Clinical experiences with trandolapril

Gaillard, CA; Leeuw, Peter W. de

doi:10.1016/0002-8703(93)90453-g

Cited by 13 publications

(2 citation statements)

References 18 publications

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“…Both systolic and diastolic blood pressures were signi®cantly reduced in the present patients, but somewhat unexpectedly by a similar degree in both groups. Serum trandolapril concentrations con®rmed that the active drug was only administered to group T and would be expected to reduce blood pressure [35]. Apart from regression to the mean, there is no clear reason why the blood pressure should have fallen quite so dramatically during the placebo treatment.…”

Section: Discussionmentioning

confidence: 99%

Insulin sensitivity in hypertensive Type 2 diabetic patients after 1 and 19 days' treatment with trandolapril

2000

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Section: Discussionmentioning

confidence: 99%

Insulin sensitivity in hypertensive Type 2 diabetic patients after 1 and 19 days' treatment with trandolapril

2000

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“…After completing these basal investigations the patients were randomized, in a double blind manner, to receive placebo (P), trandolapril 0.5 mg once daily (L) or trandolapril 4 mg daily (H). Trandolapril 4 mg day ±1 causes systemic hypotension whereas 0.5 mg day ±1 does not reduce systemic blood pressure but may affect renal haemodynamics [22]. After 10 days' treatment the renal clearances and metabolic parameters were remeasured.…”

Section: Methodsmentioning

confidence: 99%

Renal autoregulation is normal in newly diagnosed, normotensive, NIDDM patients

1998

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Abnormalities of renal autoregulation with glomerular hyperfiltration and raised intraglomerular pressure have been suggested as important factors in the initiation and development of diabetic nephropathy. Angiotensin converting enzyme (ACE) inhibition appears to have a specific reno-protective role in diabetic nephropathy, possibly by reducing intraglomerular pressure. The acute effects of ACE inhibition on renal haemodynamics in normotensive, non-insulin-dependent diabetes mellitus (NIDDM) have not been previously reported. We measured simultaneous glomerular filtration rate (GFR) and renal plasma flow (RPF) in 29 (4 female) subjects, mean age 52 years (range 27-70), using 51Cr EDTA and 125I Hippuran. Clearances were corrected to 1.73 m(-2). All patients were normotensive (blood pressure < 75th centile for age and sex), newly diagnosed (< 30 days), taking no antihypertensive or hypoglycaemic medication. Subjects were randomly allocated (double blind) to receive the ACE inhibitor trandolapril 4mg day(-1) (H) (hypotensive dose), trandolapril 0.5 mg day(-1)(L) (non-hypotensive dose) or placebo (P) for 10 days after which renal haemodynamics were remeasured. For all subjects baseline GFR, RPF and filtration fraction (FF) were 97+/-21 ml min(-1) mean+/-SD, 439+/-120 ml min(-1) and 22.3+/-2.9 % respectively. Glomerular hyperfiltration (GFR> 120 ml min[-1]) was only demonstrated in 3 subjects (10.3 %). In group H mean arterial pressure (103+/-8 vs 93+/-9 mmHg, p < 0.001) and FF (23.8+/-2.3 vs 20.0+/-4.0%, p = 0.03) fell while RPF increased (376+/-111 vs 426+/-60 ml min(-1), p = 0.02), there was no significant change in GFR. No significant change in mean arterial pressure, GFR, RPF or FF occurred in groups P and L. These studies suggest that in newly diagnosed normotensive NIDDM subjects normal renal autoregulation occurs and glomerular hyperfiltration is uncommon.

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