{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T20:57:18Z","timestamp":1778273838412,"version":"3.51.4"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2005,11]]},"abstract":"<jats:p>Despite recent evidence indicating sustained activation of the baroreflex during chronic infusion of angiotensin II (Ang II), sinoaortic denervation does not exacerbate the severity of the hypertension. Therefore, to determine whether Ang II hypertension is relatively resistant to the blood pressure-lowering effects of the baroreflex, the carotid baroreflex was electrically activated bilaterally for 7 days in 5 dogs both in the presence and absence of a continuous infusion of Ang II (5 ng\/kg per minute) producing high physiological plasma levels of the peptide. Under control conditions, basal values for mean arterial pressure (MAP) and plasma norepinephrine concentration (NE) were 93\u00b11 mm Hg and 99\u00b125 pg\/mL, respectively. By day 7 of baroreflex activation, MAP and NE were reduced to 72\u00b14 mm Hg (\u221221\u00b13 mm Hg) and 56\u00b115 pg\/mL, respectively, but PRA was unchanged (control=0.41\u00b10.06 ng ANG I\/mL per hour). All values returned to basal levels by the end of a 7-day recovery period. After 7 days of Ang II infusion, MAP increased from 93\u00b13 to 129\u00b13 mm Hg, whereas NE fell from 117\u00b115 to 86\u00b123 pg\/mL. During the next 7 days of baroreflex activation\/Ang II infusion, further reductions in NE were not statistically significant, and on the final day of baroreflex activation, the reduction in MAP was only 5\u00b11 mm Hg, compared with 21\u00b13 mm Hg in the control normotensive state. These findings indicate that long-term baroreflex-mediated reductions in arterial pressure are markedly diminished, but not totally eliminated, in the presence of hypertension produced by chronic infusion of Ang II.<\/jats:p>","DOI":"10.1161\/01.hyp.0000187011.44201.2e","type":"journal-article","created":{"date-parts":[[2005,10,11]],"date-time":"2005-10-11T00:33:41Z","timestamp":1128990821000},"page":"1194-1200","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":96,"title":["Influence of Prolonged Baroreflex Activation on Arterial Pressure in Angiotensin Hypertension"],"prefix":"10.1161","volume":"46","author":[{"given":"Thomas E.","family":"Lohmeier","sequence":"first","affiliation":[{"name":"From the Department of Physiology (T.E.L., T.M.D., D.A.H.) and Surgery (D.A.H.), University of Mississippi Medical Center, Jackson, Miss; Trauma Center (E.D.I.), North Memorial Medical Center, Robbinsdale, Minn; CVRx, Inc (M.A.R., D.J.S., R.S.K.), Maple Grove, Minn."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Terry M.","family":"Dwyer","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (T.E.L., T.M.D., D.A.H.) and Surgery (D.A.H.), University of Mississippi Medical Center, Jackson, Miss; Trauma Center (E.D.I.), North Memorial Medical Center, Robbinsdale, Minn; CVRx, Inc (M.A.R., D.J.S., R.S.K.), Maple Grove, Minn."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Drew A.","family":"Hildebrandt","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (T.E.L., T.M.D., D.A.H.) and Surgery (D.A.H.), University of Mississippi Medical Center, Jackson, Miss; Trauma Center (E.D.I.), North Memorial Medical Center, Robbinsdale, Minn; CVRx, Inc (M.A.R., D.J.S., R.S.K.), Maple Grove, Minn."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eric D.","family":"Irwin","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (T.E.L., T.M.D., D.A.H.) and Surgery (D.A.H.), University of Mississippi Medical Center, Jackson, Miss; Trauma Center (E.D.I.), North Memorial Medical Center, Robbinsdale, Minn; CVRx, Inc (M.A.R., D.J.S., R.S.K.), Maple Grove, Minn."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin A.","family":"Rossing","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (T.E.L., T.M.D., D.A.H.) and Surgery (D.A.H.), University of Mississippi Medical Center, Jackson, Miss; Trauma Center (E.D.I.), North Memorial Medical Center, Robbinsdale, Minn; CVRx, Inc (M.A.R., D.J.S., R.S.K.), Maple Grove, Minn."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David J.","family":"Serdar","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (T.E.L., T.M.D., D.A.H.) and Surgery (D.A.H.), University of Mississippi Medical Center, Jackson, Miss; Trauma Center (E.D.I.), North Memorial Medical Center, Robbinsdale, Minn; CVRx, Inc (M.A.R., D.J.S., R.S.K.), Maple Grove, Minn."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert S.","family":"Kieval","sequence":"additional","affiliation":[{"name":"From the Department of Physiology (T.E.L., T.M.D., D.A.H.) and Surgery (D.A.H.), University of Mississippi Medical Center, Jackson, Miss; Trauma Center (E.D.I.), North Memorial Medical Center, Robbinsdale, Minn; CVRx, Inc (M.A.R., D.J.S., R.S.K.), Maple Grove, Minn."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(00)00225-9"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.36.4.538"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0895-7061(01)02077-5"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.6.5.675"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.279.4.R1437"},{"key":"e_1_3_3_6_2","doi-asserted-by":"crossref","first-page":"147s","DOI":"10.1016\/S0895-7061(01)02082-9","volume":"14","year":"2001","unstructured":"Lohmeier TE. 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