First Author | Zhao D | Year | 2011 |
Journal | Am J Physiol Renal Physiol | Volume | 301 |
Issue | 3 | Pages | F574-9 |
PubMed ID | 21697239 | Mgi Jnum | J:175632 |
Mgi Id | MGI:5286787 | Doi | 10.1152/ajprenal.00065.2011 |
Citation | Zhao D, et al. (2011) Attenuated renal vascular responses to acute angiotensin II infusion in smooth muscle-specific Na+/Ca2+ exchanger knockout mice. Am J Physiol Renal Physiol 301(3):F574-9 |
abstractText | Recent studies in smooth muscle-specific Na(+)/Ca(2+) exchanger-1 knockout (NCX1(sm-/-)) mice reveal reduced arterial pressure and impaired myogenic responses compared with heterozygous littermates. In this study, we determined renal function in male anesthetized NCX1(sm-/-) mice and NCX1 heterozygous (NCX1(+/-)) littermates before and during acute ANG II infusions. Systolic blood pressure in awake mice was lower in NCX1(sm-/-) mice compared with NCX1(+/-) mice (119 +/- 4 vs. 131 +/- 3 mmHg, P < 0.05). Acute ANG II infusions (5 ng.min(-1).g(-1) body wt) increased mean arterial pressure in anesthetized NCX1(+/-) (109 +/- 2 to 134 +/- 3 mmHg, P < 0.001, n = 8) and NCX1(sm-/-) (101 +/- 8 to 129 +/- 8 mmHg, P < 0.01, n = 6) mice to a similar extent (Delta25 +/- 1 vs. Delta28 +/- 4 mmHg, P > 0.05). In response to ANG II infusions, PAH clearance (C(PAH)) decreased from 1.39 +/- 0.27 to 0.98 +/- 0.22 ml.min(-1).g(-1) (P < 0.05) and glomerular filtration rate (GFR) was reduced from 0.50 +/- 0.09 to 0.32 +/- 0.06 ml.min(-1).g(-1) (P < 0.05) in NCX1(+/-) mice. In contrast, the NCX1(sm-/-) did not exhibit significant reductions in either C(PAH) (1.16 +/- 0.30 to 1.22 +/- 0.34 ml.min(-1).g(-1), P > 0.05) or GFR (0.48 +/- 0.08 to 0.41 +/- 0.05 ml.min(-1).g(-1), P > 0.05) during acute ANG II infusions. Using flometry to measure renal blood flow continuously, NCX1(sm-/-) mice had significantly attenuated responses to ANG II infusions (-34.2 +/- 3.9%, P < 0.05) compared with those in NCX1(+/-) mice (-48 +/- 2%) or in wild-type mice (-69 +/- 7%). These data indicate that renal vascular responses to ANG II are attenuated in NCX1(sm-/-) mice compared with NCX1(+/-) mice and that NCX1 contributes to the renal vasoconstriction response to acute ANG II infusions. |