title: Role of Mas receptor antagonist (A779) on pressure diuresis and natriuresis and renal blood flow in the absence of angiotensin II receptors type 1 and 2 in female and male rats.
abstract: Sexual differences in blood pressure are associated with angiotensin 1-7 (Ang1-7) and its receptor and enzyme function targeting. Blockade of angiotensin II (AngII) receptors type 1 and 2 (AT1R and AT2R) inhibits some actions of Ang1-7. We described the role of Ang1-7 receptor (MasR) antagonist (A779) on kidney hemodynamics when AT1R and AT2R are blocked with losartan and PD123319. In anaesthetized male and female rats after blockade of both AT1R and AT2R, the renal perfusion pressure (RPP) was controlled in two levels of 80 and 100 mmHg via an adjustable clamp placed around the aorta above the level of the renal arteries. Then, the effects of saline vehicle and MasR blocker (A779) were tested on pressure natriuresis and diuresis, renal blood flow (RBF), and renal vascular resistance (RVR). In the absence of AT1R and AT2R; RVR, RBF/wet kidney tissue weight, and serum level of renin did not alter in both genders either MasR was blocked or not. However, urine flow rate (UF) and sodium excretion (UNaV) increased significantly at the pressure level of 100 mmHg in the presence of MasR in male (P<0.05) but not in female rats. When AT1R and AT2R were blocked, the impact of MasR is gender-related in pressure natriuresis and diuresis, and pressure natriuresis and diuresis in male rats (not female) increases in the presence of MasR.
authors.affiliation: Water and Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. nematbakhsh@med.mui.ac.ir.
authors.forename: A
authors.initials: A
authors.lastname: Mansoori
authors.forename: S
authors.initials: S
authors.lastname: Oryan
authors.forename: M
authors.initials: M
authors.lastname: Nematbakhsh
mesh_terms: D000804:Angiotensin II / Q000031:analogs & derivatives* / Q000494:pharmacology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D057912:Angiotensin II Type 2 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D004231:Diuresis / Q000187:drug effects* / Q000502:physiology; D005260:Female; D007093:Imidazoles / Q000494:pharmacology; D007668:Kidney / Q000187:drug effects / Q000502:physiology; D019808:Losartan / Q000494:pharmacology; D008297:Male; D009318:Natriuresis / Q000187:drug effects* / Q000502:physiology; D010446:Peptide Fragments / Q000494:pharmacology*; D011312:Pressure; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000037:antagonists & inhibitors* / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors* / Q000378:metabolism; D012079:Renal Circulation / Q000187:drug effects*; D012737:Sex Factors; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: C092006:7-Ala-angiotensin (1-7); D047228:Angiotensin II Type 1 Receptor Blockers; D057912:Angiotensin II Type 2 Receptor Blockers; D007093:Imidazoles; D010446:Peptide Fragments; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D011725:Pyridines; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D043562:Receptors, G-Protein-Coupled; D000804:Angiotensin II; C073402:PD 123319; D019808:Losartan