Why the study?
Does captopril pretreatment reduce adenosine-induced renal vasoconstriction in normotensive patients?
Does captopril pretreatment reduce adenosine-induced renal vasoconstriction in normotensive patients?
Inhibition of the angiotensin-converting enzyme with captopril blunts the vasoconstrictive effect of adenosine on renal microcirculation in humans.
Captopril may blunt adenosine-induced renal vasoconstriction; hypothesis-generating in Level 5 evidence and leaves open clinical relevance.
We sought to evaluate the possible interaction between the adenosine and angiotensin systems in the regulation of renal microcirculation in humans. Twenty normotensive patients entered the study. Ten patients (group 1) were pretreated with 50 mg of captopril, an inhibitor of angiotensin-converting enzyme, whereas 10 patients (group 2) were pretreated with placebo. Incremental doses of adenosine (from 10(-5) to 1 mg) were injected into a renal artery to all patients at 5-min intervals. Adenosine injection reduced mean renal blood flow velocity in both groups (from 17.3+/-2.8 and 16.7+/-2 cm/s to 5.1+/-1.1 and 3.8+/-0.8 cm/s, in groups 1 and 2, respectively). The decrease in flow velocity was immediate after adenosine, and its duration was proportional to dosage (y = 3.05 x -2.7; R2 = 0.46; p < 0.01). However, group 1 had a slope of regression lower than group 2 (2.37 vs. 3.82 s; p < 0.03). The index of renal resistance (mean arterial pressure/mean blood flow velocity) increased linearly in both groups with adenosine, but group I showed a lower slope of increment (2.77 vs. 5.57 mm Hg/cm/s; p < 0.01). Adenosine administration induced a marked and transient increase in human renal resistance. This vasoconstrictive effect of adenosine was blunted by captopril pretreatment.
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Marraccini et al. (2000) studied this question.
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