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Open AccessArticle

Impact of the NO-Sensitive Guanylyl Cyclase 1 and 2 on Renal Blood Flow and Systemic Blood Pressure in Mice

1
Institute of Pharmacology and Toxicology, Medical Faculty, Ruhr-University Bochum, 44801 Bochum, Germany
2
Department of Nephrology, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine-University Düsseldorf, 40225 Düsseldorf, Germany
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(4), 967; https://doi.org/10.3390/ijms19040967
Received: 23 February 2018 / Revised: 13 March 2018 / Accepted: 17 March 2018 / Published: 23 March 2018
(This article belongs to the Special Issue cGMP-Signalling in Cells: Molecular and Functional Features)
Nitric oxide (NO) modulates renal blood flow (RBF) and kidney function and is involved in blood pressure (BP) regulation predominantly via stimulation of the NO-sensitive guanylyl cyclase (NO-GC), existing in two isoforms, NO-GC1 and NO-GC2. Here, we used isoform-specific knockout (KO) mice and investigated their contribution to renal hemodynamics under normotensive and angiotensin II-induced hypertensive conditions. Stimulation of the NO-GCs by S-nitrosoglutathione (GSNO) reduced BP in normotensive and hypertensive wildtype (WT) and NO-GC2-KO mice more efficiently than in NO-GC1-KO. NO-induced increase of RBF in normotensive mice did not differ between the genotypes, but the respective increase under hypertensive conditions was impaired in NO-GC1-KO. Similarly, inhibition of endogenous NO increased BP and reduced RBF to a lesser extent in NO-GC1-KO than in NO-GC2-KO. These findings indicate NO-GC1 as a target of NO to normalize RBF in hypertension. As these effects were not completely abolished in NO-GC1-KO and renal cyclic guanosine monophosphate (cGMP) levels were decreased in both NO-GC1-KO and NO-GC2-KO, the results suggest an additional contribution of NO-GC2. Hence, NO-GC1 plays a predominant role in the regulation of BP and RBF, especially in hypertension. However, renal NO-GC2 appears to compensate the loss of NO-GC1, and is able to regulate renal hemodynamics under physiological conditions. View Full-Text
Keywords: renal blood flow; hypertension; NO-sensitive guanylyl cyclase; nitric oxide; cGMP; kidney; vasorelaxation; blood pressure; L-NAME; NO-GC renal blood flow; hypertension; NO-sensitive guanylyl cyclase; nitric oxide; cGMP; kidney; vasorelaxation; blood pressure; L-NAME; NO-GC
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MDPI and ACS Style

Mergia, E.; Thieme, M.; Hoch, H.; Daniil, G.; Hering, L.; Yakoub, M.; Scherbaum, C.R.; Rump, L.C.; Koesling, D.; Stegbauer, J. Impact of the NO-Sensitive Guanylyl Cyclase 1 and 2 on Renal Blood Flow and Systemic Blood Pressure in Mice. Int. J. Mol. Sci. 2018, 19, 967. https://doi.org/10.3390/ijms19040967

AMA Style

Mergia E, Thieme M, Hoch H, Daniil G, Hering L, Yakoub M, Scherbaum CR, Rump LC, Koesling D, Stegbauer J. Impact of the NO-Sensitive Guanylyl Cyclase 1 and 2 on Renal Blood Flow and Systemic Blood Pressure in Mice. International Journal of Molecular Sciences. 2018; 19(4):967. https://doi.org/10.3390/ijms19040967

Chicago/Turabian Style

Mergia, Evanthia; Thieme, Manuel; Hoch, Henning; Daniil, Georgios; Hering, Lydia; Yakoub, Mina; Scherbaum, Christina R.; Rump, Lars C.; Koesling, Doris; Stegbauer, Johannes. 2018. "Impact of the NO-Sensitive Guanylyl Cyclase 1 and 2 on Renal Blood Flow and Systemic Blood Pressure in Mice" Int. J. Mol. Sci. 19, no. 4: 967. https://doi.org/10.3390/ijms19040967

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