The cardiovascular action of Solanum melongena extract (SME) was investigated using in vivo and in vitro preparations. SME produced dose-dependent hypotensive responses in normotensive albino rats. The duration of response was also dose dependent. In pharmacological antagonist studies, the hypotensive action of SME was proved not to be mediated through the autonomic ganglion, the α-adrenoceptor or the histaminergic receptor. SME worked via the β-adrenoceptor and cholinergic (muscarinic) receptor inducing the hypotensive response. A dose-related attenuation of hypotension with increasing dosages of the β-adrenoceptor blocker, propranolol, and the cholinergic receptor blocker, atropine was observed. In vitro studies indicated that the vasorelaxing and negative inotropic effect of SME might be implicated in the hypotensive response. The activities of the β-adrenergic and acetylcholine receptors mediated by SME in turn promoted vasodilation of the resistant vessels and a reduction in cardiac activity respectively. It is also possible that the hypotensive effect of SME could be accounted for by its influence on the activity of the renin-angiotensin system, since a significant difference of the hypotensive response of SME was obtained with captopril. Furthermore, SME induced diuresis in water-loaded rats which might also account for the hypotensive effect observed. SME could be a very potent hypotensive agent.