ACE inhibitors improve endothelial function in type 1 diabetic patients with normal arterial pressure and microalbuminuria.

Arcaro, Guido; Zenere, B. M.; Saggiani, F.; Zenti, Maria Grazia; Monauni, Tiziano; Lechi, Alessandro; Muggeo, Michele; Bonadonna, Riccardo C.

doi:10.2337/diacare.22.9.1536

Cited by 66 publications

(54 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Not surprisingly, rat, STZ, 5-26w Heart serotonin; SNPÖ vitamin E 5-26w (T) SOD (P) Quilley et al, 1996 rat, STZ, 4-6w Heart BK; ARI 4-6w (T) COX blockade (N) Fulton et al, 1996 rat, STZ, 4-6w Kidney ACh;, BK; SNPÖ L-arginine (P) COX blockade (N) negative results were generally obtained in patients with normoalbuminuria and relatively good metabolic control (Smits et al, 1993;Lambert et al, 1996;Enderle et al, 1998). When microalbuminuric patients were included in the study population, impaired endothelium-dependent vasodilatation was consistently reported (Zenere et al, 1995;Clarkson et al, 1996;Lekakis et al, 1997;Arcaro et al, 1999). Studies investigating endothelial function in animal models of type II diabetes are scarce and have yielded con¯icting results.…”

Section: Experimental and Clinical Evidence For The Presence Of Impaimentioning

confidence: 90%

“…Similarly, ACE inhibition improved endothelium-dependent vasodilatation in type I and type II diabetes patients without a ecting the response to nitrovasodilators (Bijlstra et al, 1995;O'Driscoll et al, 1997;Arcaro et al, 1999), but other authors did not con®rm these ®ndings (Mullen et al, 1998;McFarlane et al, 1999) (Table 2B). Although the mechanisms responsible for the bene®cial e ects of ACE inhibitors have not been settled, a number of potential explanations have been put forward.…”

Section: Endothelial Dysfunction As a Therapeutic Targetmentioning

confidence: 98%

See 1 more Smart Citation

Endothelial dysfunction in diabetes

Vriese

Verbeuren

Voorde

et al. 2000

British J Pharmacology

1,015

769

View full text Add to dashboard Cite

Endothelial dysfunction plays a key role in the pathogenesis of diabetic vascular disease. The endothelium controls the tone of the underlying vascular smooth muscle through the production of vasodilator mediators. The endothelium-derived relaxing factors (EDRF) comprise nitric oxide (NO), prostacyclin, and a still elusive endothelium-derived hyperpolarizing factor (EDHF). Impaired endothelium-dependent vasodilation has been demonstrated in various vascular beds of di erent animal models of diabetes and in humans with type 1 and 2 diabetes. Several mechanisms of endothelial dysfunction have been reported, including impaired signal transduction or substrate availibility, impaired release of EDRF, increased destruction of EDRF, enhanced release of endothelium-derived constricting factors and decreased sensitivity of the vascular smooth muscle to EDRF. The principal mediators of hyperglycaemia-induced endothelial dysfunction may be activation of protein kinase C, increased activity of the polyol pathway, non-enzymatic glycation and oxidative stress. Correction of these pathways, as well as administration of ACE inhibitors and folate, has been shown to improve endothelium-dependent vasodilation in diabetes. Since the mechanisms of endothelial dysfunction appear to di er according to the diabetic model and the vascular bed under study, it is important to select clinically relevant models for future research of endothelial dysfunction.

show abstract

Section: Experimental and Clinical Evidence For The Presence Of Impaimentioning

confidence: 90%

Section: Endothelial Dysfunction As a Therapeutic Targetmentioning

confidence: 98%

Endothelial dysfunction in diabetes

Vriese

Verbeuren

Voorde

et al. 2000

British J Pharmacology

1,015

769

View full text Add to dashboard Cite

show abstract

“…A limited number of studies have shown that ACE inhibitors and AT 1 antagonist can improve endothelial-dependent vasodilator function in brachial and femoral arteries in patients with Type 1 or Type 2 diabetes [14,15,16]. While endothelium-dependent vasodilatory response induced by acetylcholine (ACh) has been shown in isolated retinal arteries [17], the effects of diabetes and RAS inhibition on vascular autoregulation in the retina in vivo have not yet been described.…”

mentioning

confidence: 99%

Angiotensin AT 1 receptor antagonism normalizes retinal blood flow and acetylcholine-induced vasodiliation in normotensive diabetic rats

