ABSTRACT
Rilmenidine is proposed as a selective imidazoline receptor rather than [2 adrenoreceptor drug. It was reported that rilmenidine causes marked centrally-mediated hypotension, whilst the incidence of its adverse effects is quite low. Clonidine is another centrally acting antihypertensive agent characterized by its wide therapeutic range. The mechanism of its antihypertensive action appears to be through stimulation of postsynaptic [2-adrenergic receptors in the nucleus tractus solitari of the medulla oblongata. The present study aimed to investigate: [1] The antihypertensive effect of rilmenidine 1mg/kg i.v versus that of clonidine 0.03mg/kg i.v in experimentally induced-hypertension in rats by renal artery occlusion. [2] Study the possible sedative effect of rilmenidine 10mg/kg i.p versus that of clonidine 0.25mg/kg i.p. [3] Evaluate the effect of yohimbine 10mg/kg i.v on rilmenidine and clonidine actions. The results of the present study revealed that at equipotent doses; both rilmenidine and clonidne induced a transient significant [p<0.05] elevation of blood pressure followed by long-lasting hypotension and bradycardia. It was also found that yohimbine significantly [p<0.05] blocked the antihypertensive effect of clonidine but produced insignificant [p>0.05] effect on rilmenidine hypotensive action. On the other hand, rilmenidine had insignificant [p>0.05] effect on sleeping time induced by pentobarbitone 30 mg/kg i.p, whilst clonidine produced significant [p<0.05] increase in the sleeping time, an action which was significantly [p<0.05] attenuated by yohimbine. In conclusion, rilmenidine proved to has high efficacy as an antihypertensive drug with less sedative side effects compared with clonidine. This may be due to its main action on the central imidazoline receptors rather than on the alpha[2] adrenoceptors