The number of AT1-B receptors was significantly higher in efferent arterioles (0.32 signals/microm3) compared to afferent arterioles (0.18 signals/microm3, p<0.05).
Absolute Event Rate: 0.32% vs 0.18%
p-value: p=<0.05
INTRODUCTION: The contractile effect of angiotensin II via AT1 receptors on the kidney arterioles is a crucial element in the kidney microcirculation. Angiotensin II also plays a role as an inhibitor via the AT1 receptors in the renin granulation of the arterioles. We have previously demonstrated that the AT1 receptors are downregulated in the renin-positive smooth muscle cells (SMCs) in contrast to renin-negative SMCs. In this study, we estimated the numbers of the AT1 receptor sub-types separately in the afferent and efferent arterioles and the renin-positive and renin-negative SMCs. METHODS: The immunohistochemical signals of the AT1-A and AT1-B receptors were counted by stereological methods. (1) RESULTS: The number of AT1-B receptors in the efferent arterioles (expressed in signals/microm3; mean (CV): 0.32 (0.33)) was significantly higher (78%; p<0.05) as compared with the number in the afferent arterioles (0.18 (0.11)). No differences were found in the AT1-A receptors. In a number of AT1-A receptors, significant differences (p<0.01) were detected between the afferent arteriolar renin-positive SMCs (0.13 (0.36)) and the number in renin-negative SMCs (0.25 (0.34)). The AT1-B receptors did not display any differences. CONCLUSIONS: These results indicate that the AT1 receptor sub-types are regulated independently in the SMCs of the normal kidney arterioles.
Rázga et al. (2008) studied Normal kidney arterioles (rats). Efferent arterioles vs. Afferent arterioles was evaluated on Number of AT1-B receptors (signals/microm3) (p=<0.05). The number of AT1-B receptors was significantly higher in efferent arterioles (0.32 signals/microm3) compared to afferent arterioles (0.18 signals/microm3, p<0.05).