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Am J Physiol Renal Physiol (January 29, 2002). doi:10.1152/ajprenal.00121.2001
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Articles in PresS, published online ahead of print January 28, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00121.2001
Submitted on April 17, 2001
Accepted on January 21, 2002

Renal Microvascular Actions of Angiotensin II Fragments

William F van Rodijnen1*, Ton A van Lambalgen1, Michiel H van Wijhe1, Geert-Jan Tangelder1, and Piet M ter Wee2

1 Physiology, VU University Medical Center, Amsterdam, Netherlands
2 Nephrology, VU University Medical Center, Amsterdam, Netherlands

In the present study, we investigated renal microvascular responses to angiotensin-(1-7) and angiotensin IV. Diameter changes of small interlobular arteries, afferent arterioles and efferent arterioles were assessed using isolated perfused hydronephrotic rat kidneys. Angiotensin-(1-7) and angiotensin IV decreased diameters of all investigated renal microvessels concentration-dependently, however, with a much lower potency than angiotensin II. The angiotensin II type 1 receptor blocker irbesartan completely reversed the responses to angiotensin-(1-7) and angiotensin IV, while the angiotensin II type 2 receptor blocker PD123319 had no effect. Both angiotensin-(1-7) and angiotensin IV failed to alter renal microvascular constriction induced by angiotensin II. In addition, subnanomolar concentrations of angiotensin-(1-7) had no effect on the myogenic-induced tone of interlobular arteries and afferent arterioles. Thus, our data indicate that, at high concentrations, angiotensin-(1-7) and angiotensin IV are able to activate the AT1-receptor, thereby inducing renal microvascular constriction. The failure of angiotensin-(1-7) and angiotensin IV to reduce the angiotensin II and pressure-induced constriction suggests that these fragments do not exert a vasodilator and/or angiotensin II antagonistic action in the kidney.




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