Why the study?
Does blockade of AT2R or MasR alter nitric oxide formation and renal blood flow in response to Angiotensin II in male and female rats with renal ischemia/reperfusion injury?
Does blockade of AT2R or MasR alter nitric oxide formation and renal blood flow in response to Angiotensin II in male and female rats with renal ischemia/reperfusion injury?
There is a gender dimorphism in nitric oxide production and renal blood flow response to Angiotensin II in renal ischemia/reperfusion injury, with females showing greater sensitivity mediated by vasodilator receptors.
Sex-specific AT2R effects on NO in rat renal I/R suggest caution extrapolating across sexes; leaves open human translation.
Background: Nitric oxide (NO) as a vasodilator factor has renoprotective effect against renal ischemia. The balance between angiotensin II (Ang II) and NO can affect kidney homeostasis. The aim of this study was to determine NO alteration in response to renin–Ang system vasodilator receptors antagonists (PD123319; Ang II type 2 receptor antagonist and A779; Mas receptor antagonist) in renal ischemia/reperfusion injury (IRI) in rats. Materials and Methods: Sixty-three Wistar male and female rats were used. Animals from each gender were divided into four groups received saline, Ang II, PD123319 + Ang II, and A779 + Ang II after renal IRI. Renal IRI induced with an adjustable hook. Blood pressure and renal blood flow (RBF) measured continuously. The nitrite levels were measured in serum, kidney, and urine samples. Results: In female rats, the serum and kidney nitrite levels increased significantly by Ang II ( P < 0.05) and decreased significantly ( P < 0.05) when PD123319 was accompanied with Ang II. Such observation was not seen in male. Ang II decreased RBF significantly in all groups ( P < 0.05), while PD + Ang II group showed significant decrease in RBF in comparison with the other groups in female rats ( P < 0.05). Conclusion: Males show more sensibility to Ang II infusion; in fact, it is suggested that there is gender dimorphism in the Ang II and NO production associated with vasodilator receptors.
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Maleki et al. (2018) studied this question.
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