scholarly journals The balance between human maternal plasma angiotensin II and angiotensin 1-7 levels in early gestation pregnancy is influenced by fetal sex

2013 ◽  
Vol 15 (4) ◽  
pp. 523-531 ◽  
Author(s):  
Shane D Sykes ◽  
Kirsty G Pringle ◽  
Ang Zhou ◽  
Gustaaf A Dekker ◽  
Claire T Roberts ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Maternal Plasma ◽  
Fetal Sex ◽  
Early Gestation ◽  
Plasma Angiotensin

161. PREDICTING GESTATIONAL HYPERTENSION AND PREECLAMPSIA FROM MATERNAL ANGIOTENSIN II AND ANGIOTENSIN 1–7 LEVELS AT 15 WEEKS GESTATION

2010 ◽  
Vol 22 (9) ◽  
pp. 79
Author(s):  
S. D. Sykes ◽  
E. R. Lumbers ◽  
K. G. Pringle ◽  
T. Zakar ◽  
G. A. Dekker ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Gestational Hypertension ◽  
Area Under The Curve ◽  
Renin Angiotensin System ◽  
Maternal Plasma ◽  
Late Gestation ◽  
Early Gestation ◽  
Predictive Strength ◽  
Hypertensive Diseases ◽  
First Time

Angiotensin II (AngII) is the main effector peptide of the renin angiotensin system (RAS). The RAS is also involved in the aetiology of hypertension. Angiotensin 1–7 (Ang1–7) acting on the Mas receptor may counteract AngII effects. RAS activity is increased in early gestation. We wanted to determine if maternal plasma AngII and Ang1–7 levels in early gestation predict the onset of hypertension in late gestation. Circulating AngII and Ang1–7 have been measured by RIA (D Casley, Prosearch Pty. Ltd.) in EDTA treated plasma from healthy nulliparous pregnant women at 15 weeks gestation from the Adelaide SCOPE cohort for preeclampsia (PE) (n = 50) and gestational hypertension (GHT) (n = 50), with 131 controls. Log transformation and linear regression showed an inverse, weak (R2 = 0.068), statistically significant relationship (P = 0.003) between AngII and Ang1–7. The predictive capability of these peptides for pregnancy outcome was determined by logistic regression and area under the curve after ROC analysis (AROC). The summaries of these analyses are shown in Table 1. AngII did not increase the predictive strength of either model and was omitted. These models show for the first time that circulating Ang1–7 levels are highly statistically significant predictors of hypertensive diseases of pregnancy as early as 15 weeks gestation, well before diagnosis of disease.

306. PREDICTING GESTATIONAL DIABETES FROM MATERNAL ANGIOTENSIN II AND ANGIOTENSIN 1–7 LEVELS AT 15 WEEKS GESTATION

2010 ◽  
Vol 22 (9) ◽  
pp. 106
Author(s):  
S. D. Sykes ◽  
E. R. Lumbers ◽  
K. G. Pringle ◽  
T. Zakar ◽  
G. A. Dekker ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Gestational Diabetes ◽  
Area Under The Curve ◽  
Renin Angiotensin System ◽  
Late Pregnancy ◽  
Early Gestation ◽  
Disease Marker ◽  
Increased Risk ◽  
Unit Increase ◽  
Plasma Angiotensin

