Relaxation kinetics of the aorta in N(ω)-nitro-L-arginine methyl ester- treated pregnant rats

Venu Jain, Yuri P. Vedernikov, George Saade, Kristof Chwalisz, Robert E. Garfield

Research output: Contribution to journalArticle

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Abstract

OBJECTIVE: To test the hypothesis that vascular relaxation kinetics are prolonged in pregnant rats treated chronically with N(ω)-nitro-L-arginine methyl ester (L-NAME). METHODS: Timed pregnant rats (on day 15 of a 22-day gestation) were implanted with infusion pumps containing vehicle (controls) or L-NAME (50 mg/d). L-NAME pumps were retained until day 22 (group 1), or removed on day 20 (group 2). All rats were killed at term. Aortic rings were mounted in organ chambers containing physiologic salt solution (PSS) for isometric tension recording, contracted with high-K+ PSS (60 mM), and allowed to relax in normal-K+ PSS. Relaxation kinetics were quantified as time for 50% and 80% relaxation. After contraction with phenylephrine, responses to cumulative concentrations of methacholine were studied in the absence and presence of L-arginine (L-Arg) (10-3 M). RESULTS: Responses to methacholine were inhibited completely in group 1 and partially in group 2 (P < .05). The inhibition in both groups was reversed by L-Arg. The rate of relaxation was significantly slower in groups 1 and 2 (P < .05) as compared with controls. Mechanical removal of the endothelium caused prolongation of relaxation in controls and group 2 (P < . 05), but not in group 1. Preincubation of aortic rings from untreated controls with L-NAME (in vitro, 10-4 M) did not affect relaxation. CONCLUSION: The endothelium modulates the rate of vascular relaxation by a factor other than nitric oxide. N(ω)- nitro-L-arginine methyl ester (L-NAME) prolongs vasorelaxation by endothelium-dependent and -independent mechanisms. Prolongation of vascular relaxation kinetics may be a mechanism to elevate blood pressure and peripheral vascular resistance in preeclampsia.

Original languageEnglish (US)
Pages (from-to)11-16
Number of pages6
JournalJournal of the Society for Gynecologic Investigation
Volume6
Issue number1
DOIs
StatePublished - Jan 1999

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NG-Nitroarginine Methyl Ester
Aorta
Endothelium
Blood Vessels
Methacholine Chloride
Salts
Vascular Resistance
Infusion Pumps
Phenylephrine
Pre-Eclampsia
Vasodilation
Arginine
Nitric Oxide
arginine methyl ester
Blood Pressure
Pregnancy
Control Groups

Keywords

  • Aorta
  • Endothelium
  • Nitric oxide
  • Preeclampsia
  • Pregnant rat
  • Relaxation kinetics

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Relaxation kinetics of the aorta in N(ω)-nitro-L-arginine methyl ester- treated pregnant rats. / Jain, Venu; Vedernikov, Yuri P.; Saade, George; Chwalisz, Kristof; Garfield, Robert E.

In: Journal of the Society for Gynecologic Investigation, Vol. 6, No. 1, 01.1999, p. 11-16.

Research output: Contribution to journalArticle

Jain, Venu ; Vedernikov, Yuri P. ; Saade, George ; Chwalisz, Kristof ; Garfield, Robert E. / Relaxation kinetics of the aorta in N(ω)-nitro-L-arginine methyl ester- treated pregnant rats. In: Journal of the Society for Gynecologic Investigation. 1999 ; Vol. 6, No. 1. pp. 11-16.
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abstract = "OBJECTIVE: To test the hypothesis that vascular relaxation kinetics are prolonged in pregnant rats treated chronically with N(ω)-nitro-L-arginine methyl ester (L-NAME). METHODS: Timed pregnant rats (on day 15 of a 22-day gestation) were implanted with infusion pumps containing vehicle (controls) or L-NAME (50 mg/d). L-NAME pumps were retained until day 22 (group 1), or removed on day 20 (group 2). All rats were killed at term. Aortic rings were mounted in organ chambers containing physiologic salt solution (PSS) for isometric tension recording, contracted with high-K+ PSS (60 mM), and allowed to relax in normal-K+ PSS. Relaxation kinetics were quantified as time for 50{\%} and 80{\%} relaxation. After contraction with phenylephrine, responses to cumulative concentrations of methacholine were studied in the absence and presence of L-arginine (L-Arg) (10-3 M). RESULTS: Responses to methacholine were inhibited completely in group 1 and partially in group 2 (P < .05). The inhibition in both groups was reversed by L-Arg. The rate of relaxation was significantly slower in groups 1 and 2 (P < .05) as compared with controls. Mechanical removal of the endothelium caused prolongation of relaxation in controls and group 2 (P < . 05), but not in group 1. Preincubation of aortic rings from untreated controls with L-NAME (in vitro, 10-4 M) did not affect relaxation. CONCLUSION: The endothelium modulates the rate of vascular relaxation by a factor other than nitric oxide. N(ω)- nitro-L-arginine methyl ester (L-NAME) prolongs vasorelaxation by endothelium-dependent and -independent mechanisms. Prolongation of vascular relaxation kinetics may be a mechanism to elevate blood pressure and peripheral vascular resistance in preeclampsia.",
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T1 - Relaxation kinetics of the aorta in N(ω)-nitro-L-arginine methyl ester- treated pregnant rats

