Angiotensin-II sensitivity and prostaglandin-synthetase inhibition in pregnancy

Jaspers, W.J.M.; Jong, P.A. de; Mulder, A.W.

doi:10.1016/0028-2243(81)90087-3

Cited by 10 publications

(3 citation statements)

References 14 publications

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“…As incubation with indomethacin caused an increase in relaxation in P-LPS infused rats, this putative role of prostacyclin during pregnancy is blunted in experimental preeclampsia. With these results, our findings seem to be in line with results in human preeclampsia [59–63], which showed decreased prostacyclin production in preeclampsia versus normal pregnancy [64], as well as with other models of preeclampsia [65,66]. The altered involvement of vasoactive PG in acetylcholine-induced relaxation responses found in our study, appeared independent of regulation of COXs expression, since we found no differences in mRNA expression of COX-1 or COX-2.…”

Section: Discussionsupporting

confidence: 91%

Endothelium-Dependent Relaxation and Angiotensin II Sensitivity in Experimental Preeclampsia

et al. 2013

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ObjectiveWe investigated endothelial dysfunction and the role of angiotensin (Ang)-II type I (AT1-R) and type II (AT2-R) receptor in the changes in the Ang-II sensitivity in experimental preeclampsia in the rat.MethodsAortic rings were isolated from low dose lipopolysaccharide (LPS) infused pregnant rats (experimental preeclampsia; n=9), saline-infused pregnant rats (n=8), and saline (n=8) and LPS (n=8) infused non-pregnant rats. Endothelium-dependent acetylcholine--mediated relaxation was studied in phenylephrine-preconstricted aortic rings in the presence of vehicle, NG-nitro-L-arginine methyl ester and/or indomethacin. To evaluate the role for AT1-R and AT2-R in Ang-II sensitivity, full concentration response curves were obtained for Ang-II in the presence of losartan or PD123319. mRNA expression of the AT1-R and AT2-R, eNOS and iNOS, COX1 and COX2 in aorta were evaluated using real-time RT-PCR.ResultsThe role of vasodilator prostaglandins in the aorta was increased and the role of endothelium-derived hyperpolarizing factor and response of the AT1-R and AT2-R to Ang-II was decreased in pregnant saline infused rats as compared with non-pregnant rats. These changes were not observed during preeclampsia.ConclusionPregnancy induced adaptations in endothelial function, which were not observed in the rat model for preeclampsia. This role of lack of pregnancy induced endothelial adaptation in the pathophysiology of experimental preeclampsia needs further investigation.

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Section: Discussionsupporting

confidence: 91%

Endothelium-Dependent Relaxation and Angiotensin II Sensitivity in Experimental Preeclampsia

et al. 2013

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“…Whether vasodilatory PG play a role is disputed (33,67,94,175), although NO is likely to contribute (3,175). Renal mesangial cells prepared from gravid rats demonstrated an attenuated rise in intracellular calcium in response to AII (72).…”

Section: Molecular Mechanisms Of Renal Vasodilation In Pregnancymentioning

confidence: 99%

The renal circulation in normal pregnancy and preeclampsia: is there a place for relaxin?

