Angiotensin-Converting Enzyme Inhibitors in the Treatment of Hypertension

Johnston, C. I.; Arnolda, Leonard F; Hiwatari, Masao

doi:10.2165/00003495-198427030-00006

Cited by 59 publications

(14 citation statements)

References 12 publications

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“…Angiotensin converting enzyme (ACE) inhibitors are of therapeutic benefit in the treatment of hypertension, heart failure and renal disease (Edwards & Padfield, 1985;Johnston et al, 1984). Lisinopril, the lysine derivative of enalaprilic acid, is a new potent orally active inhibitor of angiotensin converting enzyme (Biollaz et al, 1981).…”

Section: Introduction Methodsmentioning

confidence: 99%

Lisinopril pharmacokinetics in chronic renal failure.

Jackson

Cubela

Conway

et al. 1988

Brit J Clinical Pharma

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1 Lisinopril, a new orally active angiotensin converting enzyme inhibitor, was given to eight patients with stable chronic renal failure, in a dose of 5 mg 24 h-1 for 1 week.Creatinine clearance of the subjects ranged from 0.22 to 1.11 ml s 1 Lisinopril pharmacokinetics were studied over 8 days. 2 There was a close correlation between creatinine clearance and total 'area under the curve' over the 8 days of study (r = -0.88, P < 0.05), and plateau lisinopril concentration and creatinine clearance (r = -0.77, P < 0.05). 3 Serum angiotensin converting enzyme activity was inhibited in proportion to log serum lisinopril concentration (r = -0.99, P < 0.001). Calculated IC50 was 47 ng lisinopril ml-1 from pooled data, with individual patients IC50 ranging from 20 to 70 ng lisinopril ml-'. 4 Creatinine clearance was unaltered by treatment. Serum potassium rose to over 5 mmol 1-1 in four patients, without adverse clinical effect.

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Section: Introduction Methodsmentioning

confidence: 99%

Lisinopril pharmacokinetics in chronic renal failure.

Jackson

Cubela

Conway

et al. 1988

Brit J Clinical Pharma

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“…ACE inhibitors block the formation of angiotensin II, an octapeptide that exerts the many diverse effects of the renin-angiotensin system through its receptors (7). The angiotensin II type 1 (AT 1 ) receptor blocker also reduces lung metastasis in mice (8,9).…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II Type 2 Receptor Gene Deficiency Attenuates Susceptibility to Tobacco-Specific Nitrosamine-Induced Lung Tumorigenesis: Involvement of Transforming Growth Factor-β-Dependent Cell Growth Attenuation

et al. 2005

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To clarify an involvement of angiotensin II signaling in lung neoplasia, we have examined the effect of angiotensin II receptor deficiency on 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumorigenesis. Male angiotensin II type 2 receptor (AT 2 )-null mice with an SWR/J genetic background and control wild-type mice were treated with NNK (100 mg/kg, i.p.) or saline vehicle. NNK treatment caused the development of lung tumors in all wild-type control mice (100 % tumor prevalence), but only 85% of AT 2 -null mice developed tumors. The tumor multiplicity in AT 2 -null mice (1.9 F 0.3) was significantly smaller than that in wild-type mice (4.1 F 0.9). Primary cultured lung fibroblasts prepared from both AT 2 -null and wild-type mice markedly increased the colony counts of A549 lung cancer cells in soft agar, but a consistently higher colony count was observed with the wild-type fibroblasts ( fold increase in colony number, 5.6 F 0.5) than with the AT 2 -null fibroblasts (3.5 F 0.8). The underlying mechanism by which angiotensin II regulates cancer cell growth is due to the regulation of active transforming growth factor-B (TGF-B) production. Although the total level of TGF-B was significantly stimulated when A549 cells were cocultured with either type of fibroblasts, the level of active TGF-B in the conditioned medium was consistently higher with AT 2 -null fibroblasts than with wild-type fibroblasts. These results imply that the AT 2 receptor negatively regulates the level of active TGF-B and thus increases NNK-induced lung tumorigenesis. The AT 2 receptor function in lung stromal fibroblasts may be a potential modulator of tumor susceptibility in chemical carcinogen-induced lung tumorigenesis. (Cancer Res 2005; 65(17): 7660-5)

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“…In clinical antihypertensive therapy, angiotensin converting enzyme inhibitors decrease blood pressure without causing reflex tachycardia (Johnston et al, 1984;Campbell et al, 1985;Guidicelli et al, 1985). Although some effects on the baroreceptor reflex with converting enzyme inhibitors have been observed in animals (Kirkman & Scott, 1985), many studies show that baroreceptor reflex sensitivity is unaltered in the clinical situation (Guidicelli et al, 1985;Mancia et al, 1988;Kondowe et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

A facilitatory effect of anti‐angiotensin drugs on vagal bradycardia in the pithed rat and guinea‐pig

Rechtman

Majewski

1993

British J Pharmacology

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1 In pithed rats, preganglionic vagal nerve stimulation (at 5 Hz) elicited a bradycardia. This bradycardia was potentiated by the angiotensin converting enzyme inhibitor, captopril (1 mg kg-', i.v.) by about 40%. Subsequent angiotensin II infusion (0.03 gg kg-' min-') reversed this effect. A similar facilitatory effect was also seen with the angiotensin receptor antagonist, losartan (1Omg kg-', i.v.). These results suggest a tonic inhibitory effect of endogenous angiotensin II on vagal transmission. 2 The effect of captopril in potentiating vagal bradycardia appears to be at the level of vagal neurones, since the bradycardia elicited by the muscarinic agonist, methacholine was unaffected. 3 After the pithed rats were nephrectomized, captopril had no effect on vagally-induced bradycardia, suggesting that the formation of the endogenous angiotensin II responsible for the effect was dependent on renin release from the kidney. 4 When the sympathetic nerves of the pithed rat were electrically stimulated there was a tachycardia, and this was unaffected by captopril. However, when the sympathetic and vagus nerves were activated concurrently, the resulting tachycardia was inhibited by captopril. 5 In pithed guinea-pigs, captopril also potentiated the bradycardia caused by vagal nerve stimulation. This appears to be a tissue-selective effect since the bronchoconstriction due to the vagal stimulation was not affected by captopril. 6 These results suggest that endogenous angiotensin II can have a tonic inhibitory effect on cardiac vagal transmission. Disruption of this mechanism by anti-angiotensin drugs may attenuate the reflex tachycardia associated with the fall in blood pressure in anti-hypertensive therapy.

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Angiotensin-Converting Enzyme Inhibitors in the Treatment of Hypertension

Cited by 59 publications

References 12 publications

Lisinopril pharmacokinetics in chronic renal failure.

Lisinopril pharmacokinetics in chronic renal failure.

Angiotensin II Type 2 Receptor Gene Deficiency Attenuates Susceptibility to Tobacco-Specific Nitrosamine-Induced Lung Tumorigenesis: Involvement of Transforming Growth Factor-β-Dependent Cell Growth Attenuation

A facilitatory effect of anti‐angiotensin drugs on vagal bradycardia in the pithed rat and guinea‐pig

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