AU - Jain, Venu

AU - Vedernikov, Yuri P.

AU - Saade, George

AU - Chwalisz, Kristof

AU - Garfield, Robert E.

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N2 - OBJECTIVE: To test the hypothesis that vascular relaxation kinetics are prolonged in pregnant rats treated chronically with N(ω)-nitro-L-arginine methyl ester (L-NAME). METHODS: Timed pregnant rats (on day 15 of a 22-day gestation) were implanted with infusion pumps containing vehicle (controls) or L-NAME (50 mg/d). L-NAME pumps were retained until day 22 (group 1), or removed on day 20 (group 2). All rats were killed at term. Aortic rings were mounted in organ chambers containing physiologic salt solution (PSS) for isometric tension recording, contracted with high-K+ PSS (60 mM), and allowed to relax in normal-K+ PSS. Relaxation kinetics were quantified as time for 50% and 80% relaxation. After contraction with phenylephrine, responses to cumulative concentrations of methacholine were studied in the absence and presence of L-arginine (L-Arg) (10-3 M). RESULTS: Responses to methacholine were inhibited completely in group 1 and partially in group 2 (P < .05). The inhibition in both groups was reversed by L-Arg. The rate of relaxation was significantly slower in groups 1 and 2 (P < .05) as compared with controls. Mechanical removal of the endothelium caused prolongation of relaxation in controls and group 2 (P < . 05), but not in group 1. Preincubation of aortic rings from untreated controls with L-NAME (in vitro, 10-4 M) did not affect relaxation. CONCLUSION: The endothelium modulates the rate of vascular relaxation by a factor other than nitric oxide. N(ω)- nitro-L-arginine methyl ester (L-NAME) prolongs vasorelaxation by endothelium-dependent and -independent mechanisms. Prolongation of vascular relaxation kinetics may be a mechanism to elevate blood pressure and peripheral vascular resistance in preeclampsia.

AB - OBJECTIVE: To test the hypothesis that vascular relaxation kinetics are prolonged in pregnant rats treated chronically with N(ω)-nitro-L-arginine methyl ester (L-NAME). METHODS: Timed pregnant rats (on day 15 of a 22-day gestation) were implanted with infusion pumps containing vehicle (controls) or L-NAME (50 mg/d). L-NAME pumps were retained until day 22 (group 1), or removed on day 20 (group 2). All rats were killed at term. Aortic rings were mounted in organ chambers containing physiologic salt solution (PSS) for isometric tension recording, contracted with high-K+ PSS (60 mM), and allowed to relax in normal-K+ PSS. Relaxation kinetics were quantified as time for 50% and 80% relaxation. After contraction with phenylephrine, responses to cumulative concentrations of methacholine were studied in the absence and presence of L-arginine (L-Arg) (10-3 M). RESULTS: Responses to methacholine were inhibited completely in group 1 and partially in group 2 (P < .05). The inhibition in both groups was reversed by L-Arg. The rate of relaxation was significantly slower in groups 1 and 2 (P < .05) as compared with controls. Mechanical removal of the endothelium caused prolongation of relaxation in controls and group 2 (P < . 05), but not in group 1. Preincubation of aortic rings from untreated controls with L-NAME (in vitro, 10-4 M) did not affect relaxation. CONCLUSION: The endothelium modulates the rate of vascular relaxation by a factor other than nitric oxide. N(ω)- nitro-L-arginine methyl ester (L-NAME) prolongs vasorelaxation by endothelium-dependent and -independent mechanisms. Prolongation of vascular relaxation kinetics may be a mechanism to elevate blood pressure and peripheral vascular resistance in preeclampsia.

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KW - Endothelium

KW - Nitric oxide

KW - Preeclampsia

KW - Pregnant rat

KW - Relaxation kinetics

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