{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,17]],"date-time":"2025-09-17T14:48:02Z","timestamp":1758120482721,"version":"3.40.3"},"reference-count":31,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2001,2]]},"abstract":"<jats:p>This study was designed to determine the influence of increased superoxide anion in neuronal nitric oxide synthase (nNOS)-dependent regulation of afferent arterioles in spontaneously hypertensive rats (SHR). Afferent arteriolar diameters of male Wistar-Kyoto rats (WKY) and SHR were assessed in vitro with the blood-perfused juxtamedullary nephron technique and averaged 21.6\u00b11.6 (n=6) and 18.8\u00b11.2 (n=7) \u03bcm, respectively. The superoxide dismutase mimetic Tempol (1, 10, and 100 \u03bcmol\/L) did not influence afferent arterioles of WKY but significantly increased afferent arteriolar diameters of SHR by 20.6\u00b15.5%, 25.2\u00b15.4%, and 23.3\u00b14.9%, respectively. In WKY (n=6), the nNOS inhibitor<jats:italic>S<\/jats:italic>-methyl-<jats:sc>l<\/jats:sc>-thiocitrulline (L-SMTC; 10 \u03bcmol\/L) and the NOS inhibitor<jats:italic>N<\/jats:italic><jats:sup><jats:italic>\u03c9<\/jats:italic><\/jats:sup>-nitro-<jats:sc>l<\/jats:sc>-arginine (L-NNA; 100 \u03bcmol\/L) significantly decreased afferent arteriolar diameters (19.6\u00b11.6 \u03bcm) by 11.9\u00b13.1% and 21.0\u00b13.9%, respectively. In SHR (n=7), L-SMTC did not influence afferent arteriolar diameters (21.0\u00b11.5 \u03bcm), but L-NNA exerted an afferent arteriolar constriction (14.8\u00b13.2%) that was similar to the response observed in WKY. Experiments were also performed in the presence of 100 \u03bcmol\/L Tempol. In afferent arterioles of WKY (n=6), Tempol treatment did not modulate the basal diameters (21.5\u00b11.2 \u03bcm) or the constrictor response to L-SMTC (10.6\u00b12.1%) or L-NNA (19.3\u00b13.3%). In SHR (n=8), Tempol significantly increased afferent arteriolar diameters by 22.5\u00b14.3% and enhanced afferent arteriolar constrictor responses to L-SMTC (18.4\u00b12.7%) and L-NNA (31.9\u00b12.6%). However, the nitric oxide donor<jats:italic>S<\/jats:italic>-nitroso-<jats:italic>N<\/jats:italic>-acetylpenicillamine (10 \u03bcmol\/L), which similarly increased afferent arteriolar diameters (17.2\u00b12.3%, n=6), did not affect afferent arteriolar responses to L-SMTC (1.5\u00b12.7%) or L-NNA (18.6\u00b12.3%). These suggest that superoxide anion inhibits the control of afferent arteriolar diameters by nNOS in SHR.<\/jats:p>","DOI":"10.1161\/01.hyp.37.2.630","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"630-634","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":32,"title":["Superoxide Inhibits Neuronal Nitric Oxide Synthase Influences on Afferent Arterioles in Spontaneously Hypertensive Rats"],"prefix":"10.1161","volume":"37","author":[{"given":"Atsuhiro","family":"Ichihara","sequence":"first","affiliation":[{"name":"From the Internal Medicine, Keio University School of Medicine, Tokyo, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matsuhiko","family":"Hayashi","sequence":"additional","affiliation":[{"name":"From the Internal Medicine, Keio University School of Medicine, Tokyo, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nobuhisa","family":"Hirota","sequence":"additional","affiliation":[{"name":"From the Internal Medicine, Keio University School of Medicine, Tokyo, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takao","family":"Saruta","sequence":"additional","affiliation":[{"name":"From the Internal Medicine, Keio University School of Medicine, Tokyo, 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","first-page":"R118","volume":"270","year":"1996","unstructured":"Dubey RK, Boegehold MA, Gillespie DG, Rosselli M. 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