Angiotensin 1-7 Administration Increases Renal Blood Flow in the Absence of Bradykinin B2 Receptor in Ovariectomized Estradiol Treated Rats: The Role of Mas Receptor

  • Shadan Saberi Department of Physiology, Water and Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. AND Department of Physiology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
  • Aghdas Dehghani Department of Physiology, Water and Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. ANDDepartment of Physiology, School of Medicine, Hormozgan University of Medical Sciences, Bandar-Abbas, Iran.
  • Mehdi Nematbakhsh Department of Physiology, Water and Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. AND Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. AND IsfahanMN Institute of Basic and Applied Sciences Research, Isfahan, Iran.
Keywords: Renal blood flow, HOE-140, A779, Estradiol, Rat

Abstract

Renin angiotensin (RAS), kallikrein kinin (KKS), and sex hormonal systems demonstrate a complex contribution in kidney circulation. This study was designed to investigate the role of angiotensin 1-7 (Ang 1-7) receptor (MasR) and of bradykinin B2 receptor (B2R) in renal blood flow (RBF) response to Ang 1-7 infusion in ovariectomized estradiol treated rats. The ovariectomized rats received intramuscular vehicle (group 1, OV) or estradiol valerate (500 µg/Kg/week) (group 2, OVE) for two weeks. Then each group was divided into two subgroups subjected to receive B2R antagonist (HOE-140, subgroup A), or MasR antagonist (A779) plus HOE-140 (subgroup B). RBF and renal vascular resistance (RVR) responses to graded Ang 1-7 infusion were determined. In condition of B2R alone blocking, RBF response to Ang 1-7 in OVE group was significantly greater than that of OV group (P=0.05), however this response difference was failed by co-blockades of MasR and B2R. Estradiol could promote RBF response to graded Ang 1-7 infusion in the absence of B2R alone, however when both receptors (MasR and B2R) were blocked the role of estradiol was limited.

References

Alhenc-Gelas F, Bouby N, Richer C, Potier L, Roussel R, Marre M. Kinins as therapeutic agents in cardiovascular and renal diseases. Current pharmaceutical design. 2011;17(25):2654-62.

Imig JD. Epoxide hydrolase and epoxygenase metabolites as therapeutic targets for renal diseases. American Journal of Physiology-Renal Physiology. 2005;289(3):F496-F503.

Bądzyńska B, Sadowski J. Differential action of bradykinin on intrarenal regional perfusion in the rat: waning effect in the cortex and major impact in the medulla. The Journal of physiology. 2009;587(15):3943-53.

Yu H, Carretero OA, Juncos LA, Garvin JL. Biphasic effect of bradykinin on rabbit afferent arterioles. Hypertension. 1998;32(2):287-92.

Ren Y, Garvin J, Carretero OA. Mechanism involved in bradykinin-induced efferent arteriole dilation. Kidney international. 2002;62(2):544-9.

Sànchez R, Nolly H, Giannone C, Baglivo HP, Ramírez AJ. Reduced activity of the kallikrein-kinin system predominates over renin-angiotensin system overactivity in all conditions of sodium balance in essential hypertensives and family-related hypertension. Journal of hypertension. 2003;21(2):411-7.

El-Dahr SS, Gee J, Dipp S, Hanss BG, Vari RC, Chao J. Upregulation of renin-angiotensin system and downregulation of kallikrein in obstructive nephropathy. AMERICAN JOURNAL OF PHYSIOLOGY. 1993;264:F874-F.

Tschöpe C, Schultheiss H-P, Walther T. Multiple interactions between the renin-angiotensin and the kallikrein-kinin systems: role of ACE inhibition and AT1 receptor blockade. Journal of cardiovascular pharmacology. 2002;39(4):478-87.

Ueda S, Masumori-Maemoto S, Wada A, Ishii M, Brosnihan KB, Umemura S. Angiotensin (1-7) potentiates bradykinin-induced vasodilatation in man. Journal of hypertension. 2001;19(11).

