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- W2076309035 abstract "This study concerned the effects and mechanisms of action of endothelin-1 on the cerebral circulation. Cerebral blood flow was electromagnetically measured in awake goats. Endothelin-1 (0.01–0.3 nmol) produced dose-dependent decreases in this flow (maximal reduction=34%) and increases in cerebrovascular resistance (maximal increase=74%) (P<0.01). IRL 1620 (Suc-[Glu9, Ala11,15]endothelin-1-(8–21), agonist for endothelin ETB receptors, 0.01–0.3 nmol) slightly decreased cerebral blood flow. The effects of endothelin-1, but not those of IRL 1620, on cerebral blood flow were diminished by 50% during infusion of the antagonist for endothelin ETA receptors, BQ-123 (cyclo-(d-Asp–Pro–d-Val–Leu–Trp), 2 nmol min−1), but not affected during infusion of the antagonist for endothelin ETB receptors, BQ-788 (N-[N-[N-[(2,6-dimethyl-1-piperidinyl)carbonyl]-4-methyl-l-Leucyl-1-(methoxycarbonyl)-d-tryptophyl]-d-norleucine monosodium), 2 nmol min−1). Intravenous administration of NW-nitro-l-arginine methyl ester (l-NAME, 47 mg kg−1) or NW-nitro-l-arginine (l-NNA, 47 mg kg−1) reduced basal cerebral blood flow by 39 and 33%, increased cerebrovascular resistance by 108 and 98% and mean arterial pressure by 23 and 17%, and decreased heart rate by 27 and 25%, respectively (all at least P<0.05). The increases in cerebrovascular resistance (as absolute values) induced by endothelin-1 were not affected during either l-NAME or l-NNA (as absolute values and percentages). Intravenous administration of meclofenamate (5 mg kg−1) did not change the cerebrovascular effects of endothelin-1 and IRL 1620. In isolated goat cerebral arteries under control, resting conditions, endothelin-1 (10−11–10−7 M) induced concentration-dependent contractions (EC50=4.78×10−9 M; maximal contraction=3177±129 mg), whereas IRL 1620 (10−11–10−7 M) produced no effect. This contraction produced by endothelin-1 was competitively blocked by BQ-123 (10−7–3×10−6 M), and was not affected by BQ-788 (10−6 and 10−5 M). l-NAME (10−4 M), meclofenamate (10−5 M), indomethacin (10−5 M), l-NAME (10−4 M) plus meclofenamate (10−5 M) and phosphoramidon (10−4 M) did not affect the contraction in response to endothelin-1. Endothelium removal increased the response to endothelin-1, as well as the BQ-123 antagonism against endothelin-1 (pA2 values, 7.62 vs. 6.88; P<0.01). In both intact and de-endothelized arteries precontracted with prostaglandin F2α, endothelin-1 induced a further contraction, and IRL 1620 caused no effect. These results suggest that: (1) endothelin-1 produces cerebral vasoconstriction by activating endothelin ETA receptors probably located in smooth muscle; (2) endothelin ETB receptors, nitric oxide and prostanoids might be not involved in the cerebrovascular action of endothelin-1, and (3) endothelium removal may increase cerebrovascular reactivity by increasing sensitivity of endothelin ETA receptors to endothelin-1." @default.
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- W2076309035 date "1998-05-01" @default.
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- W2076309035 title "In vivo and in vitro action of endothelin-1 on goat cerebrovascular bed" @default.
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- W2076309035 doi "https://doi.org/10.1016/s0014-2999(98)00144-7" @default.
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