{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T22:35:56Z","timestamp":1771626956848,"version":"3.50.1"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2002,12]]},"abstract":"<jats:p>\n            To define the role of angiotensin type 1A (AT\n            <jats:sub>1A<\/jats:sub>\n            ) receptor in modulating tubuloglomerular feedback signals and to determine its relationship to neuronal NO synthase (nNOS), the diameter of the afferent arterioles of wild-type and AT\n            <jats:sub>1A<\/jats:sub>\n            receptor\u2013deficient mice was measured by the blood-perfused juxtamedullary nephron technique. The afferent arteriolar diameter of wild-type and AT\n            <jats:sub>1A<\/jats:sub>\n            receptor\u2013deficient mice averaged 16.7\u00b10.6 (n=9) and 16.8\u00b10.7 \u03bcm (n=9), respectively. In the wild-type mice, addition of 10 \u03bcmol\/L acetazolamide to the blood perfusate exerted a biphasic afferent arteriolar constriction, with the initial response and sustained response averaging 47.2\u00b13.8% and 33.9\u00b13.3%, respectively. In AT\n            <jats:sub>1A<\/jats:sub>\n            receptor\u2013deficient mice, the initial response and sustained response averaged 51.6\u00b13.6% and 9.5\u00b11.3%, respectively, and the sustained response was significantly attenuated compared with that of wild-type mice. Inhibition of nNOS with 10 \u03bcmol\/L\n            <jats:italic>S<\/jats:italic>\n            -methyl-\n            <jats:sc>l<\/jats:sc>\n            -thiocitrulline significantly decreased the afferent arteriolar diameter of AT\n            <jats:sub>1A<\/jats:sub>\n            receptor\u2013deficient mice, from 15.1\u00b11.2 to 5.0\u00b10.3 \u03bcm (n=7), and the decrease was significantly greater than that observed in wild-type mice (from 15.9\u00b11.2 to 10.6\u00b11.3 \u03bcm; n=8). During nNOS inhibition, the initial and sustained afferent arteriolar constrictor responses to acetazolamide in wild-type mice averaged 54.4\u00b16.4% and 44.8\u00b111.3%; respectively, and were similar to those in AT\n            <jats:sub>1A<\/jats:sub>\n            receptor\u2013deficient mice (53.2\u00b16.4% and 59.5\u00b14.4%, respectively). These results suggest that AT\n            <jats:sub>1A<\/jats:sub>\n            receptors enhance tubuloglomerular feedback\u2013mediated afferent arteriolar constriction, at least in part, through reducing the counteracting modulation by nNOS.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.0000041220.88322.6d","type":"journal-article","created":{"date-parts":[[2002,12,5]],"date-time":"2002-12-05T21:43:15Z","timestamp":1039124595000},"page":"934-939","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":20,"title":["Blunted Tubuloglomerular Feedback by Absence of Angiotensin Type 1A Receptor Involves Neuronal NOS"],"prefix":"10.1161","volume":"40","author":[{"given":"Atsuhiro","family":"Ichihara","sequence":"first","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine (A.I., M.H., Y.K., Y.T., N.H., T. Saruta), Tokyo; and Nephrology Discovery Research Laboratory, Tanabe Seiyaku (T. Sugaya), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matsuhiko","family":"Hayashi","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine (A.I., M.H., Y.K., Y.T., N.H., T. Saruta), Tokyo; and Nephrology Discovery Research Laboratory, Tanabe Seiyaku (T. Sugaya), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yukako","family":"Koura","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine (A.I., M.H., Y.K., Y.T., N.H., T. Saruta), Tokyo; and Nephrology Discovery Research Laboratory, Tanabe Seiyaku (T. Sugaya), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuko","family":"Tada","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine (A.I., M.H., Y.K., Y.T., N.H., T. Saruta), Tokyo; and Nephrology Discovery Research Laboratory, Tanabe Seiyaku (T. Sugaya), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takeshi","family":"Sugaya","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine (A.I., M.H., Y.K., Y.T., N.H., T. Saruta), Tokyo; and Nephrology Discovery Research Laboratory, Tanabe Seiyaku (T. Sugaya), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nobuhisa","family":"Hirota","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine (A.I., M.H., Y.K., Y.T., N.H., T. Saruta), Tokyo; and Nephrology Discovery Research Laboratory, Tanabe Seiyaku (T. Sugaya), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takao","family":"Saruta","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, Keio University School of Medicine (A.I., M.H., Y.K., Y.T., N.H., T. Saruta), Tokyo; and Nephrology Discovery Research Laboratory, Tanabe Seiyaku (T. Sugaya), Osaka, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.1996.76.2.425"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.1988.255.3.E383"},{"key":"e_1_3_2_3_2","first-page":"F315","volume":"273","year":"1997","unstructured":"Schnermann JB, Traynor T, Yang T, Huang YG, Oliverio MI, Coffman T, Briggs JP. Absence of tubuloglomerular feedback responses in AT1A receptor\u2013deficient mice. 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