Low frequency electrical field stimulation elicits responses in segments of mouse tail artery which are slower in alpha1B-knockout mice than in control mice

An alpha1b-knockout (KO) mouse has recently been shown to have markedly reduced pressor responses to phenylephrine and reduced adrenergic receptor (AR) number in the liver, heart and brain. We have now examined the potency of exogenously applied and neuronally released noradrenaline (NA) on segments of isolated tail artery of wild type (WT) and KO mice. In WT mice the CRC to NA was shifted to the right by the high affinity alpha1-AR antagonist YM12617 (pKB 9.41) but not by the high affinity alpha2-AR antagonist delequamine (pKB 6.02). The EC50 values for NA in WT (6.93) and KO (6.64) were not significantly different. CEC caused a 20% depression in the maximum response to NA in both WT (EC50 6.27) and KO (EC50 6.46). Responses to electrical field stimulation (EFS) were transient, returning to baseline within 14 seconds. Responses to low frequency stimulation were significantly smaller in KO (4-16Hz, p < 0.1). Time to EFS induced maximum response ranged from 2.5 - 2.8sec. WT and 2.9 - 3.6sec in KO (p < 0.1 for 4 &8Hz). A 4Hz (10sec train) reached maximum amplitude at 6.9 seconds and 9.15 seconds for WT and KO respectively (p < 0.1). The slope of the KO response (mv/sec) was reduced at low frequencies (4-16Hz; p < 0.1). CEC inhibited the responses to EFS in both WT and KO arteries. These results suggest that the alpha1b-AR may play a role in sympathetic neurotransmission