Effect of ANG II receptor antagonist on albuminuria and renal function in passive Heymann nephritis

1992 ◽  
Vol 263 (2) ◽  
pp. F311-F318
Author(s):  
F. N. Hutchinson ◽  
S. K. Webster
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
Enzyme Inhibitor ◽  
Pressor Response ◽  
Plasma Renin ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Heymann Nephritis

Angiotensin-converting enzyme inhibitors reduce albuminuria in nephrotic subjects, but the hormonal mechanism of this effect is not known. To determine whether specific inhibition of angiotensin (ANG) II activity would decrease albuminuria as occurs after converting enzyme inhibition, rats with passive Heymann nephritis received enalapril or the ANG II receptor antagonist losartan (6 mg.kg-1.day-1) for 4 days. Enalapril reduced both albuminuria (from 583 +/- 53 to 286 +/- 55 mg/day, P less than 0.001) and the fractional clearance of albumin (FCAlb) each day after starting treatment but did not affect glomerular filtration rate (GFR). Losartan reduced albuminuria significantly only after 4 days of treatment, but this value was not different from controls. GFR significantly increased with losartan (from 1.24 +/- 0.09 to 1.73 +/- 0.21 ml/min, P less than 0.05) so that FCAlb was reduced (from 0.0134 +/- 0.0027 to 0.0080 +/- 0.0018, P less than 0.05). Blood pressure decreased only in the enalapril group. Although plasma renin activity increased and the pressor response to ANG I was inhibited by both enalapril and losartan, suggesting effective peripheral blockade of ANG II activity, a third group of nephrotic rats was treated with losartan (18 mg.kg-1.day-1) to ensure that adequate ANG II blockade was achieved. Blood pressure decreased 10 mmHg, GFR increased from 1.35 +/- 0.14 to 1.79 +/- 0.12 ml/min (P less than 0.01), but albuminuria and FCAlb did not change. Urinary total kallikrein excretion was increased only in nephrotic rats treated with enalapril. Although both enalapril and losartan reduce ANG II activity, only the converting enzyme inhibitor reduces albuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Domestic practice of antihypertensive treatment of diabetic hypertensive patients

2014 ◽  
Vol 155 (43) ◽  
pp. 1695-1700
Author(s):  
Veronika Szentes ◽  
Gabriella Kovács ◽  
Csaba András Dézsi
Keyword(s):  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitors ◽  
Enzyme Inhibitor ◽  
Beta Blockers ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Converting Enzyme Inhibitors ◽  
Patients With Diabetes

Diabetes mellitus as comorbidity is present in 20–25% of patients suffering from high blood pressure. Because simultaneous presence of these two diseases results in a significant increase of cardiovascular risk, various guidelines focus greatly on the anti-hyperintensive treatment of patients with diabetes. Combined drug therapy is usually required to achieve the blood pressure target value of <140/85 mmHg defined for patients with diabetes, which must be based on angiotensin converting enzyme-inhibitors or angiotensin receptor blockers. These can be/must be combined with low dose, primarily thiazid-like diuretics, calcium channel blockers with neutral metabolic effect, and further options include the addition of beta blockers, imidazolin-l-receptor antagonists, or alpha-1-adrenoreceptor blockers. Evidence-based guidelines are obviously present in local practice. Although most of the patients receive angiotensin converting enzyme-inhibitor+indapamid or angiotensin converting enzyme-inhibitor+calcium channel blocker combined therapy with favorable metabolic effects, yet the use of angiotensin converting enzyme-inhibitors containing hidrochlorotiazide having diabetogenic potencial, and angiotensin receptor blocker fixed combinations is still widespread. Similarly, interesting therapeutic practice can be observed with the use of less differentiated beta blockers, where the 3rd generation carvediolol and nebivolol are still in minority. Orv. Hetil., 2014, 155(43), 1695–1700.

Effects of modulation of renal kallikrein-kinin system in the nephrotic syndrome

1990 ◽  
Vol 258 (5) ◽  
pp. F1237-F1244
Author(s):  
F. N. Hutchison ◽  
V. I. Martin
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitors ◽  
Pressor Response ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Ang Ii ◽  
Converting Enzyme Inhibitors ◽  
Kinin System ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System

Albuminuria (UAlbV) can be reduced by converting-enzyme inhibitors (CEI), but the hormonal mechanism responsible for this effect has not previously been defined. Since CEI increase kinin activity as well as reduce angiotensin II (ANG II) activity, experiments were performed to determine the effect of isolated alterations in kinin and ANG II metabolism on UAlbV in rats with passive Heymann pephritis. Phosphoramidon was used to potentiate kinin activity without altering ANG II synthesis. Aprotinin was utilized in combination with the CEI, enalapril, to prevent the increase in kinin activity caused by CEI. UAlbV and the fractional renal clearance of albumin (FCAlb) decreased significantly after either phosphoramidon or enalapril, although only enalapril reduced blood pressure. Glomerular filtration rate (GFR) was not affected by either drug. Phosphoramidon did not affect plasma renin activity (PRA) or the pressor response to angiotensin I (ANG I), indicating that ANG II synthesis was not altered. Aprotinin prevented the reduction in UAlbV and FCAlb produced by CEI but not the hypotension, elevated PRA, or ANG I pressor blockade produced by CEI. Aprotinin alone had no effect on UAlbV, GFR, PRA, or blood pressure. UAlbV can be reduced by increasing kinin activity by a mechanism that is not dependent on suppression of ANG II activity or reduction in GFR or blood pressure. CEI may reduce proteinuria as a result of their action on the kallikrein-kinin system rather than on the renin-angiotensin system.

