TY - JOUR
T1 - Strain-dependent susceptibility for hypertension in mice resides in the natural killer gene complex
AU - Taherzadeh, Zhila
AU - VanBavel, Ed
AU - de Vos, Judith
AU - Matlung, Hanke L.
AU - van Montfrans, Gert
AU - Brewster, Lizzy M.
AU - Seghers, Leonard
AU - Quax, Paul H. A.
AU - Bakker, Erik N. T. P.
PY - 2010
Y1 - 2010
N2 - Taherzadeh Z, VanBavel E, de Vos J, Matlung HL, van Montfrans G, Brewster LM, Seghers L, Quax PH, Bakker EN. Strain-dependent susceptibility for hypertension in mice resides in the natural killer gene complex. Am J Physiol Heart Circ Physiol 298: H1273-H1282, 2010. First published February 12, 2010; doi: 10.1152/ajpheart. 00508.2009.-Hypertension is associated with chronic vascular inflammation. We tested the hypothesis that the sensitivity to develop hypertension and vascular remodeling depends on the immunological background. Blood pressure, vascular remodeling, endothelial function, vascular architecture ( number of collateral arteries), and expression of inflammatory cytokines were determined in mice that received N-G-nitro-L-arginine methyl ester (L-NAME) to inhibit nitric oxide synthesis. We studied C57BL/6, BALB/c, and BALB. B6-Cmv1r mice, a congenic strain where the natural killer (NK) gene complex of C57BL/6 mice is introduced in the BALB/c background. During a 4-wk treatment with L-NAME, blood pressure initially increased in both C57BL/6 and BALB/C mice, but after 4 wk, only C57BL/6 mice showed a significant increase in mean arterial blood pressure (+53 mmHg; P <0.001) and small artery inward remodeling. Endothelial function and vascular design were significantly different between C57BL/6 mice and BALB/C mice. The inflammatory response was similar in C57BL/6 and BALB/C mice, except for the leukocyte marker CD11b. Cellular colocalization of CD11b with NK1.1 indicated the recruitment of NK cells in C57BL/6 mice. Congenic BALB. B6-Cmv1r mice showed the same endothelial response and vascular architecture as BALB/c mice. However, BALB. B6-Cmv1r mice displayed a similar sensitivity to hypertension and vascular remodeling as C57BL/6 mice. In conclusion, we have identified the NK gene complex as an important determinant in the genetically determined sensitivity to develop L-NAME-induced hypertension in mice
AB - Taherzadeh Z, VanBavel E, de Vos J, Matlung HL, van Montfrans G, Brewster LM, Seghers L, Quax PH, Bakker EN. Strain-dependent susceptibility for hypertension in mice resides in the natural killer gene complex. Am J Physiol Heart Circ Physiol 298: H1273-H1282, 2010. First published February 12, 2010; doi: 10.1152/ajpheart. 00508.2009.-Hypertension is associated with chronic vascular inflammation. We tested the hypothesis that the sensitivity to develop hypertension and vascular remodeling depends on the immunological background. Blood pressure, vascular remodeling, endothelial function, vascular architecture ( number of collateral arteries), and expression of inflammatory cytokines were determined in mice that received N-G-nitro-L-arginine methyl ester (L-NAME) to inhibit nitric oxide synthesis. We studied C57BL/6, BALB/c, and BALB. B6-Cmv1r mice, a congenic strain where the natural killer (NK) gene complex of C57BL/6 mice is introduced in the BALB/c background. During a 4-wk treatment with L-NAME, blood pressure initially increased in both C57BL/6 and BALB/C mice, but after 4 wk, only C57BL/6 mice showed a significant increase in mean arterial blood pressure (+53 mmHg; P <0.001) and small artery inward remodeling. Endothelial function and vascular design were significantly different between C57BL/6 mice and BALB/C mice. The inflammatory response was similar in C57BL/6 and BALB/C mice, except for the leukocyte marker CD11b. Cellular colocalization of CD11b with NK1.1 indicated the recruitment of NK cells in C57BL/6 mice. Congenic BALB. B6-Cmv1r mice showed the same endothelial response and vascular architecture as BALB/c mice. However, BALB. B6-Cmv1r mice displayed a similar sensitivity to hypertension and vascular remodeling as C57BL/6 mice. In conclusion, we have identified the NK gene complex as an important determinant in the genetically determined sensitivity to develop L-NAME-induced hypertension in mice
U2 - https://doi.org/10.1152/ajpheart.00508.2009
DO - https://doi.org/10.1152/ajpheart.00508.2009
M3 - Article
C2 - 20154263
SN - 0363-6135
VL - 298
SP - H1273-H1282
JO - American journal of physiology. Heart and circulatory physiology
JF - American journal of physiology. Heart and circulatory physiology
IS - 4
ER -