Hypertension and Impaired Vessel Function in a Mouse Model of Systemic Lupus Erythematosus

• Published in: The FASEB journal 2006-03, Vol.20 (5), p.A1191-A1192
• Main Authors: Ryan, Michael J., McLemore, Gerald R.
• Format: Article
• Language: English
• ISSN: 0892-6638; 1530-6860
• DOI: 10.1096/fasebj.20.5.A1191-d

Systemic Lupus Erythematosus (SLE) is a chronic autoimmune inflammatory disease predominantly affecting women of child bearing years. A majority of individuals with SLE have hypertension. Surprisingly, little attention has been given to the role of altered vascular function in the development of hypertension during SLE. We used an established model of SLE (NZBWF1) to examine whether vessel function is impaired. Female NZBWF1 Mice were studied at 36 weeks of age. Mean arterial pressure, measured by radio‐telemetry, was increased in NZBWF1 mice (119 ± 8 mmHg, n= 5) compared to control NZWLacJ mice (101 ± 8 mmHg, n=4). Isolated carotid arteries from NZBWF1 mice, precontracted with U46619 (0.4 ug/ml) for assessment of endothelial dependent relaxation, had impaired maximal relaxation to acetylcholine (ACh, 10‐4 M) compared to controls (41 ± 5% vs. 59 ± 6%, n>10). Maximal relaxation to sodium nitroprusside was not different, suggesting impaired endothelial function during SLE. Maximal tension generated by 5‐hydroxytryptamine (5‐HT) was increased in carotid arteries from NZBWF1 mice compared to controls (0.10 ± 0.02 g vs. 0.03 ± 0.01 g, n>10), thus further supporting a role for endothelial dysfunction. Because SLE often affects the kidneys, we measured renal blood flow (RBF) in NZBWF1 and control mice using perivascular flow probes. RBF was lower in NZBWF1 mice compared to controls (4.6 ± 0.3 vs. 5.5 ± 0.9 ml/min/g kidney, n>4). In addition, we calculated renal vascular resistance to be increased in the NZBWF1 mice (23 ± 1 vs. 15 ± 2 RU, n>4). Taken together our data support a role for altered systemic and renal vascular function in the development of hypertension during SLE.