Effects of central and intravascular angiotensin I and II on the choroid plexus

1991 ◽  
Vol 261 (5) ◽  
pp. R1126-R1132
Author(s):  
M. A. Maktabi ◽  
D. D. Heistad ◽  
F. M. Faraci
Keyword(s):  
Blood Flow ◽  
Angiotensin Converting Enzyme ◽  
Choroid Plexus ◽  
Blood Vessels ◽  
Enzyme Inhibitor ◽  
Similar Degree ◽  
Ang Ii ◽  
Converting Enzyme ◽  
High Concentration ◽  
Central System

The choroid plexus contains receptors for angiotensin II (ANG II) and a very high concentration of angiotensin-converting enzyme. The goal of this study was to test the hypothesis that central, as well as circulating, ANG I and II decrease blood flow to the choroid plexus. Under control conditions in anesthetized rabbits, blood flow (microspheres) to the choroid plexus was 449 +/- 21 (mean +/- SE) ml.min-1.100 g(-1). Intravascular ANG I (30 and 100 ng.kg-1.min-1) decreased blood flow to the choroid plexus by 19 +/- 14 and 28 +/- 18%, respectively. Intravascular ANG II (30 and 100 ng.kg-1.min-1) also produced a decrease in blood flow by 28 +/- 9 and 47 +/- 7%, respectively. When administered into the lateral ventricle, ANG I and II (10 and 100 ng.kg-1.min-1) decreased blood flow to a similar degree: 22 +/- 11 and 31 +/- 10% and 12 +/- 10 and 27 +/- 8%, respectively. Cerebral blood flow was not decreased by intravascular or central ANG I or II. The angiotensin-converting enzyme inhibitor quinaprilat prevented the decrease in blood flow to the choroid plexus in response to ANG I without affecting responses to ANG II. Thus 1) circulating ANG I and II are potent constrictors of blood vessels of the choroid plexus, 2) the constrictor effect of ANG I on the blood vessels of the choroid plexus appears mediated primarily by generation of ANG II, and 3) intracerebroventricular ANG I produces large reductions in the blood flow to the choroid plexus, which suggests that there is an effective central system that converts ANG I to ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-converting enzyme determination in plasma during therapy with converting enzyme inhibitor: two methods compared

1991 ◽  
Vol 37 (8) ◽  
pp. 1390-1393 ◽  
Author(s):  
T P Gorski ◽  
D J Campbell
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Spectrophotometric Method ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Fluorometric Method ◽  
Converting Enzyme Inhibitor ◽  
Ace Activity

Abstract For normal and above-normal concentrations of angiotensin-converting enzyme (ACE; EC 3.4.15.1) activity in plasma, results of a manual fluorometric method [with hippuryl-histidyl-leucine (HHL), 5 mmol/L, as substrate] correlated well with those of an automated spectrophotometric method [with 3-(2-furylacryloyl)-L-phenylalanyl-glycyl-glycine (FAPGG), 2 mmol/L, as substrate]. However, for patients receiving converting enzyme inhibitor (CEI) therapy, the spectrophotometric method showed much greater suppression of plasma ACE activity than did the fluorometric method. To determine which of the two methods provided a more reliable indication of ACE inhibition in vivo, we measured plasma ACE, angiotensin I (ANG I), and angiotensin II (ANG II) in patients receiving the CEI perindopril. During perindopril therapy, changes in the ratio of ANG II:ANG I, an index of ACE activity in vivo, showed a close agreement with changes in plasma ACE activity measured with FAPGG as substrate, but not with HHL as substrate. We conclude that measurement of ACE activity in vitro with FAPGG as substrate provides a reliable measure of changes in conversion of ANG I to ANG II in vivo during CEI therapy.

