Effect of captopril or enalapril on renal prostaglandin E2

Katayama, Shigehiro; Inaba, Masaaki; Maruno, Yoshiko; Omoto, Akira; Itabashi, Akira; Kawazu, Shoji; Ishii, Jun

doi:10.1016/0090-6980(89)90123-8

Cited by 10 publications

(6 citation statements)

References 16 publications

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“…Recently, it has been shown that captopril in vitro suppresses production of IL‐12 ( Constantinescu et al , 1998 ) , tumour necrosis factor (TNF) and IL‐1α by human peripheral blood mononuclear cells ( Schindler et al , 1995 ). Furthermore, it was reported that captopril induces prostaglandin‐E2 (PGE2) synthesis ( Katayama et al , 1989 ; Johnsen et al , 1997 ). As the constitutive production of PGE2 during in vitro incubation of haematopoietic cells is well documented ( Goodwin et al , 1978 ) and PGE2 is a key molecule in the induction of IL‐10 in monocytes, which in turn down‐regulates the production of some cytokines including IL‐1α, IL‐1β, IL‐6, IL‐8, GM‐CSF and G‐CSF, one cannot exclude that the decrease of HPP‐CFC proportion in S‐phase observed after captopril treatment is due to an important decrease in the production of cytokines which are involved in stem cell triggering into the cell cycle ( de Waal Malefyt et al , 1991 ; Niho et al , 1998 ).…”

Section: Discussionmentioning

confidence: 99%

Captopril inhibitsin vitroandin vivothe proliferation of primitive haematopoietic cells induced into cell cycle by cytotoxic drug administration or irradiation but has no effect on myeloid leukaemia cell proliferation

et al. 2000

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Angiotensin I‐converting enzyme (ACE) has been shown to be involved in the catabolism of the tetrapeptide acetyl‐Ser–Asp–Lys–Pro (AcSDKP). As AcSDKP is a physiological inhibitor of haematopoietic stem cell proliferation, we investigated the in vitro and in vivo effects of captopril, one of the specific inhibitors of ACE, on the proliferation of primitive haematopoietic cells. Regenerating bone marrow cells obtained from mice given one injection of cytosine arabinoside (100 mg/kg) as well as SA2 myeloid leukaemia cells were incubated in vitro for 24 h with 10−6 m captopril. Captopril significantly reduced the proportion of high proliferative potential colony‐forming cells (HPP‐CFC‐1) in S‐phase, whereas it had no effect on the proportion of SA2 leukaemic colony‐forming cells in S‐phase. When given in vivo to mice 1 h after 2 Gy γ‐irradiation or cytosine arabinoside (AraC) injection, captopril (100 mg/kg) was shown to prevent HPP‐CFC‐1 entry into S‐phase induced by these cytotoxic treatments. The observed effects correlated with a reduction in ACE degradative activity and an increase in the level of endogenous AcSDKP both in the supernatants of captopril‐treated bone marrow cells and in plasma of treated animals. The present findings suggest that AcSDKP might mediate the observed in vitro and in vivo inhibitory effects of captopril on primitive haematopoietic cell proliferation.

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Section: Discussionmentioning

confidence: 99%

Captopril inhibitsin vitroandin vivothe proliferation of primitive haematopoietic cells induced into cell cycle by cytotoxic drug administration or irradiation but has no effect on myeloid leukaemia cell proliferation

et al. 2000

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“…This is sustained by the observation that other potent ACE‐inhibitors, such as ramipril, perindopril and lisinopril, do not influence cytokine production 9 . An alternative hypothesis is that captopril acts through its capacity to induce prostaglandins, 24 which are potent inhibitors of cytokine synthesis 25 . Whether valsartan may also act through other mechanisms than blockade of A‐II receptors is not known.…”

Section: Discussionmentioning

confidence: 99%

The effect of renin–angiotensin system inhibitors on pro‐ and anti‐inflammatory cytokine production

et al. 1998

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SUMMARYThe balance between pro-and anti-inflammatory cytokines has been implicated in the pathogenesis of infectious and auto-immune diseases, and its modulation has been proposed as a potential therapeutic target. The results reported in the present study show that modulators of the reninangiotensin system, such as the angiotensin-converting enzyme (ACE )-inhibitor captopril and the angiotensin II receptor type I antagonist valsartan, have potent inhibitory effects on the lipopolysaccharide (LPS )-stimulated production of pro-inflammatory cytokines tumour necrosis factor (TNF ) and interleukin-1 (IL-1) in vitro. The anti-inflammatory cytokine IL-1Ra is increased by captopril, whereas IL-6 production is decreased by valsartan. These effects are exerted mainly at high concentrations of the drugs. Administration of one dose of captopril or valsartan in therapeutic dosages to patients with essential hypertension did not influence LPS-stimulated production of cytokines by whole blood. In conclusion, despite inhibitory effects on proinflammatory cytokine production in vitro, it is unlikely that captopril or valsartan could be used in anticytokine therapeutic strategies in vivo.

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“…The elevation of ANF does not bring sodium balance back to normal, while prostaglandins are diminished or normal when they should be vigorously produced. 97 It is unlikely that other systems, such as bradykinin, play a major role in the salt retention since their inhibition does not ameliorate the worsened blood pressure. 98 This phase of the hypertension has not been as well studied as the initial phase, but it seems clear that elevated renin-angiotensin activity is not solely responsible for the sustained hypertension.…”

mentioning

confidence: 99%

Pathophysiology of renovascular hypertension.

1991

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Renovascular hypertension has its experimental counterpart in the two-kidney, one clip model (Goldblatt hypertension). From the study of this model, a general pathophysiological scheme has evolved suggesting that temporal stages in the development and maintenance of hypertension are regulated by complicated hormonal and neural interrelations. The central roles played by the renin-angiotensin system and the renal nerves is discussed as they relate to other hormones. In addition, the possible contribution of converting enzyme inhibitors to understanding the pathophysiology of this condition is discussed. (Hypertension 1991

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Effect of captopril or enalapril on renal prostaglandin E2

Cited by 10 publications

References 16 publications

Captopril inhibitsin vitroandin vivothe proliferation of primitive haematopoietic cells induced into cell cycle by cytotoxic drug administration or irradiation but has no effect on myeloid leukaemia cell proliferation

Captopril inhibitsin vitroandin vivothe proliferation of primitive haematopoietic cells induced into cell cycle by cytotoxic drug administration or irradiation but has no effect on myeloid leukaemia cell proliferation

The effect of renin–angiotensin system inhibitors on pro‐ and anti‐inflammatory cytokine production

Pathophysiology of renovascular hypertension.

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