title: The effects of NG-nitro-L-arginine methyl ester on systolic pressure, diastolic pressure and pulse pressure according to the initial level of blood pressure.
abstract: The objective of this study was to re-examine whether the effect of the nitric oxide synthesis inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on blood pressure depends on peripheral vascular tone. The effects of L-NAME (10 mg/kg, i.v.) on diastolic blood pressure (DBP), systolic blood pressure (SBP), pulse pressure (PP) and heart rate (HR) were studied in pithed rats. Sal-pithed rats received 0.9% NaCl, 10 microl/kg/min. Vascular tone was step-wise increased with 3, 10 and 30 microg/kg/min intravenous phenylephrine infusion (LPhe-pithed, MPhe-pithed and HPhe-pithed rats respectively). L-NAME elicited vasopressor responses in all the animals studied. L-NAME increases in SBP and DBP in Sal-pithed rats were significantly smaller than the ones obtained in phenylephrine infused rats. The increases in DBP elicited by L-NAME were greater in LPhe-pithed rats compared with those of MPhe-pithed and HPhe-pithed rats (i.e. the step-wise rises in DBP obtained with phenylephrine were inversely related to the increases in DBP produced by L-NAME); however, the increases in SBP were similar between these experimental groups. The PP increased during L-NAME-induced pressor responses in phenylephrine-infused rats. l-NAME increases in PP showed the following order: Sal-pithed < LPhe-pithed < MPhe-pithed < or = HPhe-pithed rats. HR was not modified by L-NAME. In conclusion, the vasopressor responses produced by L-NAME in pithed rats are influenced by the pre-existing vasomotor tone in complex form. We did not find a simple positive correlation between the vascular tone or level of arterial pressure, and the magnitude of the diastolic and systolic pressor responses elicited by L-NAME. Interestingly, the increase in PP induced by l-NAME was greater in accordance with the increasing value of baseline arterial pressure. NO synthesis inhibition in the arterial endothelium may possibly explain the increase in PP caused by L-NAME, as resulting from the reduction in proximal conduit artery compliance.
authors.affiliation: Sección de Estudios de Postgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Plan de San Luis y Diaz Mirón, Col. Casco de Santo Tomás, CP 11340 México, DF, Mexico.
authors.forename: Antonio
authors.initials: A
authors.lastname: Ruiz
authors.forename: Ruth M
authors.initials: RM
authors.lastname: López
authors.forename: Teresa
authors.initials: T
authors.lastname: Pérez
authors.forename: Carlos
authors.initials: C
authors.lastname: Castillo
authors.forename: Enrique F
authors.initials: EF
authors.lastname: Castillo
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology*; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors; D052250:Nitric Oxide Synthase Type III; D051381:Rats; D017208:Rats, Wistar
chemical_list: D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D019331:NG-Nitroarginine Methyl Ester