Converting-enzyme inhibition abolishes polydipsia induced by dietary NaCl and K depletion

1990 ◽  
Vol 258 (5) ◽  
pp. F1164-F1172
Author(s):  
A. J. McKay ◽  
C. D. Poirier ◽  
L. N. Peterson
Keyword(s):  
Water Intake ◽  
Enzyme Inhibitor ◽  
Pressor Response ◽  
Plasma Renin ◽  
High Water ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Daily Water Intake ◽  
High Water Intake ◽  
Converting Enzyme Inhibition

The present studies were designed to test the hypothesis that angiotensin II (ANG II) mediates nonosmotic thirst in animals fed the low-NaCl K-free diet by preventing the increased generation of ANG II using the converting-enzyme inhibitor, enalapril. Animals were fed either a control salt or low-NaCl K-free diet and were treated with or without enalapril. Water intake in rats fed the low-NaCl K-free diet increased more than twofold on day 3 and remained elevated over the 10-day period of study. Treatment with enalapril (40 mg.kg-1.day-1) 1) prevented the striking rise in plasma renin activity in rats fed the low-NaCl K-free diet, 2) led to complete blockade of the pressor response to a 50-ng injection of angiotensin I but not ANG II, 3) did not affect daily water intake in rats consuming the control salt diet, 4) did not reduce basal water intake in rats fed the low-NaCl K-free diet below values measured in control animals, and 5) did not abolish water intake in response to osmotic stimulation. However, enalapril treatment abolished the increase in water intake that occurs in animals fed the low-NaCl K-free diet. In a double crossover study using two groups of rats fed the low-NaCl K-free diet, enalapril prevented increased water intake in rats initially fed the low-NaCl K-free diet and rapidly inhibited increased water intake in rats fed the low-NaCl K-free diet after the high water intake had been established.(ABSTRACT TRUNCATED AT 250 WORDS)

Dangers of Captopril Therapy in Newborns

PEDIATRICS ◽  
1989 ◽  
Vol 83 (6) ◽  
pp. 1076-1076
Author(s):  
VIVIAN REZNIK ◽  
WILLIAM GRISWOLD ◽  
STANLEY MENDOZA
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Angiotensin Converting Enzyme ◽  
Premature Infant ◽  
Enzyme Inhibitors ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Treatment Of Hypertension

Angiotensin-converting enzyme inhibitors are effective at lowering blood pressure in the neonate and the child. However, these drugs, when used for the treatment of hypertension in the premature infant, must be used with caution to avoid the complications that are well documented in the literature. All of the infants described in the article by Perlman and Volpe had extreme hypotension and oligunia. A group of nine infants with renal failure complicating captopril therapy were recently reported from the same institution.

scholarly journals Prediction Models of Albumin Renal Excretion in Type 2 Diabetes Mellitus Patients

2019 ◽  
Vol 70 (11) ◽  
pp. 3802-3807
Author(s):  
Amorin Remus Popa ◽  
Claudia Teodora Judea Pusta ◽  
Cosmin Mihai Vesa ◽  
Simona Bungau ◽  
Camelia Liana Buhas ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Enzyme Inhibitors ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Converting Enzyme ◽  
Angiotensin Ii Receptor ◽  
Converting Enzyme Inhibitors ◽  
Positive Correlation

Microalbuminuria is a cardiovascular risk factor in type 2 diabetes mellitus patients. It is very important to know which the predictor factors for albuminuria are, because these elements may be influenced by pharmacological measures. In our study we propose three models for the prediction of albumin glomerular excretion in a group of 446 type 2 diabetes mellitus patients: the clinical-biochemical model, the pharmacological model, and the integrative model that reunites the two models. In the clinical-biochemical model, albumin excretion was statistically significant influenced by HbA1c (positive correlation) and blood pressure (positive correlation). In the pharmacological model, albumin excretion was influenced by angiotensin converting enzyme inhibitors or angiotensin II receptor blockers treatment (negative correlation). In the integrative model, the factors were HbA1c (positive correlation), diastolic blood pressure (positive correlation), angiotensin converting enzyme inhibitors or angiotensin II receptor blockers treatment (negative correlation) and statins treatment (negative correlation). The prevalence of microalbuminuria was 16.14 %. Patients with microalbuminuria had statistically significant higher values of HbA1c, systolic blood pressure, diastolic blood pressure, triglycerides and lower values of HDL-cholesterol. A low glucose control was the most important risk factor for an increased albumin glomerular elimination. The importance of our study consists in the fact that all the elements that predict albuminuria can be influenced: HbA1c, blood pressure, therapy with angiotensin converting enzyme inhibitors or angiotensin II receptor blockers and statins.

