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• W2022856894 abstract "Clonidine and a series of structural analogs with α-adrenergic properties that have been previously characterized were evaluated for their antihypertensive activity following systemic (intravenous) administration to spontaneously hypertensive rats, and for their ability to elevate blood pressure following central (intracisternal) administration to reserpine-pretreated rats. The peripheral pressor activity after intravenous administration in pithed rats was also determined to evaluate possible differences among the compounds in α-adrenergic activity in the peripheral vasculature. Dose-response relationships for the peripheral pressor activities of the compounds indicate that the α-adrenergic activities of these imidazolidines are similar, consistent with our previous observation. A wide range in the potencies of these imidazolidines was observed when their antihypertensive activities were evaluated after systematic (intravenous) administration to spontaneously hypertensive rats. There was an excellent correlation between the antihypertensive activities of these compounds following systemic administration and their ionization constants (r = 0.90, P<0.05). In the reserpine-pretreated rat, sympathetic outflow is abolished by catecholamine depletion, and blood pressure is maximally reduced. When clonidine-like α-adrenergic agonists are administered intracisternally to reserpine-pretreated rats, a pressor response is observed which results from diffusion of the α-agonist out of the brain into the periphery where vascular α-adrenergic receptors are activated to produce the elevation in blood pressure. A wide range in pressor potencies was observed for these clonidine-like imidazolidines when administered intracisternally to reserpine-pretreated rats, and these potencies were also highly correlated with ionization constants (r = 0.94, P<0.01). Since no significant correlation (r = −0.41, P>0.05) existed between the pKa values and the pressor potencies of these compounds when administered intravenously to pithed rats, we conclude that the correlation observed above is not the result of differences in the peripheral vasoconstrictor effects of the compounds, and that the pressor effects observed after intracisternal administration of these agents to reserpine-pretreated rats resulted from their peripheral vasoconstrictor effects following their exit from the brain via diffusion through the blood-brain barrier. These results are consistent with the hypothesis that one major factor affecting the antihypertensive activity of clonidine-like imidazolidines is the blood-brain barrier and that this barrier is more easily penetrated, in either direction, by the un-ionized relative to the ionized species." @default.
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• W2022856894 title "Receptor interactions of imidazolines influence of ionization constant on the diffusion of clonidine and a series of structurally related imidazolidines into and out of the central nervous system" @default.
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• W2022856894 doi "https://doi.org/10.1016/0014-2999(82)90101-7" @default.
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