of Tokyo, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kenjiro","family":"Kimura","sequence":"additional","affiliation":[{"name":"From the Second Department of Internal Medicine (Y.H., H.H., E.S., K. Kimura, M.O.) and Faculty of Pharmaceutical Sciences (K. Kikuchi, T.N., M.H.), University of Tokyo, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuya","family":"Kikuchi","sequence":"additional","affiliation":[{"name":"From the Second Department of Internal Medicine (Y.H., H.H., E.S., K. Kimura, M.O.) and Faculty of Pharmaceutical Sciences (K. Kikuchi, T.N., M.H.), University of Tokyo, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tetsuo","family":"Nagano","sequence":"additional","affiliation":[{"name":"From the Second Department of Internal Medicine (Y.H., H.H., E.S., K. Kimura, M.O.) and Faculty of Pharmaceutical Sciences (K. Kikuchi, T.N., M.H.), University of Tokyo, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masaaki","family":"Hirobe","sequence":"additional","affiliation":[{"name":"From the Second Department of Internal Medicine (Y.H., H.H., E.S., K. Kimura, M.O.) and Faculty of Pharmaceutical Sciences (K. 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