title: Intrarenal AT(1) receptor and ACE binding in ANG II-induced hypertensive rats.
abstract: The intrarenal expression of angiotensin II (ANG II) type 1 (AT(1)) receptors and angiotensin-converting enzyme (ACE) was determined in ANG II-induced hypertensive rats (80 ng/min; 2 wk). Systolic blood pressure averaged 184 +/- 3 and 125 +/- 1 mmHg in ANG II-infused compared with Sham rats on day 12. Total kidney AT(1) receptor protein levels were not altered significantly. AT(1) receptor binding mapped by quantitative in vitro autoradiography was significantly decreased in glomeruli (172 +/- 25 vs. 275 +/- 34 disintegrations. min(-1). mm(-2)) and the inner stripe of the outer medulla (121 +/- 17 vs. 178 +/- 19 disintegrations. min(-1). mm(-2)), but not proximal convoluted tubules (48 +/- 9 vs. 58 +/- 6 disintegrations. min(-1). mm(-2)) of ANG II-infused compared with Sham rats. Proximal tubule ACE binding was significantly augmented (132 +/- 4 vs. 97 +/- 3 disintegrations. min(-1). mm(-2)) in ANG II-infused rats. In summary, during ANG II-induced hypertension, glomeruli and inner stripe of the outer medulla have reduced AT(1) receptor binding. Proximal convoluted tubules exhibit maintained AT(1) receptor density and increased ACE binding, which together with the elevated ANG II levels suggest that ANG II exerts a sustained influence on tubular reabsorption and consequently contributes to the development and maintenance of ANG II-dependent hypertension.
authors.affiliation: Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112, USA. lharris@tulane.edu
authors.forename: Lisa M
authors.initials: LM
authors.lastname: Harrison-Bernard
authors.forename: Jialong
authors.initials: J
authors.lastname: Zhuo
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kobori
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Ohishi
authors.forename: L Gabriel
authors.initials: LG
authors.lastname: Navar
mesh_terms: D000804:Angiotensin II; D000818:Animals; D001345:Autoradiography; D001794:Blood Pressure; D015153:Blotting, Western; D006977:Hypertension, Renal / Q000139:chemically induced / Q000378:metabolism*; D007678:Kidney Glomerulus / Q000737:chemistry / Q000378:metabolism*; D007679:Kidney Medulla / Q000737:chemistry / Q000378:metabolism; D007687:Kidney Tubules, Proximal / Q000737:chemistry / Q000378:metabolism; D008297:Male; D009997:Osmotic Pressure; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000032:analysis / Q000378:metabolism*; D012083:Renin / Q000097:blood; D014662:Vasoconstrictor Agents
chemical_list: D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A; D012083:Renin