It is known that clonidine exerts a hyperpolarizing action and alpha(2
)-adrenergic activity. The experimental work investigates the conditio
ns under which each action of clonidine is developed on vascular smoot
h muscle. Two parameters were studied in vitro on bovine aortic media,
Ca2+ uptake and vascular tone. The Ca2+ uptake measurement was perfor
med by incubating in Krebs' solution small slices of the preparation i
n the presence of Ca-45. Studies on vascular tone were performed on de
endothelialized bovine aortic rings suspended in Krebs' solution. Low
concentrations of clonidine (1 nM-1 mu M) decrease Ca2+ uptake and rel
ax the preparation, indicating dominance of the inhibiting action of c
lonidine may be due to an hyperpolarization. Clonidine IO mu M results
in equalization of the opposing actions of Ca2+ uptake and vascular t
one. When the preparation is stimulated by alpha(1)-adrenergic against
phenylephrine I mu M, clonidine I nM-10 mu M potentates the Ca2+ upta
ke and vascular contraction in a monophasic way, indicating that the d
epolarizing mechanisms connected with the alpha(1)-adrenergic stimulat
ion totally inhibit the relaxing action of clonidine possibly due to h
yperpolarization. This action is restricted in the presence of yohimbi
ne (alpha(2)-adrenergic blocker). (C) 1998 Pious Science. Ail rights r
eserved.