Conrad

Davison

2014

American Journal of Physiology-Renal Physiology

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Conrad KP, Davison JM. The renal circulation in normal pregnancy and preeclampsia: is there a place for relaxin?. Am J Physiol Renal Physiol 306: F1121-F1135, 2014. First published March 19, 2014 doi:10.1152/ajprenal.00042.2014.-During the first trimester of human pregnancy, the maternal systemic circulation undergoes remarkable vasodilation. The kidneys participate in this vasodilatory response resulting in marked increases in renal plasma flow (RPF) and glomerular filtration rate (GFR). Comparable circulatory adaptations are observed in conscious gravid rats. Administration of the corpus luteal hormone relaxin (RLN) to nonpregnant rats and humans elicits vasodilatory changes like those of pregnancy. Systemic and renal vasodilation are compromised in midterm pregnant rats by neutralization or elimination of circulating RLN and in women conceiving with donor eggs who lack a corpus luteum and circulating RLN. Although RLN exerts both rapid (minutes) and sustained (hours to days) vasodilatory actions through different molecular mechanisms, a final common pathway is endothelial nitric oxide. In preeclampsia (PE), maternal systemic and renal vasoconstriction leads to hypertension and modest reduction in GFR exceeding that of RPF. Elevated level of circulating soluble vascular endothelial growth factor receptor-1 arising from the placenta is implicated in the hypertension and disruption of glomerular fenestrae and barrier function, the former causing reduced K f and the latter proteinuria. Additional pathogenic factors are discussed. Last, potential clinical ramifications include RLN replacement in women conceiving with donor eggs and its therapeutic use in PE. Another goal has been to apply knowledge gained from investigating circulatory adaptations in pregnancy toward identifying and developing novel therapeutic strategies for renal and cardiovascular disease in the nonpregnant population. So far, one candidate to emerge is RLN and its potential therapeutic use in heart failure. renal hemodynamics; glomerular filtration; osmoregulation; relaxin; nitric oxide; assisted reproductive technology; glomerular endotheliosis; soluble vascular endothelial growth factor receptor-1; heart failure Renal Plasma Flow and Glomerular Filtration in Normal PregnancyMARKED VASODILATION OF THE MATERNAL CIRCULATION occurs in the first trimester of human pregnancy. Consequently, there is a precipitous and profound decline in systemic vascular resistance (SVR) that in turn abets a reciprocal increase in cardiac output (CO) of ϳ40% or 2 l/min lasting throughout pregnancy (23,163). Vasodilation of nonreproductive organs like the kidneys accounts mostly for the early gestational fall in SVR and rise in CO. The fall in SVR is nearly offset by the rise in CO; hence, mean arterial pressure (MAP) declines, but only modestly, by 5-10 mmHg (23,38,163). Although counterintuitive, this metamorphosis of the maternal circulation is virtually complete by the end of the first or beginning of the second trimester, when fetal crown rump length and place...

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“…It is not a direct consequence of the high endogenous levels of AII, since volume expansion, which suppresses endogenous activity of the renin-angiotensin system, is not associated with a change in pressor response (Everett et al, 1978a). Experiments in pregnant rabbits (O'Brien et al, 1977) and humans (Everett et al, 1978b;Jaspers et al, 1981) have shown that the administration of prostaglandin synthetase inhibitors, such as indomethacin, is associated with an enhanced pressor response to AII. Conversely, the administration of prostaglandin E2, prostaglandin E1 or epoprostenol is associated with a blunting of response, which is more pronounced than in non-pregnant subjects (Broughton Pipkin et al, 1982a,b, 1984.…”

Section: Discussionmentioning

confidence: 99%

The effect of dietary supplementation with linoleic and gammalinolenic acids on the pressor response to angiotensin II‐a possible role in pregnancy‐induced hypertension?

O'brien¹,

Morrison²,

Pipkin³

1985

Brit J Clinical Pharma

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Dietary supplementation with 3 g/day linoleic acid, 32 mg/day gammalinolenic acid and co‐factors for prostaglandin synthesis was given to 10 pregnant and 10 non‐pregnant subjects for a week. Their pressor response to the infusion of three doses of angiotensin II (AII) (pregnant: 4, 8, 16 ng kg‐1 min‐1: non‐pregnant: 1, 2, 4 ng kg‐1 min‐1) was then compared with that of 40 pregnant and 24 non‐pregnant controls who had not been given such supplementation. Dietary supplementation was not associated with changes in basal systolic or diastolic blood pressure or heart rate during the week of treatment in pregnant or non‐ pregnant subjects. Basal systolic blood pressure, diastolic blood pressure and heart rate values did not differ between the treated and untreated subjects in each group. The diastolic pressor response to AII was significantly less after treatment at all doses; the effect was more marked in the pregnant subjects. The systolic response to AII, normally less than the diastolic, was somewhat blunted in the treated pregnant patients at the two higher infusion doses. No significant effect was found in the non‐pregnant group. Evidence from other studies suggests that increasing plasma linoleic acid concentrations leads to increased plasma concentrations of epoprostenol (prostacyclin, PGI2) while increased availability of gammalinolenic acid is associated with a rise in prostaglandin E1 and E2 production. Pregnancy‐induced hypertension is associated with a diminished tissue production of both epoprostenol and E series prostaglandins, and with an enhanced pressor response to AII.(ABSTRACT TRUNCATED AT 250 WORDS)

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Angiotensin-II sensitivity and prostaglandin-synthetase inhibition in pregnancy

Cited by 10 publications

References 14 publications

Endothelium-Dependent Relaxation and Angiotensin II Sensitivity in Experimental Preeclampsia

Endothelium-Dependent Relaxation and Angiotensin II Sensitivity in Experimental Preeclampsia

The renal circulation in normal pregnancy and preeclampsia: is there a place for relaxin?

The effect of dietary supplementation with linoleic and gammalinolenic acids on the pressor response to angiotensin II‐a possible role in pregnancy‐induced hypertension?

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