Objective: Clonidine is a centrally acting antihypertensive drug. Hypotensive effect of
clonidine is mediated mainly by central α2-adrenoceptors and/or imidazoline receptors located in a
complex network of the brainstem. Unfortunately, clonidine produces side effects such as sedation,
mouth dry, and depression. Moxonidine and rilmenidine, compounds of the second generation of
imidazoline drugs, with fewer side effects, display a higher affinity for the imidazoline receptors
compared with α2-adrenoceptors. The antihypertensive action of these drugs is due to inhibition of
the sympathetic outflow primarily through central I1-imidazoline receptors in the RVLM, although
others anatomical sites and mechanisms/receptors are involved. Agmatine is regarded as the
endogenous ligand for imidazoline receptors. This amine modulates the cardiovascular function.
Indeed, when administered in the RVLM mimics the hypotension of clonidine.
Results: Recent findings have shown that imidazoline drugs also exert biological response directly
on the cardiovascular tissues, which can contribute to their antihypertensive response. Currently,
new imidazoline receptors ligands are in development.
Conclusion: In the present review, we provide a brief update on the cardiovascular effects of
clonidine, moxonidine, rilmenidine, and the novel imidazoline agents since representing an
important therapeutic target for some cardiovascular diseases.
Keywords: Imidazoline, Agmatine, Nischarin, Sympathoinhibition, Heart, Blood Vessels, Hypertension, Cardiovascular diseases
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