scholarly journals Angiotensin Converting Enzyme Inhibition Reduces Cardiovascular Responses to Acute Stress in Myocardially Infarcted and Chronically Stressed Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
A. Cudnoch-Jedrzejewska ◽  
K. Czarzasta ◽  
L. Puchalska ◽  
J. Dobruch ◽  
O. Borowik ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Acute Stress ◽  
Cardiovascular Responses ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Converting Enzyme Inhibition ◽  
Acute Stressor

Previous studies showed that chronically stressed and myocardially infarcted rats respond with exaggerated cardiovascular responses to acute stress. The present experiments were designed to elucidate whether this effect can be abolished by treatment with the angiotensin converting enzyme (ACE) inhibitor captopril. Sprague Dawley rats were subjected either to sham surgery (Groups 1 and 2) or to myocardial infarction (Groups 3 and 4). The rats of Groups 2 and 4 were also exposed to mild chronic stressing. Four weeks after the operation, mean arterial blood pressure (MABP) and heart rate (HR) were measured under resting conditions and after application of acute stress. The cardiovascular responses to the acute stress were determined again 24 h after administration of captopril orally. Captopril significantly reduced resting MABP in each group. Before administration of captopril, the maximum increases in MABP evoked by the acute stressor in all (infarcted and sham-operated) chronically stressed rats and also in the infarcted nonchronically stressed rats were significantly greater than in the sham-operated rats not exposed to chronic stressing. These differences were abolished by captopril. The results suggest that ACE may improve tolerance of acute stress in heart failure and during chronic stressing.

scholarly journals Acute angiotensin-converting enzyme inhibition evokes bradykinin-induced sympathetic activation in diabetic rats

2007 ◽  
Vol 293 (6) ◽  
pp. R2260-R2266 ◽  
Author(s):  
Robert A. Augustyniak ◽  
Maria Maliszewska-Scislo ◽  
Haiping Chen ◽  
John Fallucca ◽  
Noreen F. Rossi
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Ace Inhibition ◽  
Diabetic Rats ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Sprague Dawley ◽  
Renal Sympathetic Nerve Activity ◽  
Sprague Dawley Rats ◽  
Converting Enzyme Inhibition ◽  
Angiotensin Receptor Blockade

We have previously shown that acute intravenous injection of the angiotensin-converting enzyme (ACE) inhibitor enalapril in diabetic rats evokes a baroreflex-independent sympathoexcitatory effect that does not occur with angiotensin receptor blockade alone. As ACE inhibition also blocks bradykinin degradation, we sought to determine whether bradykinin mediated this effect. Experiments were performed in conscious male Sprague-Dawley rats, chronically instrumented to measure mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), 2 wk after streptozotocin (55 mg/kg iv, diabetic, n = 11) or citrate vehicle (normal, n = 10). Enalapril (2.5 mg/kg iv) decreased MAP in normal rats (−15 ± 3 mmHg), while a smaller response (−4 ± 1 mmHg) occurred in diabetic rats. Despite these different depressor responses to enalapril, HR (+44 ± 8 vs. +26 ± 7 bpm) and RSNA (+90 ± 21 vs +71 ± 8% baseline) increased similarly between the groups ( P ≥ 0.22 for both). Pretreatment with the bradykinin B2 receptor antagonist Hoe 140 (10 μg/kg bolus followed by 0.8·μg−1kg·min−1 infusion) attenuated the decrease in MAP observed with enalapril in normal rats but had no effect in diabetic rats. Moreover, the normal group had smaller HR and RSNA responses (HR: +13 ± 8 bpm; RSNA: +32 ± 13% baseline) that were abolished in the diabetic group (HR: −4 ± 5 bpm; RSNA: −5 ± 9% baseline; P < 0.05 vs. preenalapril values). Additionally, bradykinin (20 μg/kg iv) evoked a larger, more prolonged sympathoexcitatory effect in diabetic compared with normal rats that was further potentiated after treatment with enalapril. We conclude that enhanced bradykinin signaling mediates the baroreflex-independent sympathoexcitatory effect of enalapril in diabetic rats.

Angiotensin converting enzyme inhibition from birth reduces body weight and body fat in Sprague–Dawley rats

2008 ◽  
Vol 93 (4-5) ◽  
pp. 820-825 ◽  
Author(s):  
Harrison S. Weisinger ◽  
Denovan P. Begg ◽  
Gary F. Egan ◽  
Anura P. Jayasooriya ◽  
Fanny Lie ◽  
...  
Keyword(s):  
Body Weight ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibition ◽  
Body Fat ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Converting Enzyme Inhibition

Angiotensin-converting enzyme inhibition increases collateral-dependent muscle blood flow

1993 ◽  
Vol 75 (1) ◽  
pp. 452-457 ◽  
Author(s):  
H. T. Yang ◽  
R. L. Terjung
Keyword(s):  
Blood Flow ◽  
Angiotensin Converting Enzyme ◽  
Muscle Blood Flow ◽  
Ace Inhibition ◽  
Angiotensin Converting Enzyme Inhibition ◽  
High Dose ◽  
Converting Enzyme ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Converting Enzyme Inhibition

