Arterial endothelial permeability and vascular disease the “trap door” effect

Robertson, Abel L.; Khairallah, Philip A.

doi:10.1016/0014-4800(73)90022-1

Cited by 95 publications

(20 citation statements)

References 19 publications

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“…(3) Metabolic changes: Captopril may have beneficial effects on postischemic tissue damage because of its ability (provided by the sulfhydryl group) to scavenge highly toxic free radicals, by its antagonism of the leukotactic effect of angiotensin,s and by its beneficial action on interendothelial cell junctions and endothelial permeability. 28 In AMI, the effects of ACE inhibitors are likely to be due not only to a general plasmatic but also to a local inhibition of the renin-angiotensin system. In addition, the potentiation of local kinin effects,29 a bradykinin-induced stimulation of prostacyclin biosynthesis, a tissue plasminogen activator, and an endothelium-derived relaxing factor30 may also be involved.…”

Section: -mentioning

confidence: 99%

Captopril in acute myocardial infarction: Beneficial effects on infarct size and arrhythmias

Bussmann

Micke

Hildenbrand

et al. 1995

Clinical Cardiology

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Summary:It is known from experiments that angiotensinconverting enzyme inhibitors can limit infarct size. In a prospective. randomized, placebo-controlled double-blind study, 22 patients were given 1.5-2.0 mg captoprilh I.V., while 24 patients were given placebo. Medication was started between 2 and I8 h from the onset of infarction. The two groups were matched for age, infarct location, and time of intervention. With the exception of one patient in either group, all were concurrently given nitroglycerin. The necrosis parameters were provided by the quantitative measurement of the QRS complex. The Q wave decreased with captopril treatment (-0.003 mV), but increased with placebo (+0.14 mV, p < 0.05). The number of ventricular premature beats at 24 h from the start of treatment was 2 5 h with placebo, and 9/h with captopril (p < 0.02). Ventricular fibrillation occurred seven times in the placebo group, but did not occur in the captopril group. The creatine kinase infarct weight was 59 gram-equivalents (gEq) with placrebo, and 45 gEq with captopril (p = NS). Mean arterial pressure was reduced by 12 mmHg with captopril treatment. The results show a beneficial effect of captopril on infarct size and electrical instability, over and above the effect of standard management with nitroglycerin and thrombolysis.

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Section: -mentioning

confidence: 99%

Captopril in acute myocardial infarction: Beneficial effects on infarct size and arrhythmias

Bussmann

Micke

Hildenbrand

et al. 1995

Clinical Cardiology

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“…The following vasoactive agents were used in this study: prostaglandins Ej and F-, a , 2 8-Ala-AII (5),* 4-His-6-Tyr-AII(6), 3 4-Phe-8-Ala-AII(7),» 1-succinic acid (Suc)-4-Phe-8-Tyr-AII (7), :! and 4-Phe-8-Tyr-AII (8) •'Synthesized in our laboratory by Dr. M. C. Khosla in collaboration with Drs.…”

Section: Robertson Khairallahmentioning

confidence: 99%

Effects of Angiotensin II and Some Analogues on Vascular Permeability in the Rabbit

Robertson

Khairallah

1972

Circulation Research

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127

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“…A wide variety of biologic activities has been attributed to angiotensin II, including hemodynamic effects such as elevation of blood pressure (15), decreased mesenteric blood flow in cats, dogs, and humans (16)(17)(18)(19), and reduced blood flow and vasoconstriction in perfused limbs of rabbits, cats and dogs (16,20). Angiotensin II enhances vascular permeability (21,22) and induces widening of interendothelial cell spaces in aortic, coronary, mesenteric, and peripheral arteries (16,21,(23)(24)(25). In addition, this peptide is dipsogenic when administered into the central nervous system of rat (26) and stimulates aldosterone secretion from the adrenal cortex (27,28).…”

Section: Discussionmentioning

confidence: 99%

A human neutrophil-dependent pathway for generation of angiotensin II. Purification of the product and identification as angiotensin II.

Wintroub¹,

Klickstein²,

Watt³

1981

J. Clin. Invest.

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A B S T R A C T A human neutrophil lysosomal protease interacts at physiologic pH with a 62,000-67,000-mol wt plasma protein substrate to generate a vasoactive, smooth muscle-contracting "neutral" peptide. The peptide product of this system, previously designated the "neutral" peptide-generating pathway, was generated from purified components and purified by Bio-Gel P2 gel filtration and reverse-phase high performance liquid chromatography with a 50-60% yield of starting activity. The purified peptide had an amino acid composition of Asx, Pro, Val, Ile, Tyr, Phe, His, Arg, a composition identical to that of angiotensin II. The peptide and synthetic angiotensin II each filtered at 48-52% bed volume on Bio-Gel P2, had an isoelectric point of pH 7.8-8.1 at 4°C, migrated 3 cm toward the cathode during pH 6.4 low-voltage paper electrophoresis, and had a retention time of 44.8 min during reverse-phase high-performance liquid chromatography. In addition, the functional activity of the peptide at each purification step correlated with angiotensin II content determined by specific radioimmunoassay. The amino acid sequence of 25 nmol of the peptide was Asp-Arg-Val-Tyr-Ile-His-Pro-Phe, the same covalent structure as that ofangiotensin II. Therefore, under

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Arterial endothelial permeability and vascular disease the “trap door” effect

Cited by 95 publications

References 19 publications

Captopril in acute myocardial infarction: Beneficial effects on infarct size and arrhythmias

Captopril in acute myocardial infarction: Beneficial effects on infarct size and arrhythmias

Effects of Angiotensin II and Some Analogues on Vascular Permeability in the Rabbit

A human neutrophil-dependent pathway for generation of angiotensin II. Purification of the product and identification as angiotensin II.

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