Comparison of zofenopril and lisinopril to study the role of the sulfhydryl‐group in improvement of endothelial dysfunction with ACE‐inhibitors in experimental heart failure

Buikema, Hendrik; Monnink, Shj; Tio, R. A.; Crijns, Hjgm; Zeeuw, Dick de; Gilst, Wiek H. van

doi:10.1038/sj.bjp.0703498

Cited by 70 publications

(49 citation statements)

References 34 publications

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“…A putative local effect of Ang-(1-7) would be in line with a previous study, 17 in which 12 days of Ang-(1-7) infusion was found to inhibit restenosis after balloon-catheter injury of carotid arteries. Interestingly, infusing Ang-(1-7) to levels obtained with ACE inhibition 6 yields similar beneficial effects, including reduction of left ventricular end-diastolic pressure, 15 preservation of aortic endothelial function, 14,18 improvement of coronary flow, 14 and reduction of myocyte hypertrophy. 19 On the other hand, differences seem to exist between Ang-(1-7) infusion and ACE inhibition.…”

Section: Discussionmentioning

confidence: 87%

“…14 To examine the effects of Ang-(1-7) treatment on this aspect of cardiac failure, we investigated endothelium-dependent relaxation in isolated aortic rings. Phenylephrine elicited similar contractile responses in all 3 groups (data not shown).…”

Section: Endothelial Functionmentioning

confidence: 99%

“…Sham-operated controls (nϭ10) received saline. After 8 weeks of treatment, hemodynamic studies were performed under isoflurane anesthesia with a microtip pressure transducer, 15 coronary flow was measured in a Langendorff setup, 14 endothelial function was tested in isolated aortic rings, 14 and plasma Ang-(1-7) levels were measured by radioimmunoassay. 16 In the remainder of the text, the maximal rate of change in ventricular pressure is indicated as dP/dt.…”

Section: Experimental Designmentioning

confidence: 99%

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Angiotensin-(1–7) Attenuates the Development of Heart Failure After Myocardial Infarction in Rats

et al. 2002

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Background-The renin-angiotensin system (RAS) is a key player in the progression of heart failure. is thought to modulate the activity of the RAS. Furthermore, this peptide may play a part in the beneficial effects of angiotensin-converting enzyme inhibitors in cardiovascular disease. We assessed the effects of angiotensin-(1-7) on the progression of heart failure. Methods and Results-Male Sprague-Dawley rats underwent either coronary ligation or sham surgery. Two weeks after induction of myocardial infarction, intravenous infusion of angiotensin-(1-7) (24 g/kg per hour) or saline was started by minipump. After 8 weeks of treatment, hemodynamic parameters were measured, endothelial function was assessed in isolated aortic rings, and plasma angiotensin-(1-7) levels were determined. Myocardial infarction resulted in a significant deterioration of left ventricular systolic and diastolic pressure, dP/dt, and coronary flow. Raising plasma levels 40-fold, angiotensin-(1-7) infusion attenuated this impairment to a nonsignificant level, markedly illustrated by a 40% reduction in left ventricular end-diastolic pressure. Furthermore, angiotensin-(1-7) completely preserved aortic endothelial function, whereas endothelium-dependent relaxation in aortas of saline-treated infarcted rats was significantly decreased. Conclusions-Angiotensin-(1-7) preserved cardiac function, coronary perfusion, and aortic endothelial function in a rat model for heart failure.

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Section: Discussionmentioning

confidence: 87%

Section: Endothelial Functionmentioning

confidence: 99%

Section: Experimental Designmentioning

confidence: 99%

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Angiotensin-(1–7) Attenuates the Development of Heart Failure After Myocardial Infarction in Rats

et al. 2002

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“…The area under each individual curve (AUC) was determined (Sigma Plot; SPSS Inc., Chicago, IL) and expressed in arbitrary units. The AUC was used to present total (individual) ACh dilation, and for subsequent analysis of differences in ACh dilation with and without indomethacin (Buikema et al, 2000). Data are expressed as mean Ϯ S.E.M.…”

Section: Methodsmentioning

confidence: 99%

Low Sodium Modifies the Vascular Effects of Angiotensin-Converting Enzyme Inhibitor Therapy in Healthy Rats

