Key result
A single 50 mg dose of captopril induced significantly less increase in effective renal plasma flow (p<0.02) and fall in renal vascular resistance (p<0.01) in subjects with the DD genotype.
Why the study?
Does the renal hemodynamic response to a single dose of captopril differ according to ACE gene I/D polymorphism in healthy human volunteers?
Observational (n=27)
Does the renal hemodynamic response to a single dose of captopril differ according to ACE gene I/D polymorphism in healthy human volunteers?
p-value: p=<0.02
Intrarenal ACE inhibition by captopril differs according to ACE gene I/D polymorphism in healthy humans, with the DD genotype showing a blunted hemodynamic response.
ACE I/D polymorphism may modulate captopril renal response in healthy subjects; hypothesis-generating and should not yet guide therapy.
We studied the relationship between renal hemodynamic changes induced by a single acute administration of captopril (50 mg p.o.) and angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism in 27 healthy human volunteers, 7 with DD genotype, 10 with ID, and 10 with II genotype. The increase in effective renal plasma flow (p < 0.02) and the fall in renal vascular resistance (p < 0.01) in response to captopril were significantly less in subjects with the DD genotype than in subjects with the other genotypes. These data suggest that intrarenal ACE inhibition by captopril differs according to ACE gene ID polymorphism in healthy humans.
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Mizuiri et al. (2008) conducted an observational in Healthy human volunteers (n=27). Captopril vs. ID and II genotypes was evaluated on Renal hemodynamic changes (effective renal plasma flow and renal vascular resistance) (p=<0.02). A single 50 mg dose of captopril induced significantly less increase in effective renal plasma flow (p<0.02) and fall in renal vascular resistance (p<0.01) in subjects with the DD genotype.
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