Angioedema induced by angiotensin-converting enzyme inhibitors: an analysis of hospitalizations during the COVID-19 pandemic

2021 ◽  
Author(s):  
Tatsiana М. Sabalenka ◽  
Volha V. Zakharava ◽  
Natallia R. Prakoshyna
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibitors ◽  
Enzyme Inhibitor ◽  
Angiotensin Receptor Blockers ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Converting Enzyme Inhibitors ◽  
Converting Enzyme Inhibitor ◽  
Receptor Blockers

Backgraund: The pathogenesis of angioedema induced by angiotensin-converting enzyme inhibitors is based on the accumulation of bradykinin as a result of angiotensin-converting enzyme blockade. The SARS-CoV-2 virus by binding to the angiotensin-converting enzyme 2 receptor, may inhibit its production, which in turn leads to an increase in bradykinin levels. Thus, infection with SARS-CoV-2 may be a likely trigger for the development of angioedema. Aims: to analyze the cases of hospitalizations of patients with angioedema associated with the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers during the COVID-19 pandemic. Materials and methods: a retrospective analysis of the medical records of inpatient patients admitted to the Vitebsk Regional Clinical Hospital in May-December 2020 with isolated (without urticaria) angioedema while receiving angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was performed. All patients received smears from the naso- and oropharynx for COVID-19 by polymerase chain reaction. Results: there were admitted 15 patients (9 men and 6 women) aged 44-72 years for emergency indications, which was 53.6% among all patients with isolated angioedema. In two cases, a concomitant diagnosis of mild COVID-19 infection was established with the predominance symptoms of angioedema in the clinical picture with localization in the face, tongue, sublingual area, soft palate. All patients had a favorable outcome of the disease. Conclusions: patients with аngiotensin-converting enzyme inhibitor-induced angioedema may need to be hospitalized to monitor upper respiratory tract patency. There were cases of a combination of аngiotensin-converting enzyme inhibitor-induced angioedema and mild COVID-19 infection. Issues requiring additional research: the effect of SARS-CoV-2 infection on the levels of bradykinin and its metabolites; the trigger role of COVID-19 infection in the development of angioedema in patients receiving angiotensin-converting enzyme inhibitors/angiotensin receptor blockers; recommendations for the management of patients with аngiotensin-converting enzyme inhibitor-induced angioedema and a positive result for COVID-19.

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Endogenous Formation

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

scholarly journals Overexpression of Central ACE2 (Angiotensin-Converting Enzyme 2) Attenuates the Pressor Response to Chronic Central Infusion of Ang II (Angiotensin II)

Hypertension ◽  
2020 ◽  
Vol 76 (5) ◽  
pp. 1514-1525
Author(s):  
Anyun Ma ◽  
Lie Gao ◽  
Ahmed M. Wafi ◽  
Li Yu ◽  
Tara Rudebush ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Angiotensin Converting Enzyme ◽  
Pressor Response ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Intracerebroventricular Infusion

We investigated the mechanism by which ACE2 (angiotensin-converting enzyme 2) overexpression alters neurohumoral outflow and central oxidative stress. Nrf2 (nuclear factor [erythroid-derived 2]-like 2) is a master antioxidant transcription factor that regulates cytoprotective and antioxidant genes. We hypothesized that upregulation of central ACE2 inhibits the pressor response to Ang II (angiotensin II) by reducing reactive oxygen species through a Nrf2/antioxidant enzyme–mediated mechanism in the rostral ventrolateral medulla. Synapsin human Angiotensin Converting Enzyme 2 positive (SynhACE2 +/+ ) mice and their littermate controls synhACE2 −/− were used to evaluate the consequence of intracerebroventricular infusion of Ang II. In control mice, Ang II infusion evoked a significant increase in blood pressure and norepinephrine excretion, along with polydipsia and polyuria. The pressor effect of central Ang II was completely blocked in synhACE2 +/+ mice. Polydipsia, norepinephrine excretion, and markers of oxidative stress in response to central Ang II were also reduced in synhACE2 +/+ mice. The MasR (Mas receptor) agonist Ang 1–7 and blocker A779 had no effects on blood pressure. synhACE2 +/+ mice showed enhanced expression of Nrf2 in the rostral ventrolateral medulla which was blunted following Ang II infusion. Ang II evoked nuclear translocation of Nrf2 in cultured Neuro 2A (N2A) cells. In synhACE2 −/− mice, the central Ang II pressor response was attenuated by simultaneous intracerebroventricular infusion of the Nrf2 activator sulforaphane; blood pressure was enhanced by knockdown of Nrf2 in the rostral ventrolateral medulla in Nrf2 floxed (Nrf2 f/f ) mice. These data suggest that the hypertensive effects of intracerebroventricular Ang II are attenuated by selective overexpression of brain synhACE2 and may be mediated by Nrf2-upregulated antioxidant enzymes in the rostral ventrolateral medulla.

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