Effects of indomethacin, during pregnancy in the rat, on responses to noradrenaline and angiotensin II in vivo, and responses to phenylephrine in vitro

Jansakul, Chaweewan; King, R; Boura, A. L. A.

doi:10.1071/rd9900587

Cited by 3 publications

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“…Similar observations have been made in rats (Jansakul, King & Boura, 1990) and sheep (Blair-West, Coghlan, Denton, Scoggins & Wintour, 1972;Naden & Rosenfeld, 1981;Rosenfeld & Gant, 1981;Rosenfeld & Naden, 1989). Loss of this refractoriness is a pathophysiological feature in pregnant women who are, or who subsequently become, hypertensive (pre-eclampsia; Cook & Trudinger, 1991;Erkkola & Pirhonen, 1992).…”

Section: Introductionsupporting

confidence: 53%

“…In normal human pregnancy, the blunted pressor response, especially within the uteroplacental vasculature, to intravenously infused angiotensin (All) is considered to protect fetal oxygen and nutrient delivery in the presence of a hyperactive renin-AII system (Loquet, Broughton-Pipkin, Symonds & Rubin, 1990;Ito, Nakamura, Yoshimura, Koyama & Okamura, 1992). Similar observations have been made in rats (Jansakul, King & Boura, 1990) and sheep (Blair-West, Coghlan, Denton, Scoggins & Wintour, 1972;Naden & Rosenfeld, 1981; Rosenfeld & Gant, 1981;Rosenfeld & Naden, 1989). Loss of this refractoriness is a pathophysiological feature in pregnant women who are, or who subsequently become, hypertensive (pre-eclampsia; Cook & Trudinger, 1991;Erkkola & Pirhonen, 1992).…”

Section: Introductionmentioning

confidence: 83%

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Haemodynamic responses to an angiotensin II receptor antagonist (GR 117289) in maternal and fetal sheep

Forhead

Fowden²,

Silver³

et al. 1995

Experimental Physiology

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SUMMARYAn ATI-specific angiotensin II receptor antagonist (GRI 17289; 1 mg/kg I.v. bolus) was administered daily to ten chronically catheterized, normotensive ewes during late pregnancy (from 126 ± 1 days) until parturition (139 + 1 days); five control animals received an equivalent volume of vehicle solution. Following drug administration, mean maternal blood pressure decreased from 87 ± 1 mmHg to a minimum of 79 ± 1 mmHg at 0 5 h (P < 005; n = 10) and remained low for 4-6 h without any concomitant change in fetal blood pressure or maternal and fetal heart rates. In animals fitted with flow probes, uterine blood flow decreased from 443 ± 21 to 363 ± 27 ml/min at 0-5 h post-drug (P < 0 05; n = 6); this change was positively correlated with the reduction in maternal blood pressure. The mean decrements in uterine and umbilical blood flows measured by steady-state infusion of tritiated water were -611 ± 171 ml/min at 4-6 h (P < 0 05; n = 5) and -71 + 19 ml/min at 0-5-1 h (P < 0 05; n = 5), respectively. Significant reductions (P < 0-05; n = 10) in fetal arterial oxygen tension (-1 6 ± 0 4 mmHg), saturation (-6.6 ± 1 6 %) and content (-0.3 ± 0-1 4umol/ml) were evident at 0.5 h post-drug and were maintained for 6-12 h. Umbilical oxygen delivery decreased at 0 5-1 h following drug administration (P <001; n = 5), but was unaccompanied by any significant change in fetal oxygen consumption. Chronic decreases in daily fetal pH and blood oxygen content occurred in GRl 17289-treated ewes. There were no significant differences in gestational length or neonatal outcome between vehicle-and GRI 17289-treated groups of ewes with single fetuses.

