Pregnancy-induced alterations of neurogenic constriction and dilation of human uterine artery.
The responses to electrical field stimulation (EFS) of perivascular nerves in human uterine arteries were characterized. The arteries were removed from pregnant and nonpregnant patients undergoing hysterectomy. Tetrodotoxin, guanethidine, and phentolamine blocked EFS (2 min, 80 V, 0.1-ms duration)-induced constriction. The constrictions and the endogenous norepinephrine levels were lower (P < 0.01) in uterine arteries from pregnant than from nonpregnant patients. When arterial rings were precontracted, the response to EFS was biphasic, consisting of an initial constriction followed by a postconstriction relaxation. The EFS-induced relaxation was endothelium independent and was greater (P < 0.01) in uterine arteries from pregnant than from nonpregnant patients. The relaxation was enhanced by guanethidine and superoxide dismutase, inhibited by nitric oxide synthase inhibitors, blocked by tetrodotoxin, and unaffected by atropine, propranolol, or indomethacin. The results demonstrate that human uterine arteries respond to EFS with contraction and relaxation and that these responses may be mediated, respectively, by norepinephrine and, in part, by nitric oxide released from periarterial nerves. The decrease in neuronally mediated uterine arterial constriction and the increase in dilation could be physiological mechanisms for ensuring appropriate uteroplacental perfusion.
Nelson
S H
SH
Department of Anesthesiology, University of Texas Medical Branch, Galveston 77555, USA.
Steinsland
O S
OS
Johnson
R L
RL
Suresh
M S
MS
Gifford
A
A
Ehardt
J S
JS
D000328:Adult; D001158:Arteries / Q000294:innervation / Q000502:physiology; D004558:Electric Stimulation; D005260:Female; D006801:Humans; D008875:Middle Aged; D009424:Nervous System Physiological Phenomena; D009569:Nitric Oxide / Q000037:antagonists & inhibitors; D009638:Norepinephrine / Q000378:metabolism; D011247:Pregnancy / Q000502:physiology*; D012146:Rest; D014599:Uterus / Q000098:blood supply*; D014661:Vasoconstriction / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology*
D009569:Nitric Oxide; D009638:Norepinephrine