The converting enzyme inhibitor captopril stimulates prostacyclin synthesis by isolated rat aorta

Düsing, Rainer; Scherhag, R; Landsberg, G.; Glänzer, K; Kramer, Herbert J.

doi:10.1016/0014-2999(83)90176-0

Cited by 49 publications

(9 citation statements)

References 10 publications

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“…Further possible mechanisms may relate to angiotensin II independent actions of CEO. CEI has been shown to enhance the cyclooxygenase pathway of arachidonic acid metabolism in blood vessels and isolated glomeruli (38,(49)(50)(51). Products ofthe cyclooxygenase pathway, in turn, directly or indirectly attenuate cell proliferation (38,(52)(53)(54)(55)(56)(57)(58).…”

Section: Resultsmentioning

confidence: 99%

Serial micropuncture analysis of glomerular function in two rat models of glomerular sclerosis.

Fogo

Yoshida²,

Glick³

et al. 1988

J. Clin. Invest.

175

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We have recently developed a micropuncture technique to assess repeatedly function of the same nephrons in chronic renal disease and subsequently examine the morphology of their glomeruli by serial thin-section histological analysis. Using this approach, a potential causal linkage between early functional patterns and late structural abnormalities was examined in glomeruli of two established rat models of glomerular sclerosis. The models are (a) puromycin aminonucleoside (PAN) administration in unilaterally nephrectomized Munich-Wistar rats and (b) adriamycin (ADM) treatment in nonnephrectomized Munich-Wistar rats. Single nephron GFR (SNGFR) and glomerular capillary hydraulic pressure (PGc) were measured repeatedly for 8 (PAN rats) or 31 wk (ADM rats). In all animals studied, values for PGC remained at, or slightly below, levels measured before PAN or ADM administration. SNGFR values declined progressively in all glomeruli in PAN rats. Although some glomeruli in ADM rats had an increase in SNGFR above levels observed in nonnephrectomized control rats, these hyperfiltering glomeruli did not have abnormally high PGC nor did they exhibit glomerular sclerosis at the completion of the study. Histological analysis revealed the existence of a significant inverse correlation between the degree of sclerosis and SNGFR assessed at the time of sacrifice in both PAN and ADM groups. Chronic administration of captopril, an angiotensin I converting enzyme inhibitor, in PAN rats substantially attenuated development of glomerular sclerosis without affecting PGC in earlier stages. The observations in these models indicate that glomerular hyperfiltration and hypertension are not required for the development of glomerular sclerosis in renal diseases, and angiotensin I converting enzyme inhibitor can exert its protective effect independently of its effect on glomerular capillary pressure.

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Section: Resultsmentioning

confidence: 99%

Serial micropuncture analysis of glomerular function in two rat models of glomerular sclerosis.

Fogo

Yoshida²,

Glick³

et al. 1988

J. Clin. Invest.

175

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“…Similarly, in preliminary studies, captopril has been reported to increase the synthesis of PGE 2 in renomedullary interstitial cells in culture 33 and the synthesis of PGI 2 in isolated aortic strips. 34 Captopril may also increase renal PGE^ synthesis indirectly. One possibility is that captopril may increase renal prostaglandin synthesis by its effect on endogenous kinins.…”

mentioning

confidence: 99%

Renal vasodilation by converting enzyme inhibition. Role of renal prostaglandins.

Oliver¹,

Sciacca²,

Cannon³

1983

Hypertension

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SUMMARY The present study was designed to determine whether renal prostaglandins are involved in the renal vasodilation evoked by angiotensin II inhibition in sodium depletion. The converting enzyme inhibitor (CEI) captopril was administered to sodium-depleted control dogs and sodiumdepleted dogs that had previously received the inhibitors of prostaglandin synthesis, indomethacin or meclofenamate. CEI in control dogs increased renal blood flow (RBF) from a mean value of 220 to 309 ml/min (p < 0.01) and decreased renal vascular resistance (RVR) from 0.64 to 0.38 arbitrary resistance units (ru) (p < 0.01). Renal venous prostaglandin E 2 (PGE2) concentration also increased from 52 to 85 pg/ml (p < 0.01). In the dogs that received inhibitors of prostaglandin synthesis, RBF fell from 214 to 168 ml/min (p < 0.01), RVR increased from 0.61 to 0.82 ru (p < 0.05), and renal venous PGE 2 fell from 114 to 20 pg/ml.(p < 0.01). The subsequent administration of captopril increased RBF from 168 to 221 ml/min (p < 0.01), lowered RVR from 0.82 to 0.43 ru (p < 0.01), but failed to significantly increase renal venous~RGE 2 (20 to 25 pg/ml). The decrease in RVR induced by captopril was not significantly different in the control dogs and in the dogs with prostaglandin synthesis inhibition. However, in the control dogs RBF after captopril was significantly higher than during the control period; this was not the case in the dogs with prostaglandin synthesis inhibition. RBF after captopril and prostaglandin inhibition was not significantly different from RBF during the control period. The results indicate that the acute renal vasodilator effect of captopril in sodium depletion does not require renal prostaglandins; however, the level of RBF after captopril is dependent upon renal prostaglandins, suggesting that endogenous prostaglandins increase renal blood flow when angiotensin II is inhibited. The results confirm previous studies indicating that captopril increases renal PGE 2 synthesis. (Hypertension 5: 166-171, 1983) KEY WORDS • captopril • renal blood flow • sodium depletion

