February 1, 1991Circulation
Endothelin-1-induced vasoconstriction in humans. Reversal by calcium channel blockade but not by nitrovasodilators or endothelium-derived relaxing factor.
Key result
Endothelin-1 induces vasodilation at low doses and vasoconstriction at high doses; calcium channel blockade converts high-dose ET-induced vasoconstriction to vasodilation (P<0.05).
Why the study?
Do calcium channel blockers, nitrovasodilators, or endothelium-derived relaxing factor reverse endothelin-1-induced vasoconstriction in healthy volunteers?
Population
25 healthy volunteers
Comparison
Brachial artery infusions of endothelin-1 at low… vs Endothelin-1 infusion alone
Design
Other
Authors
Discussion
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Implication
Hypothesis-generating for calcium channel blockade in endothelin-mediated vasoconstriction; leaves open clinical translation in patients.
Structured PICO
Do calcium channel blockers, nitrovasodilators, or endothelium-derived relaxing factor reverse endothelin-1-induced vasoconstriction in healthy volunteers?
P
Population
25 healthy volunteers who received brachial artery infusions to investigate the vascular effects of endothelin-1.
I
Intervention
Brachial artery infusions of endothelin-1 (ET) at low (0.5 ng/min/100 ml) and high (25 and 50 ng/min/100 ml) dosages, alone and in combination with sodium nitroprusside, acetylcholine, nifedipine, or verapamil
C
Comparator
Endothelin-1 infusion alone
O
Outcome
Forearm blood flow and forearm vascular resistancesurrogate
Blockade of voltage-operated calcium channels, but not cyclic GMP-dependent vasodilation, prevents endothelin-1-induced vasoconstriction in human resistance vessels.
Cite This Study
Kiowski et al. (1991) studied Healthy volunteers (n=25). Endothelin-1 infusion vs. Baseline was evaluated on Forearm blood flow and forearm vascular resistance. Endothelin-1 induces vasodilation at low doses and vasoconstriction at high doses; calcium channel blockade converts high-dose ET-induced vasoconstriction to vasodilation (P<0.05).