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Lisinopril improves endothelial dysfunction in hypertensive NIDDM subjects with diabetic nephropathy
F S Nielsen1, P Rossing, M A Gall
1Steno Diabetes Center, Gentofte, Denmark.
Insights
Lisinopril improved endothelial function and reduced albuminuria in hypertensive patients with type 2 diabetes and kidney disease, unlike atenolol. This suggests lisinopril offers both kidney and blood vessel protection.
Area of Science:
- Cardiology
- Nephrology
- Endocrinology
Background:
- Endothelial dysfunction is common in non-insulin dependent diabetes mellitus (NIDDM) with hypertension and albuminuria, contributing to cardiovascular disease.
- Cardiovascular disease is a leading cause of morbidity and mortality in NIDDM patients.
- Diabetic nephropathy is a significant complication associated with increased cardiovascular risk.
Purpose of the Study:
- To compare the effects of angiotensin-converting enzyme (ACE) inhibition with lisinopril versus conventional antihypertensive treatment with atenolol on endothelial dysfunction.
- To evaluate whether lisinopril could ameliorate endothelial dysfunction more effectively than atenolol in hypertensive NIDDM patients with diabetic nephropathy.
- To assess the impact of lisinopril and atenolol on blood pressure, albuminuria, and endothelial function markers.
Main Methods:
- A 12-month prospective, randomized, double-blind, parallel study.
- Involved 43 hypertensive NIDDM patients with diabetic nephropathy.
- Measured 24-h ambulatory blood pressure (ABP), transcapillary escape rate of albumin (TERalb), serum von Willebrand factor (vWF), and urinary albumin excretion rate (UAE).
Main Results:
- Both lisinopril and atenolol equally reduced mean ambulatory blood pressure.
- Lisinopril significantly decreased TERalb (a marker of endothelial function), while atenolol increased it (p=0.015).
- Urinary albumin excretion rate (UAE) was reduced by 45% with lisinopril versus 10% with atenolol (p=0.014).
Conclusions:
- Lisinopril demonstrated reno- and vasculoprotective properties in hypertensive NIDDM patients with diabetic nephropathy.
- ACE inhibition with lisinopril appears more beneficial for endothelial function and albuminuria than atenolol in this patient population.
- These findings highlight the potential of lisinopril in managing cardiovascular risk in diabetic nephropathy.
Abstract:
Endothelial dysfunction is a prevalent phenomenon in non-insulin dependent diabetic (NIDDM) patients with hypertension and albuminuria, and may contribute to the development and progression of cardiovascular disease, which is the main cause of the high morbidity and mortality observed in these patients. Therefore the aim of our study was to evaluate whether inhibition of angiotensin-converting enzyme (with lisinopril 10-20 mg day-1) could ameliorate endothelial dysfunction more than reducing blood pressure with conventional antihypertensive treatment (atenolol 50-100 mg day-1), usually in combination with a diuretic. We performed a 12-month prospective, randomized, double-blind, parallel study in 43 hypertensive NIDDM patients with diabetic nephropathy (21 treated with lisinopril and 22 with atenolol). The following variables were measured: 24-h ambulatory blood pressure (ABP); transcapillary escape rate of albumin (TERalb; i.e. initial disappearance of intravenously injected 125I-labelled human serum albumin); serum concentrations of von Willebrand factor (vWF), using ELISA, and urinary albumin excretion rate (UAE). Data are presented for 32 patients (16 lisinopril and 16 atenolol; age 60 years, SD 8; 25 males) out of 35 who completed the study and had valid measurements of TERalb. At baseline the two groups were comparable; TERalb (8.5 (SEM 0.6) vs. 7.2 (0.4)%); vWF (2.09 (range 0.82-4.34) vs. 1.97 (0.95-3.86) IU ml-1; UAE 916 (x/divided by antilog SEM 1.3) vs. 1444 (1.2), and mean ABP 110 (SEM 3) vs. 113 (2) mmHg, in the lisinopril and atenolol group, respectively. During follow up, the mean ABP was equally reduced in the lisinopril and atenolol group, by 12 (SEM 2) vs. 10 (2) mmHg, respectively, TERalb decreased in the lisinopril group by 0.6 (SEM 0.7)%, whereas it increased in the atenolol group 1.5 (0.5)%; the mean difference was 2.2% (95% CI, 0.5 to 3.9; p = 0.015). UAE was reduced by 45% (95% CI, 25 to 60) in the lisinopril group vs. 10% (-15 to 30) in the atenolol group (p = 0.014). Serum vWF was not changed during follow up in either group. Our study suggests that lisinopril has both reno- and vasculoprotective properties in hypertensive NIDDM patients with diabetic nephropathy.