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“…14-17 ACE inhibitors have a variety of effects on the ischemic myocardium: (1) increasing bradykinin, 18 (2) stimulation of nitric oxide formation, 19 (3) enhancing prostacyclin production, 20,21 and (4) reduction of catecholamines. 22 In the present study, the ACE inhibitor, temocaprilat, had a cardioprotective effect and, furthermore, the ACE inhibitor in combination with the ETA/ETB receptor antagonist, TAK-044, had a marked cardioprotective effect during ischemia and reperfusion, which suggests that the reninangiotensin system may be involved in the development of myocardial ischemia and reperfusion injury due to ET-1.…”

Section: Discussionmentioning

confidence: 99%

Effect of an Endothelin Receptor Antagonist and an Angiotensin Converting Enzyme Inhibitor on Metabolism and Contraction in the Ischemic and Reperfused Rabbit Heart

1999

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ince the first report on endothelin (ET), 1 there have been many studies regarding its effects of cardiovascular system in various in vitro and in vivo models. Recently, ET has been reported to contribute to the extension of myocardial infarct size 2 and, moreover, ET-1 interacts with several neuroendocrine systems such as the renin-angiotensin system. 3 The effect of ET-1 in conjunction with the renin-angiotensin system on myocardial ischemia and reperfusion injury has not been clearly identified.The purpose of the present study was to examine the effect of the ETA/ETB receptor antagonist, TAK-044, and/or an angiotensin converting enzyme (ACE) inhibitor, temocaprilat, on the myocardial metabolism, contraction and relaxation of the ischemic and reperfused rabbit heart. Myocardial energy metabolism was measured by phosphorus 31-nuclear magnetic resonance ( 31 P-NMR) spectrometer. The administration of these agents was found to improve abnormal myocardial energy metabolism. Methods Isolated Heart PreparationMale Japanese white rabbits weighing 1.6-1.7 kg were anesthetized by intravenous injection of sodium pentobarbital (30 mg/kg). The chest was opened and heparin sodium (1,000 IU/kg) was injected through the right atrial appendage. The heart was quickly removed and after aortic cannulation the retrograde Langendorff perfusion was initiated without delay.The hearts were perfused at a constant perfusion pressure of 80 mmHg with modified Tyroide's solution at 37°C of the following composition (in mmol/L); NaCl 108, KCl 5, MgCl2 1, HEPES 5, CaCl2 2, glucose 10, sodium acetate 20. The perfusate was oxygenated with 100% O2 using a bubble-type artificial lung (Japan Medical Supply Co, Ltd, Hiroshima, Japan) adjusted to pH 7.40. The perfusate was recycled to an artificial lung after passing through the heart. A 40-m Swank filter (Nipro Co, Ltd, Tokyo, Japan) was placed within this route to remove any contaminants.To measure left ventricular (LV) pressure, a latex balloon was inserted into the left ventricle via a left atrial incision. The balloon was large enough so that no pressure was generated by itself over the range of left ventricular volumes used in the experiment. The balloon was filled with bubblefree saline and attached to a pressure transducer (Millar Instruments Inc, Houston, TX, USA) connected to a polygraph system RM-6000 (Nihon Kohden Co, Tokyo, Japan). The effect of an endothelin (ET) A/ETB receptor antagonist, TAK-044, and/or an angiotensin converting enzyme (ACE) inhibitor, temocaprilat, on myocardial metabolism and contraction during ischemia and reperfusion was examined by phosphorus 31-nuclear magnetic resonance ( 31 P-NMR) in Langendorff rabbit hearts. After normothermic 15 min global ischemia, 60 min of postischemic reperfusion was carried out. TAK-044 and/or temocaprilat was administered from 40 min prior to the global ischemia. Adenosine triphosphate (ATP), creatine phosphate, inorganic phosphate, pH, left ventricular systolic developed pressure (LVDev.P), left ventricular end-diastolic pressure ...

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The converting enzyme inhibitor captopril stimulates prostacyclin synthesis by isolated rat aorta

Cited by 49 publications

References 10 publications

Serial micropuncture analysis of glomerular function in two rat models of glomerular sclerosis.

Serial micropuncture analysis of glomerular function in two rat models of glomerular sclerosis.

Renal vasodilation by converting enzyme inhibition. Role of renal prostaglandins.

Effect of an Endothelin Receptor Antagonist and an Angiotensin Converting Enzyme Inhibitor on Metabolism and Contraction in the Ischemic and Reperfused Rabbit Heart

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