Diminished Prostaglandin-Mediated Inhibition of Norepinephrine Release from the Sympathetic Nerve Endings in Spontaneously Hypertensive Rats

Abstract

This study was performed to investigate prostaglandin(PG)-mediated regulation of norepinephrine release from the sympathetic nerve endings in spontaneously hypertensive rats(SHR). The effects of PGE₂ on the pressor responses and norepinephrine overflow during the periarterial nerve stimulation were examined in the perfused mesenteric vascular beds from SHR and age-matched Wistar Kyoto rats(WKY). In preliminary studies using normotensive Wistar rats, PGE₂ inhibited the overflow of norepinephrine in response to the electrical nerve stimulation. On the contrary, when indomethacin was infused into the preparations, the norepinephrine overflow induced by the nerve stimulation was increased. In SHR, the neurogenic vasoconstriction and norepinephrine overflow during the nerve stimulation were significantly greater than in WKY. PGE₂ in the medium inhibited the pressor responses and norepinephrine overflow during the nerve stimulation dose-dependently in WKY, while the inhibitory effects of PGE₂ in SHR were blunted. These results suggest that PGE₂ is an important hormone in regulating sympathetic vascular tone and that presynaptic inhibition of vascular adrenergic transmission by PGE₂ is attenuated in SHR.

Key Words:

• Spontaneously hypertensive rats
• norepinephrine release
• sympathetic nervous system
• presynaptic inhibition
• prostaglandin E₂
• indomethacin