Vasomotor responses in cyclosporin A-treated rats after chronic angiotensin blockade. Chronic angiotensin II infusion but not bradykinin blockade abolishes the antiproteinuric response to angiotensin-converting enzyme inhibition in established adriamycin nephrosis. Angiotensin-converting enzyme and myocardial fibrosis in the rat receiving angiotensin II or aldosterone. Rx drugs

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Hypertension. 1994 Jun;23(6 Pt 2):832-7.
Vasomotor responses in cyclosporin A-treated rats after chronic angiotensin blockade.

Auch-Schwelk W, Duske E, Hink U, Betz M, Unkelbach M, Fleck E.

Department of Cardiology, German Heart Institute Berlin.

Chronic angiotensin-converting enzyme (ACE) inhibition prevents endothelial dysfunction in hypertension and hypercholesterolemia. Long-term treatment with cyclosporin A impairs endothelium-dependent relaxations and augments contractions to angiotensin II in the rat aorta. The present study compares vasomotor responses to several vasoconstrictor and dilator stimuli after 6 weeks of oral treatment with either the angiotensin-converting enzyme inhibitor lisinopril (10 mg/kg per day), the angiotensin subtype 1 receptor antagonist D 8731 (10 mg/kg per day), cyclosporin A (15 mg/kg per day), or a combination of cyclosporin A with lisinopril or D 8731 (n = 15 rats per group). Twenty-four hours after the last treatment, aortic rings were mounted in organ chambers for measurement of isometric force. Endothelium-dependent relaxations to acetylcholine and calcium ionophore were impaired by cyclosporin A but not affected by the vasodilators. Cyclosporin A-induced endothelial dysfunction was prevented by cotreatment with lisinopril or D 8731. Relaxations to nitroglycerin, SIN-1, and forskolin were not affected by any treatment. Contractions to phenylephrine and serotonin were reduced by lisinopril but not by D 8731. In contrast, contractions to angiotensin II were augmented by cyclosporin A, lisinopril, and the combination of both but not by D 8731 or D 8731 plus cyclosporin A. The data suggest a role for angiotensin II in cyclosporin A-induced endothelial dysfunction. Chronic ACE inhibition reduces overall smooth muscle contractility. The selective augmentation of angiotensin II effects by ACE inhibition and cyclosporin A suggests upregulation of angiotensin receptors in the aortic smooth muscle by these treatments. Chronic angiotensin subtype 1 receptor blockade does not appear to affect angiotensin receptor function.

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J Am Soc Nephrol. 2000 Mar;11(3):490-6.
Chronic angiotensin II infusion but not bradykinin blockade abolishes the antiproteinuric response to angiotensin-converting enzyme inhibition in established adriamycin nephrosis.

Wapstra FH, Navis G, de Jong PE, de Zeeuw D.

Groningen Institute of Drug Studies, Division of Nephrology, University Hospital and Groningen School of Medicine, The Netherlands.

Angiotensin-converting enzyme (ACE) inhibition reduces proteinuria in established adriamycin nephrosis. To investigate whether the reduction in proteinuria is due to decreased generation of angiotensin II (AngII) or to decreased degradation of bradykinin, four series of experiments in established adriamycin nephrosis were performed. In the first series, 2 mg/kg lisinopril reduced BP from 117 +/- 4 to 67 +/- 2 mmHg and proteinuria from 335 +/- 66 to 57 +/- 10 mg/24 h after 2 wk of treatment. Subsequent continuous intraperitoneal infusion of AngII (250 ng/kg per min) for 2 wk partially restored proteinuria to 180 +/- 42 mg/24 h, whereas BP increased to 97 +/- 3 mmHg. Subsequent withdrawal of AngII restored the antiproteinuric effects of lisinopril, whereas subsequent withdrawal of lisinopril restored proteinuria to pretreatment values. In the second series, AT1 receptor blockade induced a fall in BP and proteinuria similar to that by lisinopril. In the third series, lisinopril reduced BP from 121 +/- 5 to 68 +/- 2 mmHg and proteinuria from 355 +/- 90 to 101 +/- 10 mg/24 h. Subsequent intraperitoneal infusion of bradykinin antagonist (HOE 140; 1 mg/kg per 24 h) for 2 wk did not affect BP (72 +/- 2 mmHg) or proteinuria (92 +/- 15 mg/24 h). In the fourth series, bradykinin (3 mg/kg per 24 h) was infused for 2 wk to mimic decreased bradykinin breakdown. This did not affect proteinuria, but induced a fall in BP from 114 +/- 3 to 93 +/- 4 mmHg. The BP-lowering effect of exogenous bradykinin was completely reversed by 1 wk infusion of HOE 140 (93 +/- 4 to 113 +/- 4 mmHg), while proteinuria remained unchanged. In conclusion, the antiproteinuric effect of ACE inhibition appears to be independent of bradykinin in this model, supporting a main role for reduction of AngII in the antiproteinuric action of ACE inhibition.

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J Lab Clin Med. 1993 Oct;122(4):395-403.
Angiotensin-converting enzyme and myocardial fibrosis in the rat receiving angiotensin II or aldosterone.

Sun Y, Ratajska A, Zhou G, Weber KT.

Department of Internal Medicine, University of Missouri-Columbia.

Angiotensin-converting enzyme (ACE) is present in tissues composed largely of fibrillar collagen such as heart valves, the adventitia of great vessels and intramyocardial coronary arteries, and the scar that follows myocardial infarction. We tested the hypothesis that such tissue ACE is related to fibrous tissue formation and that its appearance is independent of circulating renin and angiotensin peptides. For this purpose we selected experimental models that simulate primary and secondary hyperaldosteronism, each of which are associated with the appearance of myocardial fibrosis. ACE in the excised heart and aorta was localized by in vitro autoradiography with [125I]351A, while fibrosis was identified by light microscopy in sections stained with collagen specific picrosirius red. Tissue was obtained at 2, 4, and 6 weeks from various experimental groups: unoperated, untreated, age- and sex-matched controls; age- and sex-matched uninephrectomized control rats on a high sodium diet; and rats that had received either aldosterone (ALDO) or angiotensin II (AII). Compared with controls, we found ACE binding (1) unchanged after 2 weeks of ALDO, but increased in the adventitia of intramural coronary arteries after 4 weeks, in keeping with the perivascular fibrosis that appeared in each ventricle; (2) markedly increased after 6 weeks of ALDO, where it not only involved coronary vessels but also microscopic scars that appeared in atria and ventricles; (3) increased in the coronary adventitia and sites of scarring, each of which were present 2 weeks after AII; and (4) markedly increased after 4 and 6 weeks of AII as fibrosis became more extensive.(ABSTRACT TRUNCATED AT 250 WORDS)

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