Gestational diabetes (GD), a pregnancy complication defined by glucose intolerance with onset during pregnancy, is a condition affecting 5.5%–8.8% of Australian pregnancies1. Untreated GD increases perinatal mortality and babies from GD pregnancies have an increased risk of diabetes and obesity, whilst mothers have an increased risk of type II diabetes later in life1. Circulating levels of angiotensin 1–7 (Ang1–7), a peptide of the renin angiotensin system, have been reported to be reduced in third trimester pregnancies with GD2. The effects of Ang1–7 generally oppose those of angiotensin II (AngII) and it is possible that in early gestation pro-angiogenic functions of AngII are counterbalanced by Ang1–7, causing placental insufficiency and pregnancy complications. We wanted to determine the predictive capability of AngII and Ang1–7, in early gestation, for GD. Healthy nulliparous pregnant women from the Adelaide SCOPE cohort with GD (n = 36) or serving as controls (n = 131) had both peptides measured at 15 weeks using an RIA (D. Casley, Prosearch Pty. Ltd.) on EDTA treated plasma. A predictive model was constructed using logistic regression and area under the curve after ROC analysis (AROC, Table 1). AngII did not change the model and was omitted. This model shows that for every one unit increase of Log (Ang1–7 pg/mL) peptide levels the odds of acquiring GD increase five times, suggesting that Ang1–7 levels in early gestation may be a better disease marker than those seen at late pregnancy. (1) Hoffman L, Nolan C, Wilson JD, et al., 1998. Gestational diabetes mellitus – management guidelines. The Australasian Diabetes in Pregnancy Society. Med. J. Aust. 169, 93–97.(2) Nogueira AI, Santos RAS, Simoes e Silva AC, et al., 2007. The pregnancy-induced increase of plasma angiotensin-(1–7) is blunted in gestational diabetes. Regul. Pep., 141, 55–60.

Chemoreflex and endocrine components of cardiovascular responses to acute hypoxemia in the llama fetus

1996 ◽  
Vol 271 (1) ◽  
pp. R73-R83 ◽  
Author(s):  
D. A. Giussani ◽  
R. A. Riquelme ◽  
F. A. Moraga ◽  
H. H. McGarrigle ◽  
C. R. Gaete ◽  
...  
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
High Altitude ◽  
Chronic Exposure ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Cardiovascular Responses ◽  
Pronounced Increase ◽  
Plasma Vasopressin ◽  
Plasma Angiotensin

We tested the hypothesis that the llama fetus has a blunted cardiovascular chemoreflex response to hypoxemia by investigating the effects of acute hypoxemia on perfusion pressure, heart rate, and the distribution of the combined ventricular output in 10 chronically instrumented fetal llamas at 0.6-0.7 gestation. Four llama fetuses had the carotid sinus nerves sectioned. In the intact fetuses, there was a marked bradycardia, an increase in perfusion pressure, and a pronounced peripheral vasoconstriction during hypoxemia. These cardiovascular responses during hypoxemia in intact fetuses were accompanied by a pronounced increase in plasma vasopressin, but not in plasma angiotensin II concentrations. Carotid denervation prevented the bradycardia at the onset of hypoxemia, but it did not affect the intense vasoconstriction during hypoxemia. Plasma vasopressin and angiotensin II levels were not measured in carotid-denervated fetuses. Our results do not support the hypothesis that the carotid chemoreflex during hypoxemia is blunted in the llama fetus. However, they emphasize that other mechanisms, such as increased vasopressin concentrations, operate to produce an intense vasoconstriction in hypoxemia. This intense vasoconstriction in the llama fetus during hypoxemia may reflect the influence of chronic exposure to the hypoxia of high altitude on the magnitude and gain of fetal cardiovascular responses to a superimposed acute episode of hypoxemia.

scholarly journals Update on angiotensin II: new endocrine connections between the brain, adrenal glands and the cardiovascular system

2017 ◽  
Vol 6 (7) ◽  
pp. R131-R145 ◽  
Author(s):  
Frans H H Leenen ◽  
Mordecai P Blaustein ◽  
John M Hamlyn
Keyword(s):  
Angiotensin Ii ◽  
Sympathetic Activity ◽  
Endocrine Function ◽  
Lv Function ◽  
Slow Pathway ◽  
Ang Ii ◽  
Endogenous Ouabain ◽  
Plasma Angiotensin ◽  
Synthase Inhibitor ◽  
The Brain