The purpose of this study was to evaluate the effect of angiotensin-converting enzyme (ACE) inhibition on collateral-dependent blood flow (BF) during exercise. Adult male Sprague-Dawley rats (approximately 320 g) were fed zabicipril, an ACE inhibitor, mixed with powdered food at 0.0, 0.3, and 3.0 mg.kg-1 x day-1 (n = 12/group) for 5–7 days. Under ketamine-acepromazine anesthesia, the carotid and caudal arteries were catheterized for BF determination, and both femoral arteries were ligated to remove the primary route for BF to the distal limb tissue. Later on the same day, collateral-dependent hindlimb BF was determined at two treadmill speeds (15 and 25 m/min at 15% grade) with 85Sr- and 141Ce-labeled 15-microns microspheres. Zabicipril ingestion induced 50 and 65% inhibition of plasma ACE activity in the low- and high-dose group, respectively (P < 0.001). ACE inhibition did not affect body weight, blood pressure, or heart rate of the rats during exercise. However, BFs to the total hindlimb were 44 and 36% higher (P < 0.001) in zabicipril-treated animals than in the zero-dose controls (approximately 45 ml.min-1 x 100 g-1). Furthermore, BFs to the proximal hindlimb, distal hindlimb, and gastrocnemius-plantaris-soleus group were 33–44% greater in drug-treated than in control animals (P < 0.025). Higher speed (25 m/min) failed to further increase muscle BF; therefore peak BFs were likely achieved. These results indicate that collateral-dependent BF was improved by ACE inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Kinins in humans

2000 ◽  
Vol 278 (4) ◽  
pp. R897-R904 ◽  
Author(s):  
Ann-Maree Duncan ◽  
Athena Kladis ◽  
Garry L. Jennings ◽  
Anthony M. Dart ◽  
Murray Esler ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibition ◽  
Reactive Hyperemia ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Blood Levels ◽  
Converting Enzyme ◽  
Glandular Kallikrein ◽  
Arterial Blood ◽  
Peptide System ◽  
Converting Enzyme Inhibition

The kinin peptide system in humans is complex. Whereas plasma kallikrein generates bradykinin peptides, glandular kallikrein generates kallidin peptides. Moreover, a proportion of kinin peptides is hydroxylated on proline3 of the bradykinin sequence. We established HPLC-based radioimmunoassays for nonhydroxylated and hydroxylated bradykinin and kallidin peptides and their metabolites in blood and urine. Both nonhydroxylated and hydroxylated bradykinin and kallidin peptides were identified in human blood and urine, although the levels in blood were often below the assay detection limit. Whereas kallidin peptides were more abundant than bradykinin peptides in urine, bradykinin peptides were more abundant in blood. Bradykinin and kallidin peptide levels were higher in venous than arterial blood. Angiotensin-converting enzyme inhibition increased blood levels of bradykinin, but not kallidin, peptides. Reactive hyperemia had no effect on antecubital venous levels of bradykinin or kallidin peptide levels. These studies demonstrate differential regulation of the bradykinin and kallidin peptide systems, and indicate that blood levels of bradykinin peptides are more responsive to angiotensin-converting enzyme inhibition than blood levels of kallidin peptides.

Angiotensin-converting enzyme inhibition and Na appetite: microbehavioral analysis and nycthemeral physiology

1993 ◽  
Vol 265 (1) ◽  
pp. R7-R13 ◽  
Author(s):  
N. E. Rowland ◽  
T. M. Nicholson ◽  
J. C. Smith
Keyword(s):  
Enzyme Inhibitor ◽  
Chronic Administration ◽  
Plasma Renin ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Sprague Dawley ◽  
Sodium Appetite ◽  
Angiotensin I Converting Enzyme ◽  
Sprague Dawley Rats ◽  
Converting Enzyme Inhibition

The present experiments describe a marked nycthemeral rhythm in both the appetite for 0.3 M NaCl solution and components of the renin-angiotensin-aldosterone axis stimulated in Sprague-Dawley rats by chronic administration of enalapril, an angiotensin I-converting enzyme inhibitor. Continuous recording of water, NaCl, and food intakes shows that the sodium appetite is manifest as discrete bouts of salt ingestion in temporal proximity to meals and is partially independent of water bouts. In particular, salt bouts occur without water bouts in the late afternoon of a 12:12-h light-dark cycle and continue periprandially with water bouts during the night. Intake of all three commodities is minimal in the morning. In a second experiment, it was determined that plasma renin activity (PRA) was maximally elevated by chronic enalapril in the daytime and that plasma aldosterone was reduced by enalapril but continued to show nycthemeral rhythm peaking in the afternoon. The concurrent maxima in PRA and aldosterone in the afternoon in enalapril-treated rats thus coincides with NaCl intake in the absence of water intake.

Angiotensin-Converting Enzyme Inhibition and the Progression of Congestive Cardiomyopathy

Circulation ◽  
1995 ◽  
Vol 92 (3) ◽  
pp. 562-578 ◽  
Author(s):  
Francis G. Spinale ◽  
Henry H. Holzgrefe ◽  
Rupak Mukherjee ◽  
R. Barry Hird ◽  
Jennifer D. Walker ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibition ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Congestive Cardiomyopathy ◽  
Converting Enzyme Inhibition
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