et al. 2004

View full text Add to dashboard Cite

Aims/hypothesis. The renin angiotensin system is emerging as a potential therapeutic target for diabetic retinopathy. This study examines the effects of angiotensin-converting-enzyme inhibition by captopril and angiotensin AT 1 receptor antagonism using candesartan-cilexetil on retinal blood flow and acetylcholinestimulated vasodilatation in normotensive diabetic rats. Methods. Non-diabetic or streptozotocin-induced diabetic rats were treated for 2 weeks with captopril (100 mg/kg/day) or candesartan cilexetil (2 mg/kg/day). Retinal haemodynamics were measured using video fluorescein angiography. Effects of exogenous acetylcholine on retinal haemodynamics were examined following intravitreal injection. Total retinal diacylglycerol was labelled using diacylglycerol kinase, separated by thin-layer chromatography, and quantified using autoradiography. Results. Diabetic rats had prolonged retinal mean circulation time and decreased retinal blood flow compared with non-diabetic rats. Treatment of diabetic rats with either captopril or candesartan blocked the development of these blood flow abnormalities. Intraviteral injection of acetylcholine (10 −5 mol/l) in non-diabetic rats increased retinal blood flow by 53.9±22.0% relative to baseline whereas this response to acetylcholine was blunted in diabetic rats (4.4±19.6%, p<0.001). Candesartan treatment of diabetic rats restored the acetylcholine-stimulated retinal blood flow response to 60.0±18.7% compared with a 56.2+20.1% response in candesartan-treated non-diabetic rats. Total retinal diacylglycerol levels were increased in diabetic rats (3.75±0.98 nmol/mg, p<0.05) compared with non-diabetic rats (2.13±0.25 nmol/mg) and candesartan-treatment of diabetic rats normalized diacylglycerol levels (2.10±0.25 nmol/mg, p<0.05). Conclusion/interpretation. This report provides evidence that angiotensin-converting enzyme inhibition and AT 1 receptor antagonism ameliorates retinal haemodynamic dysfunctions in normotensive diabetic rats. [Diabetologia (2004) 47:113-123]

show abstract

“…Özellikle mikroalbüminürililerde bu bozulma daha belirgindir. [16] Ayr›ca, tip 1 DM'de mikroalbüminürinin varl›¤›, kardiyovasküler hastal›k-lar› (KVH) ve koroner arter hastal›klar› (KAH) için de risk faktörü olarak bildirilmifltir. [15] Mikroalbüminürinin ve sessiz iskeminin birlikteli¤i gösterilmifltir.…”

Section: Hipergliseminin Neden Oldu¤u Mikrovasküler De¤iflikliklerunclassified

“…[15] Mikroalbüminüri erken vasküler hasar›n, nefropatinin ve kardiyovasküler komplikasyonlar›n belirleyicisidir. [16] Küçük dozlarda al›nan ACEI'nin kan bas›nc›n› düflürmeden albüminüriyi azaltt›¤›, [15] bu azalman›n ilk alt› ay içinde %52 oran›nda gerçekleflti¤i gösterilmifltir. [39] Di¤er antihipertansiflerle karfl›laflt›r›ld›¤›nda hem kan bas›nc›-n›, hem de proteinüriyi düflürmede daha etkili oldu¤u bulunmufltur.…”

Section: D‹yabette H‹pertans‹yonun Tedav‹s‹unclassified

Diabetes mellitus and hypertension

Tuğrul¹

1999

PharmacoEcon Outcomes News

View full text Add to dashboard Cite

Diabetes Mellitus and Hypertension Arma¤an TU⁄RULHipertansiyon tüm dünyada önemli bir sa¤l›k sorunudur. Diyabetlilerde hipertansiyon s›kl›¤›, diyabetli olmayanlardan 1.5-2 kat yüksektir. Tip 1 diyabette geliflen hipertansiyon patogenezinden diyabetik nefropati sorumludur. Tip 2 diyabette ise hipertansiyon patogenezi multifaltöriyeldir. Diyabetlilerde hipertansiyon tedavisi için çeflitli olumlu etkileri nedeniyle ilk seçenek olarak, ACE inhibitörleri öneril-mektedir. Bu yaz›da, diyabet ve hipertansiyon iliflkisi, diyabetlilerdeki hipertansiyonun epidemiyolojisi, patogenezi ve tedavi konular›ndaki bilgiler gözden geçirildi.Anahtar Sözcükler: Antihipertansif ajanlar; diabetes mellitus/komplikasyon/ilaç tedavisi; hipertansiyon; komplikasyon/ilaç tedavisi; risk faktörleri.Hypertension is a major worldwide health problem. Its prevalence is 1.5-2 times higher in diabetic population than that in non-diabetic individuals. Its pathogenesis depends on diabetic nephropathy in type 1, whereas may be multifactorial in type 2 diabetes mellitus. In diabetics, angiotensin converting enzyme inhibitors are most widely preferred in the treatment of hypertension because of their numerous desirable effects. In this article, the most recent data are presented on the relationship between diabetes mellitus and hypertension, and on the epidemiology, pathogenesis, and treatments of hypertension in diabetic patients.

show abstract

ACE inhibitors improve endothelial function in type 1 diabetic patients with normal arterial pressure and microalbuminuria.

Cited by 66 publications

References 0 publications

Endothelial dysfunction in diabetes

Endothelial dysfunction in diabetes

Angiotensin AT 1 receptor antagonism normalizes retinal blood flow and acetylcholine-induced vasodiliation in normotensive diabetic rats

Diabetes mellitus and hypertension

Contact Info

Product

Resources

About