Mechanism of action of hypotensive prostaglandins in patients with essential hypertension.

Despite extensive investigation, the biological mechanisms causing essential hypertension (EHT) remain unclear. To clarify the means by which hypotensive prostaglandins (Hypo-PGs, mainly PGE1 and PGE2) act in patients with EHT, the interaction between intravenously infused Hypo-PGs and pressor substances such as an adrenergic neurotransmitter, noradrenaline (NA) and angiotensin II (AII) was examined both in patients with EHT and in perfused isolated rabbit ear artery preparations. In patients with EHT, Hypo-PGs were shown to reduce the pressor responses to intravenously infused NA or AII, although no significant difference was found between the pressor responses to NA under basal conditions and the responses during intravenous infusion of Hypo-PGs. Animal studies were undertaken to investigate the inhibitory action of Hypo-PGs on the vasoconstrictive responses to electrical stimulation of the perivascular sympathetic nerves (VSNS) and to exogenous NA at pre- and postjunctional sites in blood vessel walls. The suppressive action of Hypo-PGs on the response to VSNS was shown to be more potent than that to their action on the response to exogenous NA. Thus, it was concluded that the hypotensive action of intravenously infused Hypo-PGs in patients with EHT may be more dependent on prejunctional sites than on the postjunctional sites in the walls of blood vessels.