Angiotensin II induces apoptosis in human and rat alveolar epithelial cells

1999 ◽  
Vol 276 (5) ◽  
pp. L885-L889 ◽  
Author(s):  
Rongqi Wang ◽  
Alex Zagariya ◽  
Olivia Ibarra-Sunga ◽  
Claudia Gidea ◽  
Edmund Ang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Epithelial Cells ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitor ◽  
Alveolar Epithelial Cells ◽  
Receptor Subtypes ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Alveolar Epithelial

Recent work from this laboratory demonstrated potent inhibition of apoptosis in human alveolar epithelial cells (AECs) by the angiotensin-converting enzyme inhibitor captopril [B. D. Uhal, C. Gidea, R. Bargout, A. Bifero, O. Ibarra-Sunga, M. Papp, K. Flynn, and G. Filippatos. Am. J. Physiol. 275 ( Lung Cell. Mol. Physiol. 19): L1013–L1017, 1998]. On this basis, we hypothesized that apoptosis in this cell type might be induced by angiotensin II (ANG II) through its interaction with the ANG II receptor. Purified ANG II induced dose-dependent apoptosis in both the human AEC-derived A549 cell line and in primary type II pneumocytes isolated from adult Wistar rats as detected by nuclear and chromatin morphology, caspase-3 activity, and increased binding of annexin V. Apoptosis also was induced in primary rat AECs by purified angiotensinogen. The nonselective ANG II-receptor antagonist saralasin completely abrogated both ANG II- and angiotensinogen-induced apoptosis at a concentration of 50 μg/ml. With RT-PCR, both cell types expressed the ANG II-receptor subtypes 1 and 2 and angiotensin-converting enzyme (ACE). The nonthiol ACE inhibitor lisinopril blocked apoptosis induced by angiotensinogen, but not apoptosis induced by purified ANG II. These data demonstrate the presence of a functional ANG II-dependent pathway for apoptosis in human and rat AECs and suggest a role for the ANG II receptor and ACE in the induction of AEC apoptosis in vivo.

Enalapril decreases angiotensin II receptors in subfornical organ of SHR

1989 ◽  
Vol 256 (6) ◽  
pp. H1609-H1614 ◽  
Author(s):  
A. J. Nazarali ◽  
J. S. Gutkind ◽  
F. M. Correa ◽  
J. M. Saavedra
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitor ◽  
Area Postrema ◽  
Subfornical Organ ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Wky Rats ◽  
Enalapril Treatment

We studied brain angiotensin II (ANG II) receptors by quantitative autoradiography in adult normotensive Wistar-Kyoto (WKY) rats and in spontaneously hypertensive rats (SHR) after treating the rats with the converting-enzyme inhibitor enalapril, 25 mg/kg, po daily for 14 days. Enalapril treatment decreased blood pressure in only SHR, inhibited plasma angiotensin-converting enzyme activity by 85%, and increased plasma ANG I concentration and renin activity in both WKY and SHR. In the untreated SHR animals, ANG II receptor concentrations were higher in the subfornical organ, the area postrema, the nucleus of the solitary tract, and the inferior olive when compared with the untreated WKY rats. Enalapril treatment produced a large decrease in only subfornical organ ANG II receptors of SHR. The selective reversal of the alteration in subfornical organ ANG II receptors in SHR may indicate a decreased central response to ANG II and may be related to the mode of action of angiotensin-converting enzyme inhibitors in this model.

Angiotensin-converting enzyme inhibitor inhibits dehydration-enhanced fever induced by endotoxin in rats

2000 ◽  
Vol 279 (4) ◽  
pp. R1512-R1516 ◽  
Author(s):  
Tatsuo Watanabe ◽  
Makoto Hashimoto ◽  
Minoru Wada ◽  
Toshiaki Imoto ◽  
Michio Miyoshi ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Angiotensin Converting Enzyme Inhibitor ◽  
Intravenous Injection ◽  
Enzyme Inhibitor ◽  
Interleukin 1Β ◽  
Bacterial Endotoxin ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitor

It has been reported that a host develops a marked fever under dehydrated conditions compared with normally hydrated conditions (11). The present study was carried out to investigate whether ANG II is involved in the enhancement seen in dehydrated rats of the fever induced by bacterial endotoxin. The results showed that intravenous injection of bacterial endotoxin produced a fever in dehydrated rats (rats deprived of water for 24 h) that was significantly greater than that seen in normally hydrated rats. In contrast, dehydration had no effect on the fever induced by intravenous interleukin-1β (IL-1β). Under dehydrated conditions, the enhanced endotoxin-induced fever was significantly inhibited by the angiotensin-converting enzyme inhibitor lisinopril, but the IL-1β fever was not. These results suggest that the dehydration-induced enhancement of endotoxin fever is due, at least in part, to the action of ANG II, which elicits an increased production of pyrogenic cytokines such as IL-1.

