Hypertension is associated with the imbalance of
vasoconstrictor and
vasodilator systems. Vasodilation is usually evaluated in isolated blood vessels, but except for
nitric oxide (NO), relatively little attention is given to the in vivo efficiency of particular
vasodilator mechanisms. The aim of our study was to evaluate the contribution of endogenous
vasodilator prostanoids, Ca(2+)-activated K(+) channels and NO to blood pressure (BP) maintenance in rats with three different forms of experimental
hypertension. Both principal vasopressor systems (the renin-angiotensin system and the sympathetic nervous system) were blocked by
captopril and
pentolinium in conscious spontaneously hypertensive rats (SHRs), Dahl
salt-hypertensive (DS-HS) rats and rats with NO-deficient
hypertension, as well as in their normotensive controls. Thereafter, we monitored BP changes in rats subjected to either a sequential or an isolated blockade of
prostanoid synthesis by the non-selective
cyclooxygenase inhibitor,
indomethacin, of Ca(2+)-activated K(+) channels by
tetraethylammonium and of NO formation by
N(G)-nitro-L-arginine methyl ester. All three forms of experimental
hypertension were characterized by augmented sympathetic vasoconstriction. The vasodilatation exerted by endogenous
prostanoids and Ca(2+)-activated K(+) channels was enhanced in all forms of
hypertension, almost proportionally to BP elevation. On the contrary, NO-dependent vasodilatation was not enhanced in any form of experimental
hypertension, and there was a severe relative NO deficiency in both, SHRs and DS-HS rats. In conclusion, our data suggested that there is a compensatory activation of
vasodilator prostanoids and Ca(2+)-activated K(+) channels in rats with experimental
hypertension, whereas NO-dependent vasodilatation is not augmented. Thus, the overall activity of
vasodilator systems failed to compensate for augmented sympathetic vasoconstriction in hypertensive animals.