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We further investigated whether 3-week oral treatment with the angiotensin II type I receptor antagonist TCV-116 would improve the baroreflex in rats with myocardial infarction. The maximal gain of the mean arterial pressure-RSNA relation in spontaneously hypertensive rats with myocardial infarction and treated with vehicle (1.7\u00b10.1% control per mm Hg) was smaller than the gain in sham-operated hypertensive rats (2.3\u00b10.1% control per mm Hg). After 3-week oral treatment with TCV-116, the maximal gain of the arterial pressure-RSNA relation in hypertensive rats with myocardial infarction was 2.3\u00b10.1% control per mm Hg and significantly greater than the gain in infarcted and vehicle-treated hypertensive rats. In hypertensive rats, the maximal gain of the arterial pressure-heart rate relation of infarcted and TCV-116-treated rats was larger than in infarcted and vehicle-treated rats but significantly smaller than in sham-operated rats. These results demonstrate that oral treatment with an angiotensin receptor antagonist is effective in restoring the impaired baroreflex caused by myocardial infarction and that endogenous angiotensin II is one of the critical factors involved in the impaired baroreflex in myocardial infarction.<\/jats:p>","DOI":"10.1161\/01.hyp.29.1.458","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:53:46Z","timestamp":1339462426000},"page":"458-463","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":18,"title":["Improvement in Baroreflex Function by an Oral Angiotensin Receptor Antagonist in Rats With Myocardial Infarction"],"prefix":"10.1161","volume":"29","author":[{"given":"Masahiko","family":"Nishizawa","sequence":"first","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan, and the Kidney Disease Center, Saitama (Japan) Medical School (H.S.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroo","family":"Kumagai","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan, and the Kidney Disease Center, Saitama (Japan) Medical School (H.S.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masashi","family":"Ichikawa","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan, and the Kidney Disease Center, Saitama (Japan) Medical School (H.S.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naoki","family":"Oshima","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan, and the Kidney Disease Center, Saitama (Japan) Medical School (H.S.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiromichi","family":"Suzuki","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan, and the Kidney Disease Center, Saitama (Japan) Medical School (H.S.)."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takao","family":"Saruta","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan, and the Kidney Disease Center, Saitama (Japan) Medical School (H.S.)."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"doi-asserted-by":"publisher","key":"e_1_3_2_1_2","DOI":"10.1161\/hyp.26.3.425"},{"doi-asserted-by":"publisher","key":"e_1_3_2_2_2","DOI":"10.1161\/hyp.27.2.209"},{"key":"e_1_3_2_3_2","first-page":"R109","volume":"263","year":"1992","unstructured":"Kumagai H, Averill DB, Ferrario CM. 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