scholarly journals Effects of hypotension and fluid depletion on central angiotensin-induced thirst and salt appetite

2001 ◽  
Vol 281 (5) ◽  
pp. R1726-R1733 ◽  
Author(s):  
Robert L. Thunhorst ◽  
Alan Kim Johnson
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Salt Appetite ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Nacl Solution ◽  
Subcutaneous Injections ◽  
Sodium Ingestion ◽  
Vasodilator Drug

We examined the effects of hypotension and fluid depletion on water and sodium ingestion in rats in response to intracerebroventricular infusions of ANG II. Hypotension was produced by intravenous infusion of the vasodilator drug minoxidil (25 μg · kg−1 · min−1) concurrently with the angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) to prevent endogenous ANG II formation. Hypotension increased water intake in response to intracerebroventricular ANG II (30 ng/h) but not intake of 0.3 M NaCl solution and caused significant urinary retention of water and sodium. Acute fluid depletion was produced by subcutaneous injections of furosemide (10 mg/kg body wt) either alone or with captopril (100 mg/kg body wt sc) before intracerebroventricular ANG II (15 or 30 ng/h) administration. Fluid depletion increased water intake in response to the highest dose of intracerebroventricular ANG II but did not affect saline intake. In the presence of captopril, fluid depletion increased intakes of both water and saline in response to both doses of intracerebroventricular ANG II. Because captopril administration causes hypotension in fluid-depleted animals, the results of the two experiments suggest that hypotension in fluid-replete animals preferentially increases water intake in response to intracerebroventricular ANG II and in fluid-depleted animals increases both salt and water intake in response to intracerebroventricular ANG II.

scholarly journals Dysregulation of the placental renin–angiotensin system in human fetal growth restriction

Reproduction ◽  
2019 ◽  
Vol 158 (3) ◽  
pp. 237-245 ◽  
Author(s):  
Sarah J Delforce ◽  
Eugenie R Lumbers ◽  
Stacey J Ellery ◽  
Padma Murthi ◽  
Kirsty G Pringle
Keyword(s):  
Blood Flow ◽  
Angiotensin Converting Enzyme ◽  
Mrna Expression ◽  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Renin Angiotensin System ◽  
Mrna Levels ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin System

Fetal growth restriction (FGR) is a pregnancy complication wherein the foetus fails to reach its growth potential. The renin–angiotensin system (RAS) is a critical regulator of placental function, controlling trophoblast proliferation, angiogenesis and blood flow. The RAS significantly influences uteroplacental blood flow through the balance of its vasoconstrictive and vasodilatory pathways. Although the RAS is known to be dysregulated in placentae from women with preeclampsia, the expression of the RAS has not yet been studied in pregnancies compromised by FGR alone. This study investigated the mRNA expression and protein levels of RAS components in placentae from pregnancies compromised by FGR. Angiotensin II type 1 receptor (AGTR1) and angiotensin-converting enzyme 2 (ACE2) mRNA levels were reduced in FGR placentae compared with control (P = 0.012 and 0.018 respectively). Neprilysin (NEP) mRNA expression was lower in FGR placentae compared with control (P = 0.004). mRNA levels of angiotensinogen (AGT) tended to be higher in FGR placentae compared with control (P = 0.090). Expression of prorenin, AGT, angiotensin-converting enzyme (ACE) or ACE2 proteins were similar in control and FGR placentae. The renin-AGT reaction is a first order reaction so levels of expression of placental AGT determine levels of Ang II. Decreasing levels of ACE2 and/or NEP by limiting the production of Ang-(1-7), which is a vasodilator, and increasing placental Ang II levels (vasoconstrictor) may result in an imbalance between the vasoconstrictor and vasodilator arms of the placental RAS. Ultimately this dysregulation of the placental RAS could lead to reduced placental perfusion that is evident in FGR.

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