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Ann Ital Med Int. 1992 Jul-Sep;7(3):148-52.
[ACE inhibitors and vagal activity: the effect of captopril and lisinopril on cardiovascular reflexes]

[Article in Italian]

Quadri R, Papotti GM, La Grotta A, Maule S, Zanone M, Valentini M, Fonzo D, Chiandussi L.

Cattedra di Medicina Interna, Ospedale San Vito.

The influence of the ACE-inhibitors captopril and lisinopril on parasympathetic activity in normotensive subjects was evaluated. Three cardiovascular tests which explored chiefly parasympathetic function (deep breathing, lying to standing and Valsalva test) were performed in 10 normotensive volunteers (mean age 26.1 years) in both basal conditions and after four days of treatment with either captopril (25 mg twice a day) or lisinopril (20 mg once a day). Mean blood pressure was not influenced by captopril, whereas it was significantly lowered with lisinopril (from 94.4 +/- 6.8 to 88.7 +/- 5.7 mmHg; p < 0.05). Neither drug interfered with heart rate or with the results of the deep breathing and Valsalva tests. The 30/15 ratio, an index of heart rate variability during the lying to standing test, significantly worsened after assumption of both captopril (from 1.37 +/- 0.18 to 1.21 +/- 0.14; p < 0.05) and lisinopril (from 1.31 +/- 0.17 to 1.20 +/- 0.11; p < 0.05). Although our subjects had a lisinopril-induced drop in blood pressure, their heart rate remained steady. This finding confirms previous studies reporting the lack of reflex tachycardia during ACE-inhibition. The slight effect of ACE-inhibitors on the results of deep breathing and Valsalva tests suggests that such drugs do not directly stimulate vagal activity; the significant decrease of the 30/15 ratio may be due to a functional impairment of the baroreflex mechanism.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1333780&dopt=Abstract

path.azg.nl

Long-term renin-angiotensin system blockade is beneficial in a variety of renal diseases. This study examines the long-term (34 weeks) effects of the angiotensin-converting enzyme inhibitor lisinopril and the angiotensin II receptor type I blocker L158,809 in the Fisher to Lewis rat model of chronic renal transplant failure. Treatment in allografted rats with lisinopril or L158,809 was initiated 10 days after transplantation, or at the time when proteinuria exceeded 50 mg/24 h. Untreated allografts and syngrafts served as controls. In contrast to syngrafts, untreated allografts developed proteinuria, hypercholesterolaemia, interstitial damage, and glomerulosclerosis. Lisinopril or L158,809 treatment in allografts starting at day 10 after transplantation completely prevented this, with the exception of interstitial damage, but this treatment also caused a reduction in blood pressure and renal function. Moreover, the intimal surface area of the renal arteries was dramatically increased in allografts treated with either lisinopril or L158,809 compared with untreated allografted rats. Treatment once proteinuria had developed was less effective in preventing glomerulosclerosis, but also caused less intimal expansion. Thus, chronic renin-angiotensin system blockade preserves glomerular morphology in the absence of proteinuria, but enhances intimal hyperplasia and reduces renal function in experimental transplantation. In view of these results, it should be questioned whether such treatment benefits renal transplant patients in the long term. Copyright 2001 John Wiley & Sons, Ltd.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11329151&dopt=Abstract




J Vasc Surg. 2001 May;33(5):1057-64.
Suppression of experimental abdominal aortic aneurysms in the rat by treatment with angiotensin-converting enzyme inhibitors.

Liao S, Miralles M, Kelley BJ, Curci JA, Borhani M, Thompson RW.

Department of Surgery (Section of Vascular Surgery), Washington University School of Medicine, St Louis, MO, USA.

PURPOSE: Pathologic remodeling of the extracellular matrix is a critical mechanism in the development and progression of abdominal aortic aneurysms (AAAs). Although angiotensin-converting enzyme (ACE) inhibitors are known to alter vascular wall remodeling in other conditions, their effects on AAAs are unknown. In this study we assessed the effect of ACE inhibitors in a rodent model of aneurysm development. METHODS: Male Wistar rats underwent transient aortic perfusion with porcine pancreatic elastase, followed by treatment with one of three ACE inhibitors (captopril [CP], lisinopril [LP], or enalapril [EP]), an angiotensin (AT)1 receptor antagonist (losartan [LOS]), or water alone (9 rats in each group). Blood pressure and aortic diameter (AD) were measured before elastase perfusion and on day 14, with an AAA defined as an increase in AD (DeltaAD) of more than 100%. The structural features of the aortic wall were examined by means of light microscopy. RESULTS: Aneurysmal dilatation consistently developed within 14 days of elastase perfusion in untreated rats, coinciding with the development of a transmural inflammatory response and destruction of the elastic media (mean DeltaAD, 223% +/- 28%). All three ACE inhibitors prevented AAA development (mean DeltaAD: CP, 67% +/- 4%; LP, 18% +/- 12%; and EP, 14% +/- 3%; each P <.05 vs controls). ACE inhibitors also attenuated the degradation of medial elastin without diminishing the inflammatory response. Surprisingly, the aneurysm-suppressing effects of ACE inhibitors were dissociated from their effects on systemic hemodynamics, and LOS had no significant effect on aneurysm development compared with untreated controls (mean DeltaAD, 186% +/- 19%). CONCLUSION: Treatment with ACE inhibitors suppresses the development of elastase-induced AAAs in the rat. Although this is associated with the preservation of medial elastin, the mechanisms underlying these effects appear to be distinct from hemodynamic alterations alone or events mediated solely by AT1 receptors. Further studies are needed to elucidate how ACE inhibitors influence aortic wall matrix remodeling during aneurysmal degeneration.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11331849&dopt=Abstract












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