Carvalho MB, Duarte FV, Faria-Silva R, Fauler B, da Mata Machado LT, de Paula RD, et al. Evidence for Mas-mediated bradykinin potentiation by the angiotensin-(1-7) nonpeptide mimic AVE 0991 in normotensive rats. Hypertension. 2007;50(4):762-7.

Lu J, Zhang Y, Shi J. Effects of intracerebroventricular infusion of angiotensin-(1–7) on bradykinin formation and the kinin receptor expression after focal cerebral ischemia–reperfusion in rats. Brain research. 2008;1219:127-35.

Madeddu P, Emanueli C, Varoni MV, Demontis MP, Anania V, Gorioso N, et al. Regulation of bradykinin B2‐receptor expression by oestrogen. British journal of pharmacology. 1997;121(8):1763-9.

Roesch DM, Tian Y, Zheng W, Shi M, Verbalis JG, Sandberg K. Estradiol Attenuates Angiotensin-Induced Aldosterone Secretion in Ovariectomized Rats 1. Endocrinology. 2000;141(12):4629-36.

Maranon R, Reckelhoff JF. Sex and gender differences in control of blood pressure. Clinical Science. 2013;125(7):311-8.

Ji H, Menini S, Zheng W, Pesce C, Wu X, Sandberg K. Role of angiotensin-converting enzyme 2 and angiotensin (1–7) in 17β-oestradiol regulation of renal pathology in renal wrap hypertension in rats. Experimental physiology. 2008;93(5):648-57.

Santos RA, e Silva ACS, Maric C, Silva DM, Machado RP, de Buhr I, et al. Angiotensin-(1–7) is an endogenous ligand for the G protein-coupled receptor Mas. Proceedings of the National Academy of Sciences. 2003;100(14):8258-63.

Nematbakhsh M, Safari T. Role of Mas receptor in renal blood flow response to angiotensin (1-7) in male and female rats. General physiology and biophysics. 2013;33(3):365-72.

Sullivan JC, Bhatia K, Yamamoto T, Elmarakby AA. Angiotensin (1-7) Receptor Antagonism Equalizes Angiotensin II–Induced Hypertension in Male and Female Spontaneously Hypertensive Rats. Hypertension. 2010;56(4):658-66.

Crews JK, Khalil RA. Gender‐specific inhibition of Ca2+ entry mechanisms of arterial vasoconstriction by sex hormones. Clinical and experimental pharmacology and physiology. 1999;26(9):707-15.

Kanashiro CA, Khalil RA. Gender-related distinctions in protein kinase C activity in rat vascular smooth muscle. American Journal of Physiology-Cell Physiology. 2001;280(1):C34-C45.

Higashi Y, Sanada M, Sasaki S, Nakagawa K, Goto C, Matsuura H, et al. Effect of estrogen replacement therapy on endothelial function in peripheral resistance arteries in normotensive and hypertensive postmenopausal women. Hypertension. 2001;37(2):651-7.

Brosnihan KB, Li P, Ferrario CM. Angiotensin-(1-7) dilates canine coronary arteries through kinins and nitric oxide. Hypertension. 1996;27(3):523-8.

Li P, Chappell MC, Ferrario CM, Brosnihan KB. Angiotensin-(1–7) augments bradykinin-induced vasodilation by competing with ACE and releasing nitric oxide. Hypertension. 1997;29(1):394-8.

Aparecida Oliveira M, Bruno Fortes Z, Santos RA, Kosla MC, De Carvalho MHC. Synergistic effect of angiotensin-(1–7) on bradykinin arteriolar dilation in vivo. Peptides. 1999;20(10):1195-201.

Safari T, Nematbakhsh M, Hilliard LM, Evans RG, Denton KM. Sex differences in the renal vascular response to angiotensin II involves the Mas receptor. Acta Physiologica. 2012;206(2):150-6.

Published
2019-03-12
How to Cite
1.
Saberi S, Dehghani A, Nematbakhsh M. Angiotensin 1-7 Administration Increases Renal Blood Flow in the Absence of Bradykinin B2 Receptor in Ovariectomized Estradiol Treated Rats: The Role of Mas Receptor. Acta Med Iran. 57(2):103-109.
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