title: Modified histamine-induced NO-mediated relaxation in resistance arteries in pre-eclampsia.
abstract: We investigated the characteristic changes in histamine-induced, endothelium-derived nitric oxide (NO)-mediated relaxation in human omental resistance arteries seen in pre-eclampsia. Isometric contraction was provoked by a stable analogue of thromboxane A(2) in endothelium-intact strips from both pre-eclamptic and normotensive pregnant women. Histamine (0.3 nM-10 microM) produced a concentration-dependent relaxation of this contraction in both groups. The magnitude of the relaxation induced by histamine (1 microM) was significantly smaller in pre-eclampsia both in the presence and absence of famotidine (H(2)-receptor blocker). In the presence of famotidine, L-N(G)-nitroarginine significantly attenuated the histamine-induced relaxation in strips from normotensive pregnant women but not in those from pre-eclamptic women. The relaxation induced by human atrial natriuretic peptide (0. 1 nM-1 microM) was also significantly smaller in the pre-eclamptic group. It is concluded that the histamine-induced, endothelium-derived NO-mediated relaxation (mediated via H(1)-receptors) is down-regulated in resistance arteries in pre-eclampsia and we suggest that this is due, at least in part, to an attenuation of the action of cyclic GMP in smooth muscle cells.
authors.affiliation: Department of Obstetrics and Gynecology, Nagoya City University Medical School, 467-8601, Nagoya, Japan. og.yo@med.nagoya-cu.ac.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Suzuki
authors.forename: T
authors.initials: T
authors.lastname: Yamamoto
authors.forename: K
authors.initials: K
authors.lastname: Suzumori
authors.forename: J
authors.initials: J
authors.lastname: Kajikuri
authors.forename: T
authors.initials: T
authors.lastname: Itoh
mesh_terms: D000328:Adult; D001158:Arteries; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism; D015536:Down-Regulation; D004730:Endothelium, Vascular / Q000502:physiology; D015738:Famotidine / Q000494:pharmacology; D005260:Female; D006632:Histamine / Q000494:pharmacology*; D006801:Humans; D007537:Isometric Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D019335:Nitroarginine / Q000494:pharmacology; D011225:Pre-Eclampsia / Q000378:metabolism*; D011247:Pregnancy; D011738:Pyrilamine / Q000494:pharmacology; D011969:Receptors, Histamine H1 / Q000378:metabolism; D011970:Receptors, Histamine H2 / Q000378:metabolism; D014655:Vascular Resistance / Q000187:drug effects; D014664:Vasodilation / Q000502:physiology*
chemical_list: D011969:Receptors, Histamine H1; D011970:Receptors, Histamine H2; D019335:Nitroarginine; D009569:Nitric Oxide; D015738:Famotidine; D006632:Histamine; D009320:Atrial Natriuretic Factor; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D006152:Cyclic GMP; D011738:Pyrilamine