title: [Increased plasma and urinary Na+-K+ ATPase inhibitory activity and elevated blood pressure in metoclopramide-treated rats].
abstract: Our recent studies demonstrated that dopaminergic receptor may play an important role in controlling blood pressure and renal sodium handling. This study was designed to investigate whether endogenous Na+-K+ ATPase inhibitors are related to changes in blood pressure and sodium balance, caused by the administration of metoclopramide (MC), a dopamine (D2) receptor antagonist, and sodium loading. Young male Wistar rats (250 approximately 300 g) were raised under three different conditions, control (control group), 1% NaCl loading (NaCl group) and 1% NaCl plus 1.5 mg/kg/day of metoclopramide (MC group) for 7 days. Systolic blood pressure (SBP), urinary and plasma Na+-K+ ATPase inhibitory activity (ATPI), urinary sodium, potassium and catecholamine excretions were measured. SBP in the MC group elevated from 116 +/- 2 mmHg to 134 +/- 4 mmHg, but there were no changes in SBP in the control and NaCl groups. Urine volume and urinary sodium excretion significantly increased in not only the NaCl group but also in the MC group. Plasma ATPI in both the NaCl and MC groups was higher than in the control group (p less than 0.001), and the level of ATPI in the MC group was significantly higher than in the NaCl group (p less than 0.05). Urinary ATPI in the control group was not detected after 7 days, but that in the NaCl and MC groups was clearly increased. The excretions of urinary catecholamines remained unchanged in all groups.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Third Department of Internal Medicine, Fukushima Medical College, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Shigetomi
authors.forename: H
authors.initials: H
authors.lastname: Tosaki
authors.forename: H
authors.initials: H
authors.lastname: Haga
authors.forename: S
authors.initials: S
authors.lastname: Ueno
authors.forename: K
authors.initials: K
authors.lastname: Tanaka
authors.forename: A
authors.initials: A
authors.lastname: Matsunaga
authors.forename: K
authors.initials: K
authors.lastname: Satoh
authors.forename: H
authors.initials: H
authors.lastname: Kohno
authors.forename: K
authors.initials: K
authors.lastname: Mori
authors.forename: K
authors.initials: K
authors.lastname: Katoh
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D018492:Dopamine Antagonists; D004837:Epinephrine / Q000652:urine; D008297:Male; D008787:Metoclopramide / Q000494:pharmacology*; D009318:Natriuresis / Q000187:drug effects; D009638:Norepinephrine / Q000652:urine; D011188:Potassium / Q000652:urine; D011506:Proteins / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012982:Sodium, Dietary / Q000008:administration & dosage / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000097795:ATPase Inhibitory Protein
chemical_list: D018492:Dopamine Antagonists; D004837:Epinephrine; D008787:Metoclopramide; D009638:Norepinephrine; D011188:Potassium; D011506:Proteins; D012982:Sodium, Dietary; D000254:Sodium-Potassium-Exchanging ATPase; D000097795:ATPase Inhibitory Protein