Abstract
The role of prostaglandins (PGs) in the regulation of blood pressure was analysed from the point of view of vascular reactivity to PGs and also of PG-induced modulation of pressor response. The vasodepressor effect of PGE1 as more sensitive in the patients with essential hypertension than in the normotensive subjects. In the normotensive subjects or in rats, pressor response to norepinephrine was modulated by PGE1, enhanced under treatment with indomethacin, an inhibitor of PG biosynthesis, and suppressed under an infusion of PGE1. These results indicate that pressor response to norepinephrine is modulated by exogenous and endogenous PGs. The PG-induced modulation disappeared after chemical sympathectomy, suggesting that the PG-induced modulation of pressor response is regulated by the sympathetic nervous system. In sympathetic neurotransmission, PGs could play an important role in the regulation of norepinephrine release. Renal content of norepinephrine was reduced under treatment with indomethacin, indicating an enhanced release of norepinephrine and an enhanced turnover of norepinephirne in the kidneys under treatment with indomethacin. These results suggest that a deficient state of PG may enhance the pressor response and norepinephrine release. As there is much evidence indicating that the reduction of PG synthesis in patients and animals with hypertension, vascular reactivity to PGs and PG-induced modulation of pressor response may play significant roles in the regulation of blood pressure and could be causal factors of hypertension.