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Section: Introductionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 83%

Haemodynamic responses to an angiotensin II receptor antagonist (GR 117289) in maternal and fetal sheep

Forhead

Fowden²,

Silver³

et al. 1995

Experimental Physiology

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The mechanism of EDHF-mediated responses in subcutaneous small arteries from healthy pregnant women

Luksha¹,

Nisell²,

Kublickiene³

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Luksha, Leonid, Henry Nisell, and Karolina Kublickiene. The mechanism of EDHF-mediated responses in subcutaneous small arteries from healthy pregnant women. Am J Physiol Regul Integr Comp Physiol 286: R1102-R1109, 2004. First published January 29, 2004 10.1152/ajpregu.00550.2003.-We studied the importance of endothelium-derived hyperpolarizing factor (EDHF) vs. nitric oxide (NO) and prostacyclin (PGI2) in bradykinin (BK)-induced relaxation in isolated small subcutaneous arteries from normal pregnant women. We also explored the contribution of cytochrome P-450 (CYP450) product of arachidonic acid (AA) metabolism, hydrogen peroxide (H2O2), and gap junctions that have been suggested to be involved in EDHF-mediated responses. Isolated arteries obtained from subcutaneous fat biopsies of normal pregnant women (n ϭ 30) undergoing planned cesarean section were mounted in a wire-myography system. In norepinephrine-constricted vessels, incubation with N G -nitro-Larginine methyl ester (L-NAME) resulted in a significant reduction in relaxation to BK. Simultaneous incubation with L-NAME and indomethacin failed to modify this response further. BK-mediated dilatation in the presence of K ϩ -modified solution was decreased to similar level as obtained after incubation with L-NAME. Incubation with L-NAME abolished BK-induced responses in K ϩ -modified solution. Sulfaphenazole, a specific inhibitor of CYP450 epoxygenase, and catalase (an enzyme that decomposes H2O2) did not affect the EDHFmediated relaxation because concentration-response curves to BK were similar in arteries after incubation with L-NAME vs. L-NAME ϩ sulfaphenazole and L-NAME ϩ catalase. The inhibitor of gap junctions, 18␣-glycyrrhetinic acid, significantly reduced BK-mediated relaxation both without and with incubation with L-NAME. We found that both NO and EDHF, but not PGI2, are involved in the endothelium-dependent dilatation to BK. BK-induced relaxation is almost equally mediated by NO and EDHF. CYP450 epoxygenase metabolites of AA or H2O2 do not account for EDHF-mediated response; however, gap junctions are involved in the EDHF-mediated responses to BK in subcutaneous small arteries in normal pregnancy. endothelium-dependent relaxation; gap junctions; endothelium-derived hyperpolarizing factor; hydrogen peroxide MATERNAL CARDIOVASCULAR ADAPTATION to normal pregnancy is associated with decreased peripheral vascular resistance that plays an important role for blood pressure reduction despite an increase in plasma volume and cardiac output. The vascular adaptation to normal pregnancy is believed to be dependent on an enhanced endothelium-dependent dilatation (3,18,25). However, the pathways underlying these changes are not fully understood and need further investigation because an impaired cardiovascular adaptation is associated with the development of preeclampsia (18,25,42). It is generally accepted that preeclampsia is an endothelial cell disorder, and the increased vascular resistance and blood pressure during this pregnancyrelated disease are due to en...

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"Reatividade vascular de aortas isoladas de ratas ao término da gestação: participação de óxido nítrico e prostanóides"

Martinez¹

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Effects of indomethacin, during pregnancy in the rat, on responses to noradrenaline and angiotensin II in vivo, and responses to phenylephrine in vitro

Cited by 3 publications

References 0 publications

Haemodynamic responses to an angiotensin II receptor antagonist (GR 117289) in maternal and fetal sheep

Haemodynamic responses to an angiotensin II receptor antagonist (GR 117289) in maternal and fetal sheep

The mechanism of EDHF-mediated responses in subcutaneous small arteries from healthy pregnant women

"Reatividade vascular de aortas isoladas de ratas ao término da gestação: participação de óxido nítrico e prostanóides"

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