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Renal Vascular Responses Are Attenuated in Smooth Muscle‐Specific Na+/Ca2+ Exchanger Knockout Mice during Acute Angiotensin II Infusions
Author(s) -
Zhao Di,
Blaustein Mordecai P,
Navar L. Gabriel
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1059.19
Subject(s) - endocrinology , medicine , chemistry , angiotensin ii , renal function , blood pressure , renal blood flow , kidney , knockout mouse , receptor
Studies in smooth muscle‐specific Na + /Ca 2+ exchanger knockout (NCX1 sm−/− ) mice reveal reduced arterial pressure and impaired myogenic responses compared to heterozygous littermates. In this study, we determined renal function in male anesthetized NCX1 sm−/− mice (n=6) and global NCX1 heterozygous (NCX1 +/− , n=8) littermates before and during acute Ang II infusions (5 ng/g Body Weight/min). Systolic blood pressure in awake mice was lower in NCX1 sm−/− mice compared to NCX1 +/− mice (119±4 versus 131±3 mm Hg, P<0.05). Acute Ang II infusions increased mean arterial pressure in NCX1 sm−/− (98±8 to 123±8 mm Hg, P<0.001) and NCX1 +/− mice (109±2 to 134±3 mm Hg, P<0.001). Acute Ang II infusions did not change renal plasma flow (RPF; Δ0.06±0.09 ml/min, P>0.05) or glomerular filtration rate (GFR; Δ0.003±0.04 ml/min, P>0.05) in NCX1 sm−/− mice, whereas acute Ang II infusions significantly decreased RPF (Δ−0.2±0.09 ml/min, P<0.05) and GFR (Δ−0.08±0.03 ml/min, P<0.05) in NCX1 +/− mice. The urine flow responses to acute Ang II infusions were significantly greater in NCX1 sm−/− mice as compared with NCX1 +/− mice (Δ1.88±0.83 versus Δ‐0.33±0.42 μl/min, P<0.05). Urine flow and urinary sodium excretion were higher in NCX1 sm−/− mice as compared with NCX1 +/− mice during acute Ang II infusions. These data suggest that renal vascular responses to Ang II are attenuated in NCX1 sm−/− mice as compared with NCX1 +/− mice and that NCX1 contributes to the renal vasoconstriction response to acute Ang II infusions. Supported by NIH/NHLBI. Disclosure: no conflict of interest