{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,28]],"date-time":"2025-09-28T15:33:55Z","timestamp":1759073635887,"version":"3.40.3"},"reference-count":27,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[1995,4]]},"abstract":"<jats:p><jats:italic>Abstract<\/jats:italic>We have reported that in two-kidney, one clip hypertensive rats, renal perfusion is maintained by a balance between the vasodilator endothelium-derived nitric oxide and the vasoconstrictor angiotensin II. Others have suggested that endothelium-derived constricting factor, reported to be thromboxane A<jats:sub>2<\/jats:sub>and\/or endoperoxide, contributes to increased blood pressure in angiotensin II\u2013dependent hypertension. We hypothesized that in angiotensin II\u2013dependent two-kidney, one clip hypertension, endothelium-derived constricting factor contributes to vasoconstriction of the clipped kidney following nitric oxide synthesis inhibition. Using radioactive microspheres, we studied renal blood flow to the stenotic kidney of two-kidney, one clip hypertensive rats 4 weeks after clipping. The influence of nitric oxide on systemic and renal hemodynamics was evaluated by determining the response to nitric oxide synthesis inhibition using 10 mg\/kg<jats:italic>N<\/jats:italic><jats:sup>\u03c9<\/jats:sup>-nitro-<jats:sc>l<\/jats:sc>-arginine methyl ester in these rats, which were either not treated (n=8) or treated (n=8) with 4 mg\/kg of the constricting factor receptor antagonist BMS 180,291. Mean basal blood pressure in rats was 167\u00b19 mm Hg (mean\u00b1SEM).<jats:italic>N<\/jats:italic><jats:sup>\u03c9<\/jats:sup>-Nitro-<jats:sc>l<\/jats:sc>-arginine methyl ester increased blood pressure by 35\u00b17 mm Hg (<jats:italic>P<\/jats:italic>&lt;.001). In the clipped kidney,<jats:italic>N<\/jats:italic><jats:sup>\u03c9<\/jats:sup>-nitro-<jats:sc>l<\/jats:sc>-arginine methyl ester decreased renal blood flow by 40% (from 4.5\u00b10.9 to 2.7\u00b10.6 mL \u00b7 min<jats:sup>\u22121<\/jats:sup>\u00b7 g kidney<jats:sup>\u22121<\/jats:sup>;<jats:italic>P<\/jats:italic>&lt;.01) and increased renal vascular resistance by 100% (from 51.9\u00b19.6 to 105.0\u00b119.2 mm Hg \u00b7 mL<jats:sup>\u22121<\/jats:sup>\u00b7 min<jats:sup>\u22121<\/jats:sup>\u00b7 g kidney<jats:sup>\u22121<\/jats:sup>;<jats:italic>P<\/jats:italic>&lt;.005). Pretreatment with BMS 180,291 had no effect on basal blood pressure (167\u00b17 mm Hg) or blood flow to the clipped kidney. However, constricting factor blockade diminished the pressor response to<jats:italic>N<\/jats:italic><jats:sup>\u03c9<\/jats:sup>-nitro-<jats:sc>l<\/jats:sc>-arginine methyl ester by 63%, decreasing the response to only 13\u00b14 mm Hg (<jats:italic>P<\/jats:italic>&lt;.02). In rats treated with BMS 180,291,<jats:italic>N<\/jats:italic><jats:sup>\u03c9<\/jats:sup>-nitro-<jats:sc>l<\/jats:sc>-arginine methyl ester decreased blood flow to the clipped kidney by only 12% (from 5.4\u00b10.6 to 4.7\u00b10.5 mL \u00b7 min<jats:sup>\u22121<\/jats:sup>\u00b7 g kidney<jats:sup>\u22121<\/jats:sup>;<jats:italic>P<\/jats:italic>&lt;.05), while renal vascular resistance increased by only 17% (from 36.7\u00b17.1 to 43.0\u00b17.2 mm Hg \u00b7 mL<jats:sup>\u22121<\/jats:sup>\u00b7 min<jats:sup>\u22121<\/jats:sup>\u00b7 g kidney<jats:sup>\u22121<\/jats:sup>;<jats:italic>P<\/jats:italic>&lt;.005). In conclusion, although blocking endothelium-derived constricting factor in hypertensive rats affected neither basal blood pressure nor renal blood flow, it dramatically blunted both the systemic pressor and renal constrictor responses to inhibition of endothelium-derived nitric oxide synthesis. These data suggest a significant regulatory interaction between endothelium-derived constricting factor and endothelium-derived nitric oxide in renovascular hypertension.<\/jats:p>","DOI":"10.1161\/01.hyp.25.4.803","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:24:03Z","timestamp":1339460643000},"page":"803-808","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":10,"title":["Endothelium-Derived Constricting Factor in Renovascular Hypertension"],"prefix":"10.1161","volume":"25","author":[{"given":"David H.","family":"Sigmon","sequence":"first","affiliation":[{"name":"From the Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Mich."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William H.","family":"Beierwaltes","sequence":"additional","affiliation":[{"name":"From the Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, Mich."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.74.2.8293559"},{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"418","DOI":"10.1016\/S0022-3565(25)21230-7","volume":"233","year":"1985","unstructured":"Mais DE, Saussy DL, Chaikouni A, Kochel PJ, Knapp DR, Hananaka N, Halushka PV. 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