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• W2026792167 abstract "The mechanism by which neuropeptide Y (NPY) potentiates the vasoconstriction induced by α 1 ‐adrenoceptor agonists was investigated in 3rd generation mesenteric arterioles of the rat. At a maximally active concentration, nitrendipine (10 −6 m ) displaced to the right the concentration‐response curves to noradrenaline (pD 2 decreased from 6.2 ± 0.06 to 5.7 ± 0.03) and phenylephrine (pD 2 decreased from 5.6 ± 0.03 to 5.3 ± 0.03). Diltiazem (10 −5 m ) also shifted to the right the concentration‐response curve to phenylephrine (pD 2 decreased from 6.0 ± 0.06 to 5.5 ± 0.04). In addition, the maximal response to phenylephrine was significantly decreased in the presence of either nitrendipine or diltiazem. In the absence of a calcium channel blocking agent, NPY (100 n m ) produced a leftward shift of the concentration‐response curves to noradrenaline (pD 2 increased from 6.2 ± 0.06 to 6.5 ± 0.05) and phenylephrine (pD 2 increased from 5.6 ± 0.03 to 6.0 ± 0.06 and from 6.0 ± 0.06 to 6.3 ± 0.11). In the presence of either nitrendipine (10 −6 m ) or diltiazem (10 −5 m ), NPY (100 n m ) did not alter the concentration‐response curves to either noradrenaline or phenylephrine. NPY was added to arterioles brought to the same level of tension (40% of the maximal contraction) either by phenylephrine alone (1.5 × 10 −6 m ) or by a higher concentration of phenylephrine (3 × 10 −6 m ) followed by the addition of prazosin (1.3 × 10 −9 m ; a concentration at which it partially blocks α 1 ‐adrenoceptors). In these conditions, the response to phenylephrine was completely abolished by nitrendipine (10 −6 m ) or by diltiazem (10 −5 m ). Furthermore, NPY (10 −10 to 10 −7 m ) increased the arteriolar tension up to the maximal contractile capacity of the vessels with pD 2 values of 8.6 ± 0.02 and 8.7 ± 0.01, in the absence and presence of prazosin, respectively. Prazosin was replaced in the above protocol by other vasodilator agents acting through different mechanisms. Whether in the presence of 2 × 10 −7 m forskolin, 6 × 10 −7 m sodium nitroprusside (which stimulate adenylate cyclase or guanylate cyclase, respectively) or 2 × 10 −7 m diltiazem (a concentration at which calcium entry is partially blocked), NPY enhanced phenylephrine‐induced contraction to the maximum level with an identical potency (pD 2 values of the peptide ranged from 8.3 to 8.7). The results show that, in rat mesenteric arterioles, NPY potentiates only the calcium entry blocker‐sensitive component of contraction induced by stimulation of α 1 ‐adrenoceptors. In addition, they provide evidence that the peptide counteracts with an equal potency the inhibitory effect of partial block of α 1 ‐adrenoceptors and of relaxing agents acting through different mechanisms. It is suggested that NPY enhances calcium entry induced by stimulation of α 1 ‐adrenoceptors in this tissue." @default.
• W2026792167 created "2016-06-24" @default.
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• W2026792167 date "1990-02-01" @default.
• W2026792167 modified "2023-10-18" @default.
• W2026792167 title "Enhancement by neuropeptide Y (NPY) of the dihydropyridine-sensitive component of the response to α1-adrenoceptor stimulation in rat isolated mesenteric arterioles" @default.
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• W2026792167 doi "https://doi.org/10.1111/j.1476-5381.1990.tb14714.x" @default.
• W2026792167 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1917373" @default.
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