{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T03:51:36Z","timestamp":1768017096572,"version":"3.49.0"},"reference-count":31,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":2130,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2003,4]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>In mouse atria, angiotensin II and bradykinin lose much or all of their noradrenaline release\u2010enhancing effect when presynaptic <jats:italic>\u03b1<\/jats:italic><jats:sub>2<\/jats:sub>\u2010autoinhibition does not operate either because of stimulation with very brief pulse trains or because of treatment with <jats:italic>\u03b1<\/jats:italic><jats:sub>2<\/jats:sub> antagonists. We now studied this operational condition in <jats:italic>\u03b1<\/jats:italic><jats:sub>2<\/jats:sub>\u2010adrenoceptor\u2010deficient mice. Release of <jats:sup>3<\/jats:sup>H\u2010noradrenaline was elicited by electrical stimulation.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In tissues from wild\u2010type (WT) mice, angiotensin II and bradykinin increased the overflow of tritium evoked by 120 pulses at 3 Hz. This enhancement did not occur or was much reduced when tissues were stimulated by 120 pulses at 3 Hz in the presence of rauwolscine and phentolamine, or when they were stimulated by 20 pulses at 50 Hz.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In tissues from mice lacking the <jats:italic>\u03b1<\/jats:italic><jats:sub>2A<\/jats:sub>\u2010adrenoceptor (<jats:italic>\u03b1<\/jats:italic><jats:sub>2A<\/jats:sub>KO) or the <jats:italic>\u03b1<\/jats:italic><jats:sub>2B<\/jats:sub>\u2010adrenoceptor (<jats:italic>\u03b1<\/jats:italic><jats:sub>2B<\/jats:sub>KO), the concentration\u2013response curves of angiotensin II and bradykinin (120 pulses at 3 Hz) were unchanged. In tissues from mice lacking the <jats:italic>\u03b1<\/jats:italic><jats:sub>2C<\/jats:sub>\u2010adrenoceptor (<jats:italic>\u03b1<\/jats:italic><jats:sub>2C<\/jats:sub>KO) or both the <jats:italic>\u03b1<\/jats:italic><jats:sub>2A<\/jats:sub>\u2010 and the <jats:italic>\u03b1<\/jats:italic><jats:sub>2C<\/jats:sub>\u2010adrenoceptor (<jats:italic>\u03b1<\/jats:italic><jats:sub>2AC<\/jats:sub>KO), the concentration\u2013response curves were shifted to the same extent downwards.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>As in WT tissues, angiotensin II and bradykinin lost most or all of their effect in <jats:italic>\u03b1<\/jats:italic><jats:sub>2A<\/jats:sub>KO and <jats:italic>\u03b1<\/jats:italic><jats:sub>2AC<\/jats:sub>KO tissues when rauwolscine and phentolamine were present or trains consisted of 20 pulses at 50 Hz.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Rauwolscine and phentolamine increased tritium overflow evoked by 120 pulses at 3 Hz up to seven\u2010fold in WT and <jats:italic>\u03b1<\/jats:italic><jats:sub>2B<\/jats:sub>KO tissues, three\u2010fold in <jats:italic>\u03b1<\/jats:italic><jats:sub>2A<\/jats:sub>KO and <jats:italic>\u03b1<\/jats:italic><jats:sub>2C<\/jats:sub>KO tissues, and two\u2010fold in <jats:italic>\u03b1<\/jats:italic><jats:sub>2AC<\/jats:sub>KO tissues.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Results confirm that angiotensin II and bradykinin require ongoing <jats:italic>\u03b1<\/jats:italic><jats:sub>2<\/jats:sub>\u2010autoinhibition for the full extent of their release\u2010enhancing effect. Specifically, they require ongoing <jats:italic>\u03b1<\/jats:italic><jats:sub>2C<\/jats:sub>\u2010autoinhibition. The peptide effects that remain in <jats:italic>\u03b1<\/jats:italic><jats:sub>2C<\/jats:sub>\u2010autoreceptor\u2010deficient mice seem to be because of <jats:italic>\u03b1<\/jats:italic><jats:sub>2B<\/jats:sub>\u2010autoinhibition. The results hence also suggest that in addition to <jats:italic>\u03b1<\/jats:italic><jats:sub>2A<\/jats:sub>\u2010 and <jats:italic>\u03b1<\/jats:italic><jats:sub>2C<\/jats:sub>\u2010 mouse postganglionic sympathetic neurons possess <jats:italic>\u03b1<\/jats:italic><jats:sub>2B<\/jats:sub>\u2010autoreceptors.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2003) <jats:bold>138<\/jats:bold>, 1389\u20131402. doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0705223\">10.1038\/sj.bjp.0705223<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0705223","type":"journal-article","created":{"date-parts":[[2003,4,29]],"date-time":"2003-04-29T17:18:42Z","timestamp":1051636722000},"page":"1389-1402","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Crosstalk between presynaptic angiotensin receptors, bradykinin receptors and <i>\u03b1<\/i><sub>2<\/sub>\u2010autoreceptors in sympathetic neurons: a study in <i>\u03b1<\/i><sub>2<\/sub>\u2010adrenoceptor\u2010deficient mice"],"prefix":"10.1111","volume":"138","author":[{"given":"Anne\u2010Ulrike","family":"Trendelenburg","sequence":"first","affiliation":[]},{"given":"Angelika","family":"Meyer","sequence":"additional","affiliation":[]},{"given":"Werner","family":"Klebroff","sequence":"additional","affiliation":[]},{"given":"Serafim","family":"Guimar\u00e3es","sequence":"additional","affiliation":[]},{"given":"Klaus","family":"Starke","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[2009,1,29]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1124\/mol.56.1.154"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1124\/pr.54.1.43"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/978-1-4899-0952-7_19"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.1988.tb11730.x"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0703167"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1007\/BFb0049778"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00586703"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1007\/s002100100396"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1007\/BFb0117493"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/46040"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1006\/jmcc.1997.0492"},{"key":"e_1_2_7_13_1","first-page":"337","article-title":"Presynaptic regulation of the release of catecholamines","volume":"32","author":"LANGER S.Z.","year":"1977","journal-title":"Pharmacol. 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