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1 Institute of Vegetative Physiology, Charite-Universitatsmedizin Berlin, Humboldt-University of Berlin, Berlin, Germany
2 Department of Medical Cell Biology, Uppsala University, Biomedical Center, Uppsala, Sweden
3 Berlin, Germany; Institute of Vegetative Physiology, Charite-Universitatsmedizin Berlin, Humboldt-University of Berlin, Berlin, Germany
4 Institute of Pathology, Neuropathology, and Molecular Pathology, Hannover, Germany
5 Department of Internal Medicine I, Marienhospital Herne, Ruhr-University Bochum, Bochum, Germany
* To whom correspondence should be addressed. E-mail: andreas.patzak{at}charite.de.
The aim of the study is to evaluate the impact of nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) and neuronal NOS (nNOS) on the angiotensin II response in afferent arterioles (Af). Dose responses were assessed for angiotensin II in microperfused Af of mice homozygous for disruption of the eNOS gene (eNOS(-/-)), or nNOS gene (nNOS(-/-)), and their wild type controls eNOS(+/+), and nNOS(+/+). Angiotensin II at 10-8 and 10-6 mol/l reduced the lumen to 69% and 68% in eNOS(+/+), and to 59% and 50% in nNOS(+/+). NG-Nitro-L-arginine-methyl-ester (L-NAME) did not change basal arteriolar diameters, but augmented angiotensin II contraction, reducing diameters to 23% and 13% in eNOS(+/+), and 7% and 10% in nNOS(+/+) at 10-8 and 10-6 mol/l. The response to angiotensin II was enhanced in nNOS(-/-) mice (41% and 25% at 10-8 and 10-6 mol/l), and, even more enhanced in eNOS(-/-) mice (12% and 9%) compared to nNOS(+/+) and eNOS(+/+). L-NAME led to complete constriction of Af in these groups. Media/lumen ratios of Af did not differ between controls and gene deficient mice. mRNA expression of angiotensin II receptor type 1A, 1B and type 2 also did not differ. The results reveal that angiotensin II induced release of NO from both eNOS and nNOS significantly contribute to the control of Af. Results also suggest that eNOS-derived NO is of greater importance than nNOS-derived NO in this isolated arteriolar preparation.
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