Attenuated renal response to moxonidine and rilmenidine in one kidney‐one clip hypertensive rats

1 I1 non‐adrenoceptor, imidazoline receptor agonists, such as moxonidine, 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 therefore studied the renal effects of two known non‐adrenoceptor, imidazoline 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 directly into the renal artery (30 gauge needle) of 1K‐sham normotensive and 1K‐1C hypertensive rats. 3 In 1K‐sham normotensive rats, rilmenidine and moxonidine produced dose related increases in urine flow rate, sodium excretion and osmolar clearance. Both rilmenidine and moxonidine 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 moxonidine (3 and 10 nmol kg−1 min−1) did result in a small increase in urine 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 diminished in 1K‐1C hypertensive rats compared with 1K‐sham normotensive rats. Whether this decrease in activity of the natriuretic non‐adrenoceptor, imidazoline receptors contributes to the increase in blood pressure in the 1K‐1C acquired model of hypertension remains to be determined.