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Case Reports
. 2007 Nov;50(5):829-34.
doi: 10.1161/HYPERTENSIONAHA.107.096750. Epub 2007 Oct 8.

Autoimmune hypertensive syndrome

David C Kem  1 , Xichun Yu, Eugene Patterson, Shijun Huang, Stavros Stavrakis, Bela Szabo, Leann Olansky, Jon McCauley, Madeleine W Cunningham
Affiliations
Case Reports

Autoimmune hypertensive syndrome

David C Kem et al. Hypertension. 2007 Nov.
No abstract available

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Figures

Figure 1
Figure 1
The ELISA titers for both anti-β1AR and anti-β2AR from 2000 and 2006 are shown in this plot compared with values obtained in 25 normal control subjects.
Figure 2
Figure 2
Top, The dose-response effect of the 2006 serum is shown on Purkinje fiber contractility. Dilutions as low as 1:400 gave a significant increase in contractility compared with the buffer alone. Each point represents the mean±SD for 5 observations. *P=0.05, **P<0.01 vs buffer control. Bottom, ISO was used as a positive control. This preparation was able to demonstrate significance even at 10−10 mol/L concentrations. *P<0.05, **P<0.01 vs buffer control.
Figure 3
Figure 3
The effect of IgG from the patient is shown on Purkinje fiber contractility. Data are shown for 6 different studies using IgG derived from the sera, for 2 normal control subjects and for the ISO control. Only 1 assay was used with the β-blocker nadolol (NAD). The values represent mean±SD and are expressed as percentage above basal levels of the buffer control (dashed line). The nadolol was added to the perfusion buffer before the test, and new baseline data were acquired. There was an immediate rise in the contractility index when IgG was added. This effect would be maintained for 2 to 5 minutes and then would wash out over a 5-minute period, indicating that the antibodies were not of such high affinity as to remain affixed for prolonged periods. This response was completely blocked when a β-blocker was added before the addition of the IgG. *P<0.01 vs control IgG.
Figure 4
Figure 4
The effect of the 2006 sera is shown on Purkinje fiber automaticity for the patient and a normal control subject. Each value represents the mean of 20 consecutive contractions and was measured once the preparation had stabilized. The data are expressed as the percentage above basal levels of the buffer control (dashed line; mean±SD; n=3). This effect was similar to the contractility data. There was no evidence for desensitization of the response over a 5-minute exposure period. This accelerated response again was completely eliminated by previous treatment with the non-selective β-blocker nadolol (NAD). *P<0.01 vs control sera.
Figure 5
Figure 5
The effect of sera and affinity-purified IgG derived from the patient’s sera on PKA activation is shown for sera obtained in 2000 and for both sera and IgG obtained in 2006. The values are expressed as percentages above basal levels of PKA in medium control (dashed line) in the H9c2 heart cell line (mean±SD; n=3). There was no significant difference between the use of sera and affinity-purified IgG from the sera in the assay. The patient was not on a β-blocker when the first sample was obtained. There was no apparent effect of carvedilol on PKA activity in the diluted sera in 2006. This potential effect was eliminated in the purified IgG sample. The PKA activity was returned to baseline when propranolol (PROP) was added to the incubated cells. ISO was used as a positive control to activate PKA. *P<0.01 vs sera or IgG from a normal control subject.
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