Plasma angiotensin II levels in women with severe preeclampsia under magnesium sulfate regimen

2021 ◽  
Vol 23 ◽  
pp. 56-58
Author(s):  
Amanda S.D. de Lima ◽  
Ingrid P. Holanda ◽  
Paulo R.P. Nascimento ◽  
Selma M.B. Jeronimo ◽  
Leonardo C. Ferreira
Keyword(s):  
Angiotensin Ii ◽  
Magnesium Sulfate ◽  
Severe Preeclampsia ◽  
Plasma Angiotensin

Short-course postpartum (6-h) magnesium sulfate therapy in severe preeclampsia

2015 ◽  
Vol 293 (5) ◽  
pp. 983-986 ◽  
Author(s):  
Shaheen Anjum ◽  
Gade Pramod Rajaram ◽  
Imam Bano
Keyword(s):  
Magnesium Sulfate ◽  
Severe Preeclampsia ◽  
Short Course

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.

Sign in / Sign up

Export Citation Format

Share Document