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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Characterization of brain imidazoline receptors in normotensive and hypertensive rats: differential regulation by chronic imidazoline drug treatment.

The binding of [3H]idazoxan in the presence of l-epinephrine was used to characterize and quantitate imidazoline receptors in the brain of spontaneously hypertensive (SHR), normotensive Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats before and after chronic imidazoline drug treatment. In the cerebral cortex of WKY and SHR rats, the rank order of potency of imidazoli(di)ne drugs (cirazoline greater than idazoxan greater than naphazoline greater than clonidine much greater than RX821002) competing with [3H]idazoxan showed the specificity for an imidazoline receptor which also appeared heterogeneous in nature. In SHR rats, the density of imidazoline receptors (hypothalamus greater than medulla oblongata greater than cerebral cortex) and proportion of high- and low-affinity sites for the receptor were not different from those in WKY and SD rats, suggesting that the receptor itself is not altered in hypertension. However, chronic treatment with idazoxan and cirazoline (10 and 1 mg/kg, i.p., every 12 h for 7 days) consistently increased (about 35%) the density of imidazoline receptors in the brain of WKY and SD, but not in SHR rats. A similar treatment with RX821002, the 2-methoxy analog of idazoxan, which is a highly selective alpha-2 adrenoceptor antagonist, did not increase the density of brain imidazoline receptors. Moreover, the up-regulation of these receptors induced by cirazoline was still present after alkylation of the alpha-2 adrenoceptors with N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline. The lack of regulation by idazoxan and cirazoline of the density of imidazoline receptors in the brain of SHR rats suggests the existence of a relevant abnormality in the adaptive process of these receptors in this genetic model of hypertension.[1]


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