alpha-Adrenoceptor subtypes mediating regional kidney blood flow responses to renal nerve stimulation

The mechanisms underlying the relative insensitivity of the renal medullary circulation to renal sympathetic nerve stimulation (RNS) remain unknown. Therefore, we tested the effects of systemic alpha(1)- and alpha(2)-adrenoceptor blockade on responses to electrical RNS in pentobarbitone anaesthetized rabbits. Renal blood flow (RBF), cortical laser Doppler flux (CLDF), and to a lesser extent medullary LDF (MLDF) were reduced by RNS in a frequency-dependent manner. Prazosin decreased responses of RBF and CLDF, but not MLDF, to RNS. For example, during the control period 4 Hz stimulation reduced RBF, CLDF and MLDF by 85+/-3%, 89+/-2%, and 20+/-12%, respectively, but after prazosin, corresponding responses were 39+/-3%, 42+/-5% and 28+/-7%, respectively. Prazosin markedly blunted pressor and renal vasoconstrictor responses to intravenous phenylephrine, without altering pressor responses to intravenous xylazine. Rauwolscine enhanced renal vasoconstrictor responses to RNS, although this was statistically significant for RBF and CLDF but not MLDF. For example, during the control period 2 Hz stimulation reduced RBF, CLDF and MLDF by 63+/-7%, 58+/-7%, and 29+/-17%, respectively, and after rauwolscine, corresponding responses were 83+/-4%, 87+/-1%, and 53+/-12%, respectively. Rauwolscine markedly blunted renal vasoconstrictor responses to renal arterial guanabenz, but not phenylephrine. These data suggest that alpha(1)-adrenoceptors contribute to RNS-induced vasoconstriction in the renal cortex, but contribute less in vascular elements controlling medullary perfusion. Activation of alpha(2)-adrenoceptors appears to blunt RNS-induced renal vasoconstriction, but this mechanism does not underlie the relative insensitivity of medullary perfusion to RNS.