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. 2002 Sep 27;545(Pt 1):269–277. doi: 10.1113/jphysiol.2002.022384

Table 3.

Effect of diclofenac with and without CTX + apamin on bradykinin-induced hyperpolarization

Normotensive pregnant (mV) Pre-eclampsia (mV)
I. Resting membrane potential
  Control −59.9 ± 1.3 (9) −56.0 ± 1.1 (6)
  +DF −55.1 ± 0.8(9) −53.2 ± 1.2 (6)
  +DF + CTX + apamin −51.8 ± 0.4(4) −49.4 ± 0.7(4)
II. Bradykinin-induced hyperpolarization
  Control
     initial hyperpolarization −12.4 ± 1.4 (6) −11.3 ± 1.2 (6)
     second hyperpolarization −4.3 ± 0.7 (6) −2.6 ± 0.4* (6)
  +DF
     initial hyperpolarization −11.5 ± 1.8 (6) −16.4 ± 1.0 (4)
     second hyperpolarization −0.4 ± 0.6(6) −0.4 ± 1.6 (4)
  +DF + CTX + apamin
     initial hyperpolarization −0.6 ± 0.6(4) −1.2 ± 1.2 (3)

Data are expressed as mean ± s.e.m. The number of women is given in parentheses. The initial hyperpolarization was calculated as the maximum hyperpolarization obtained within a 3 min period after application of bradykinin, and the second hyperpolarization was calculated as the maximum hyperpolarization obtained within a 5–17 min period after washout of bradykinin. The cyclooxygenase inhibitor, diclofenac (DF, 3 μm), was given as pretreatment for 60 min and was present throughout the experiment. Charybdotoxin (CTX) + apamin (Ca2+-activated K+ channel inhibitors) were given as pretreatment for 15 min in the presence of diclofenac and were present thereafter.

*

P < 0.05 vs. normotensive pregnant women.

P < 0.05 vs. before application of diclofenac.

P < 0.05 vs. before application of CTX + apamin.