ATTENUATED RENAL RESPONSE TO MOXONIDINE AND RILMENIDINE IN ONE-KIDNEYONE-CLIP HYPERTENSIVE RATS

1 I-1 non-adrenoceptor, imidazoline receptor agonists, such as moxonid ine, increase urine flow rate and sodium excretion following infusion into the renal artery. The functions of these agonists in genetic and acquired models of hypertension have not been determined. 2 We therefo re studied the renal effects of two known non-adrenoceptor, imidazolin e receptor agonists, rilmenidine and moxonidine, in 1K-1C hypertensive and 1K-sham normotensive rats. Rilmenidine (0, 3, 10, 30 nmol kg(-1) min(-1)) or moxonidine (0, 1, 3, 10 nmol kg(-1) min(-1)) was infused d irectly into the renal artery (30 gauge needle) of 1K-sham normotensiv e and 1K-1C hypertensive rats. 3 In 1K-sham normotensive rats, rilmeni dine and moxonidine produced dose related increases in urine flow rate , sodium excretion and osmolar clearance. Both rilmenidine and moxonid ine failed to increase. urine flow rate, sodium excretion and osmolar clearance in 1K-1C hypertensive rats to the same extent as in 1K-sham animals. At comparable doses, rilmenidine had no effect, while moxonid ine (3 and 10 nmol kg(-1) min(-1)) did result in a small increase in u rine volume and osmolar clearance which was less than that observed in the 1K sham control animals. 4 These studies indicate that the renal effects of non-adrenoceptor, imidazoline receptor stimulation are dimi nished in 1K-1C hypertensive rats compared with 1K-sham normotensive r ats. Whether this decrease in activity of the natriuretic non-adrenoce ptor, imidazoline receptors contributes to the increase in blood press ure in the 1K-1C acquired model of hypertension remains to be determin ed.