The hyperglycemia induced by angiotensin II in rats is mediated by AT1 receptors

We have shown that the renin-angiotensin system (RAS) is involved in glucose homeostasis during acute hemorrhage. Since almost all of the physiological actions described for angiotensin II were mediated by AT1 receptors, the present experiments were designed to determine the participation of AT1 receptors in the hyperglycemic action of angiotensin II in freely moving rats. The animals were divided into two experimental groups: 1) animals submitted to intravenous administration of angiotensin II (0.96 nmol/100 g body weight) which caused a rapid increase in plasma glucose reaching the highest values at 5 min after the injection (33% of the initial values, P<0.01), and 2) animals submitted to intravenous administration of DuP-753 (losartan), a non-peptide antagonist of angiotensin II with AT1-receptor type specificity (1.63 µmol/100 g body weight as a bolus, iv, plus a 30-min infusion of 0.018 µmol 100 g body weight-1 min-1 before the injection of angiotensin II), which completely blocked the hyperglycemic response to angiotensin II (P<0.01). This inhibitory effect on glycemia was already demonstrable 5 min (8.9 ± 0.28 mM, angiotensin II, N = 9 vs 6.4 ± 0.22 mM, losartan plus angiotensin II, N = 11) after angiotensin II injection and persisted throughout the 30-min experiment. Controls were treated with the same volume of saline solution (0.15 M NaCl). These data demonstrate that the angiotensin II receptors involved in the direct and indirect hyperglycemic actions of angiotensin II are mainly of the AT1-type

A tribute to Samuel MacDonald McCann (1925-2007): in honor of one of the last pioneers of Neuroendocrinology

Submitted by Guilherme Lemeszenski ([email protected]) on 2013-08-22T18:52:46Z No. of bitstreams: 1 S0100-879X2007000500013.pdf: 480043 bytes, checksum: 62f9616a5cb6dbcff1870baa33e1b37b (MD5)Made available in DSpace on 2013-08-22T18:52:46Z (GMT). No. of bitstreams: 1 S0100-879X2007000500013.pdf: 480043 bytes, checksum: 62f9616a5cb6dbcff1870baa33e1b37b (MD5) Previous issue date: 2007-05-01Made available in DSpace on 2013-09-30T18:25:13Z (GMT). No. of bitstreams: 2 S0100-879X2007000500013.pdf: 480043 bytes, checksum: 62f9616a5cb6dbcff1870baa33e1b37b (MD5) S0100-879X2007000500013.pdf.txt: 7453 bytes, checksum: 19a2782d2d1e9ae1b4a3246afd5bd8f4 (MD5) Previous issue date: 2007-05-01Submitted by Vitor Silverio Rodrigues ([email protected]) on 2014-05-20T13:42:36Z No. of bitstreams: 2 S0100-879X2007000500013.pdf: 480043 bytes, checksum: 62f9616a5cb6dbcff1870baa33e1b37b (MD5) S0100-879X2007000500013.pdf.txt: 7453 bytes, checksum: 19a2782d2d1e9ae1b4a3246afd5bd8f4 (MD5)Made available in DSpace on 2014-05-20T13:42:36Z (GMT). No. of bitstreams: 2 S0100-879X2007000500013.pdf: 480043 bytes, checksum: 62f9616a5cb6dbcff1870baa33e1b37b (MD5) S0100-879X2007000500013.pdf.txt: 7453 bytes, checksum: 19a2782d2d1e9ae1b4a3246afd5bd8f4 (MD5) Previous issue date: 2007-05-01USP Faculdade de Medicina de Ribeirão Preto Departamento de FisiologiaUSP Faculdade de Odontologia de Ribeirão Preto Departamento de Morfologia, Estomatologia e FisiologiaUNESP Faculdade de Odontologia de Araçatuba Departamento de Apoio, Produção e SaúdeUFRJ Instituto de Biofísica Carlos Chagas FilhoUERJ Instituto de Biologia Departamento de Ciências FisiológicasUFMG ICB Departamento de Fisiologia e BiofísicaUNESP Faculdade de Odontologia de Araçatuba Departamento de Apoio, Produção e Saúd