Regulator of G protein signaling 2 (RGS2-/-) deficient mice feature an increased resting blood pressure and an excessive pressor response to stress. We measured renal sympathetic nerve activity (RSNA) directly to test the hypothesis that RSNA is increased in RGS2-/- mice, compared to RGS2+/+ mice. Seventeen mice (RGS2-/-, n = 9; RGS2+/+, n = 8) were anesthetized with isoflurane. We cannulated the left jugular vein for drug administration. Renal sympathetic nerve activity (RSNA) was recorded using bipolar electrodes. Arterial blood pressure (BP) from the femoral artery, ECG (needle electrodes), and RSNA were recorded (sample rate 10 kHz) simultaneously. RSNA was analysed off-line using a modified wavelet de-noising technique and the classical discriminator method. RSNA detected during phenylephrine bolus injections or after the animals death was subtracted from baseline values. Mean arterial blood pressure, norepinephrine plasma levels, the responsiveness to vasoactive drugs, and the sympathetic baroreflex gain were similar in anesthetized RGS2+/+ and RGS2-/- animals. RSNA was lower in RGS2-/- mice compared to wild-type controls (wavelet: spike rate in Hz: RGS2+/+ 25.5 ± 5.1; RGS2-/- 17.4 ± 4.0; discriminator method: RGS2+/+ 41.4 ± 5.7, RGS2-/- 22.0 ± 4.3, p < 0.05). Thus, the expected result proved not to be the case. Our data suggest a mismatch between sympathetic nerve traffic and plasma norepinephrine concentrations. This observation may depend on altered coupling between electrical nerve activity and norepinephrine release and/or a changed norepinephrine uptake in RGS2-/- mice.
- Cardiovascular physiology
- RGS2-deficient mice
- Renal sympathetic nerve activity