In the brain, angiotensinergic pathways play a major role in chronic regulation of cardiovascular and electrolyte homeostasis. Increases in plasma angiotensin II (Ang II), aldosterone, [Na+] and cytokines can directly activate these pathways. Chronically, these stimuli also activate a slow neuromodulatory pathway involving local aldosterone, mineralocorticoid receptors (MRs), epithelial sodium channels and endogenous ouabain (EO). This pathway increases AT1R and NADPH oxidase subunits and maintains/further increases the activity of angiotensinergic pathways. These brain pathways not only increase the setpoint of sympathetic activity per se, but also enhance its effectiveness by increasing plasma EO and EO-dependent reprogramming of arterial and cardiac function. Blockade of any step in this slow pathway or of AT1R prevents Ang II-, aldosterone- or salt and renal injury-induced forms of hypertension. MR/AT1R activation in the CNS also contributes to the activation of sympathetic activity, the circulatory and cardiac RAAS and increase in circulating cytokines in HF post MI. Chronic central infusion of an aldosterone synthase inhibitor, MR blocker or AT1R blocker prevents a major part of the structural remodeling of the heart and the decrease in LV function post MI, indicating that MR activation in the CNS post MI depends on aldosterone, locally produced in the CNS. Thus, Ang II, aldosterone and EO are not simply circulating hormones that act on the CNS but rather they are also paracrine neurohormones, locally produced in the CNS, that exert powerful effects in key CNS pathways involved in the long-term control of sympathetic and neuro-endocrine function and cardiovascular homeostasis.

scholarly journals R-PEP-27, a Potent Renin Inhibitor, Decreases Plasma Angiotensin II and Blood Pressure in Normal Volunteers

1994 ◽  
Vol 7 (4 Pt 1) ◽  
pp. 295-301 ◽  
Author(s):  
R. M. Zusman ◽  
K. Y. Hui ◽  
J. Nussberger ◽  
D. M. Christensen ◽  
J. Higgins ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Renin Inhibitor ◽  
Normal Volunteers ◽  
Plasma Angiotensin

Renal perfusion pressure and renin secretion in bilaterally renal denervated sheep

1994 ◽  
Vol 72 (7) ◽  
pp. 782-787 ◽  
Author(s):  
L. Fan ◽  
S. Mukaddam-Daher ◽  
J. Gutkowska ◽  
B. S. Nuwayhid ◽  
E. W. Quillen Jr.
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Excretion Rate ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Renal Perfusion Pressure ◽  
Plasma Angiotensin

To further investigate the influence of renal nerves on renin secretion, the renin secretion responses to step reductions of renal perfusion pressure (RPP) were studied in conscious sheep with innervated kidneys (n = 5) and with bilaterally denervated kidneys (n = 5). The average basal level of RPP in sheep with denervated kidneys (82 ± 4 mmHg; 1 mmHg = 133.3 Pa) was similar to that in sheep with innervated kidneys (83 ± 3 mmHg). RPP was reduced in four sequential 15-min steps, to a final level of 54 ± 2 mmHg in sheep with innervated kidneys and to 57 ± 1 mmHg in denervated sheep. The renin secretion rate was increased as RPP was reduced in sheep with innervated kidneys. Baseline peripheral plasma renin activity was reduced and there was almost no response of renin secretion rate to reduction of RPP in sheep with denervated kidneys. Also, baseline renal blood flow, urine flow rate, sodium excretion rate, and potassium excretion rate were higher in sheep with denervated kidneys than those with innervated kidneys. Baseline plasma angiotensin II was similar in both groups of sheep. As RPP was decreased, plasma angiotensin II was increased in sheep with innervated kidneys, but was not significantly altered in sheep with denervated kidneys. Plasma atrial natriuretic factor was unaltered by either reduction of RPP or renal denervation. In conclusion, hormonal factors, such as angiotensin II and atrial natriuretic factor, do not account for the dramatic suppression of renin secretion in response to the reduction of RPP in sheep with bilateral renal denervation. Renal nerves are a necessary component in the control of renin secretion during reduction of RPP and may contribute to the regulation of baseline plasma renin activity and sodium excretion rate in conscious ewes.Key words: renin secretion, renal perfusion pressure, renal nerves, denervation, sheep.

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