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Augmented Renal Vascular nNOS and Renin Protein Expression in Angiotensin Type 1 Receptor Null Mice

Sungmi Park and Lisa M. Harrison-Bernard

Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, Louisiana

Correspondence to: Lisa M. Harrison-Bernard, PhD, Department of Physiology, Box P7-3, Louisiana State University Health Sciences Center, 1901 Perdido Street, New Orleans, LA 70112. E-mail: lharris{at}lsuhsc.edu

The present study was performed to determine the influence of absence of angiotensin type 1A (AT_1A) and/or AT_1B receptor feedback regulation of kidney neuronal nitric oxide synthase (nNOS) and renin protein expression. Kidneys were harvested from wild-type (WT), AT_1A^–/–, AT_1B^–/–, and AT_1A^–/–AT_1B^–/– mice and immunostained for nNOS and renin protein localization. AT_1A^–/– and AT_1A^–/–AT_1B^–/– kidneys demonstrated an increase in the percentage of glomeruli with nNOS-positive afferent and interlobular arterioles compared with WT mice. Density of vascular nNOS immunostaining was 20-fold higher in kidneys of AT_1A^–/– and AT_1A^–/–AT_1B^–/– compared with WT mice. Density of macula densa nNOS immunostaining was 7-fold higher in AT_1A^–/–AT_1B^–/– than in WT mice. Percent of glomeruli positive for juxtaglomerular (JG) cell renin was 3-fold higher, whereas the density of JG cell renin immunostaining was 15-fold higher in kidneys of AT_1A^–/– and AT_1A^–/–AT_1B^–/– compared with WT mice. Kidneys of AT_1A^–/– and AT_1A^–/–AT_1B^–/– mice displayed recruitment of renin protein expression along afferent and interlobular arterioles. Absence of AT₁ receptor signaling resulted in enhanced nNOS protein expression in both microvascular and tubular structures. Enhanced NO generation may contribute to the reduced renal vascular tone and blood pressure observed with blockade of the renin–angiotensin system. (J Histochem Cytochem 56:401–414, 2008)

Key Words: neuronal nitric oxide synthase • juxtaglomerular cell • transgenic mice • renin recruitment • macula densa cells

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