Kocks

Gschwend²,

Zeeuw

et al. 2004

J Pharmacol Exp Ther

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Low dietary sodium (LS) increases the effect of angiotensinconverting enzyme (ACE) inhibitor therapy in patients and experimental models, but mechanisms underlying this enhanced efficacy are largely unknown. Because the benefits of ACE inhibition are mediated to a considerable extent by their effect on the vasculature, we studied whether low sodium alters the vascular effects of ACE inhibition. Baseline functional and morphological characteristics, and endothelium-dependent and -independent dilatory responses were studied in isolated perfused small intrarenal and mesenteric arteries obtained from control rats (CON), rats on LS, lisinopril-treated rats (CON-LIS), or rats treated with lisinopril during LS (LS-LIS). We found, first, that LS-LIS compared with CON-LIS enhances blood pressure reduction. Second, interlobar renal arteries had increased lumen diameter and reduced adrenergic contractility in CON-LIS compared with CON, without additional effects of LS. In contrast, mesenteric arteries were not altered in CON-LIS compared with CON, but became triggered for increased myogenic and adrenergic constriction in LS-LIS. Third, LS-LIS decreased acetylcholine (ACh)-induced vasodilation in both mesenteric and renal arteries compared with CON-LIS. During the latter condition, opposite prostaglandins are involved in the endothelial function of the two different vascular beds, i.e., increased involvement of contractile prostaglandins in ACh-induced vasodilatation in renal arteries, versus dilatory prostaglandins in mesenteric arteries. Whether cause or consequence of the enhanced blood pressure response, our data demonstrate a modifying effect of dietary sodium on vascular effects of ACE inhibition. These findings provide a rationale for further studies addressing the mechanism-of-actions of our therapies to find additional strategies to improve therapy response.Intervention in the renin-angiotensin system (RAS) by angiotensin-converting enzyme (ACE) inhibitors has proven to be an effective strategy to improve renal and cardiovascular prognosis in different patient populations. The response to ACE inhibition is modified by sodium intake, with a blunted response during high sodium intake, and an enhanced response during dietary sodium restriction. This occurs irrespective of the underlying disorder and applies to the effect on blood pressure, renal hemodynamic response, and proteinuria (Heeg et al., 1989;Teravainen et al., 1997;Buter et al., 1998), in experimental conditions and as well as in humans (Navis et al., 1987;Wapstra et al., 1996;Wing et al., 1998).Although ACE inhibitors have been studied extensively, the mechanism of the modifying effect of sodium intake on their efficacy is not well understood. The effects of ACE inhibition are believed to result from their hemodynamic actions, as well as from pressure-dependent and -independent effect on the vessel wall. In this respect, many studies showed improved vessel wall structure and dimension, and improved endothelial function in cardiovascular disease afte...

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“…Thiosulfate is used as a treatment for calcifylaxis in patients with end-stage renal disease (111) and has been described as a protective agent in hypertensive heart and renal disease in rats (109,157). Sulfhydrylated ACE inhibitors, such as zofenopril and captopril, show additional beneficial effects in different trials (158). Recently, it was demonstrated that the beneficial effects of sulfhydrylated ACE inhibitors are explained by H 2 S release (159).…”

Section: Future Perspectives and Treatment Optionsmentioning

confidence: 99%

Gasotransmitters in Vascular Complications of Diabetes

et al. 2016

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In the past decades three gaseous signaling molecules—so-called gasotransmitters—have been identified: nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S). These gasotransmitters are endogenously produced by different enzymes in various cell types and play an important role in physiology and disease. Despite their specific functions, all gasotransmitters share the capacity to reduce oxidative stress, induce angiogenesis, and promote vasorelaxation. In patients with diabetes, a lower bioavailability of the different gasotransmitters is observed when compared with healthy individuals. As yet, it is unknown whether this reduction precedes or results from diabetes. The increased risk for vascular disease in patients with diabetes, in combination with the extensive clinical, financial, and societal burden, calls for action to either prevent or improve the treatment of vascular complications. In this Perspective, we present a concise overview of the current data on the bioavailability of gasotransmitters in diabetes and their potential role in the development and progression of diabetes-associated microvascular (retinopathy, neuropathy, and nephropathy) and macrovascular (cerebrovascular, coronary artery, and peripheral arterial diseases) complications. Gasotransmitters appear to have both inhibitory and stimulatory effects in the course of vascular disease development. This Perspective concludes with a discussion on gasotransmitter-based interventions as a therapeutic option.

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Comparison of zofenopril and lisinopril to study the role of the sulfhydryl‐group in improvement of endothelial dysfunction with ACE‐inhibitors in experimental heart failure

Cited by 70 publications

References 34 publications

Angiotensin-(1–7) Attenuates the Development of Heart Failure After Myocardial Infarction in Rats

Angiotensin-(1–7) Attenuates the Development of Heart Failure After Myocardial Infarction in Rats

Low Sodium Modifies the Vascular Effects of Angiotensin-Converting Enzyme Inhibitor Therapy in Healthy Rats

Gasotransmitters in Vascular Complications of Diabetes

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