Rilmenidine is proposed as a selective imidazoline receptor rather than a2
adrenoreceptor drug. It was reported that rilmenidine causes marked centrallymediated
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 a2-adrenergic receptors in the nucleus
tractus solitari of the medulla oblongata. The present study aimed to investigate:
(1) The antihypertensive effect of rilmenidine lmg/kg i.v versus that of clonidine
0.03mk/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/Icg 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 & 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 ins 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 a2 adrenoceptors. |
