Neuropeptide Y (NPY) reduces field stimulation-evoked release of noradrenaline and enhances force of contraction in the rat portal vein

Dahlöf, Carl; Dahlöf, Pia; Tatemoto, Kazuhiko; Lundberg, Jan M.

doi:10.1007/bf00515562

Cited by 107 publications

(13 citation statements)

References 18 publications

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“…PYY and NPY are on the whole equipotent, whereas NPY 2-36 appears to be markedly less potent (Rioux et al, 1986). Moreover, NPY can inhibit the electrically-stimulated release of NA from sympathetic fibres in the vas deferens (Lundberg & Stjarne, 1984) and in certain blood vessels (Dahlof et al, 1985). This effect is mediated via Y2-receptors which recognize not only full length NPY/PYY but also C-terminal fragments of NPY and PYY (Wahlestedt et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Effects of various neuropeptide Y/peptide YY fragments on electrically‐evoked contractions of the rat vas deferens

Grundemar

Håkanson

1990

British J Pharmacology

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1The effects of various neuropeptide Y (NPY) and peptide YY (PYY) fragments on electrically-evoked twitches in the rat isolated vas deferens were studied and compared with the effects of full length NPY and PYY. The aim was to identify the shortest NPY/PYY fragments that are capable of suppressing the contractions. 2 NPY (1-36) and C-terminal fragments of NPY (from 11-36 to 22-36) suppressed the electricallyevoked twitches in a concentration-dependent manner. On the whole there seemed to be a gradual lowering of the pIC50 values with progressive shortening of the NPY fragments (except for fragments 16-36 and 22-36 that had rather high pIC50 values). NPY 23-36, 24-36 and 25-36 suppressed the twitches at high concentrations (3pM). NPY 26-36 was without effect as were C-terminal carboxy-deaminated NPY and glycine extended NPY (NPY-Gly-Lys-Arg). 3 PYY (1-36) and C-terminal fragments of PYY (from 11-36 to 23-36) suppressed the electricallyevoked twitches in a concentration-dependent manner. PYY 1-36 was more potent than any of the fragments. There was a tendency for shorter fragments to have lower pIC50 values. suppressed the twitches at high concentrations (3 gM). PYY 26-36 was without effect.4 The findings suggest that the 12 C-terminal amino acid residues of NPY and PYY are the minimum length required to activate the Y2-receptor.

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Section: Introductionmentioning

confidence: 99%

Effects of various neuropeptide Y/peptide YY fragments on electrically‐evoked contractions of the rat vas deferens

Grundemar

Håkanson

1990

British J Pharmacology

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“…Since exogenous NPY produces vasoconstriction via nonadrenergic mechanisms (Lundberg & Tatemoto, 1982), and since part of the sympathetic vasoconstrictor response to nerve stimulation has been shown to remain after combined alpha-and beta-adrenoceptor blockade or reserpine treatment, it has been suggested that NPY may be involved in sympathetic vascular control (see Lundberg et al, 1986d). NPY also seems to inhibit NA release via a prejunctional action (Lundberg & Stjarne, 1984; Dahlof et al, 1985). Thus, NPY may both modulate neurotransmitter release and contribute to the postjunctional response of vascular smooth muscle.…”

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confidence: 99%

Plasma neuropeptide Y‐like immunoreactivity and catecholamines during various degrees of sympathetic activation in man

Pernow

Lundberg

Kaijser

et al. 1986

Clinical Physiology

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194

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Summary. Neuropeptide Y‐like immunoreactivity (NPY‐LI) and catecholamine concentrations in plasma were analysed during and after 60 min of physical exercise at a work load corresponding to 70% of individual maximal oxygen uptake in nine healthy men of average physical fitness. Systemic plasma NPY‐LI increased progressively from 18±3 to 81±19 pmolx1‐1 in parallel with a 10‐fold increase in noradrenaline (NA) concentration. The increase in plasma NPY‐LI during exercise and the decrease after completion of exercise were much slower than the corresponding changes in NA concentration. This difference is probably related to a slower diffusion of NPY into systemic circulation after release, as well as to a longer half‐life of NPY than of NA in plasma. Reversed phase HPLC and sephadex G‐50 gel‐filtration chromatography revealed that the main component of NPY‐LI in plasma during exercise eluted in a similar position as synthetic human NPY. During exercise plasma NPY‐LI correlated well with the plasma concentration of NA (r=0·80), but not with that of adrenaline (ADR), suggesting a neuronal origin of NPY. The self‐ratings of perceived exertion (RPE) were well correlated with the plasma concentrations of both NPY‐LI and NA. No clear‐cut veno‐arterial concentration difference was observed for NPY‐LI. Isometric handgrip and orthostatic test doubled plasma NA concentrations but did not cause any increase in plasma NPY‐LI. No change in plasma tachykinin‐like immunoreactivity was detected during exercise. The present data suggest that NPY is released together with NA during strong, but probably not during mild, sympathetic activation under physiological conditions in man.

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“…Thus, NPY has been found to inhibit transmural nerve-stimulation evoked contraction of mouse and rat vas deferens, rat uterus, and rat and guinea pig heart, as well as mesenteric arteries [84][85][86][87][88]. The effect has been shown to be due to a presynaptic inhibitory action of the peptide on the release of noradrenaline [87][88][89]. In the isolated perfused mesenteric arterial bed of the rat, inhibition of the electrically stimulated release of noradrenaline was observed over a concentration range of NPY of 10 -1~ to 10 -7 M. The low concentrations (10 -1~ and 10 -9 M) decreased the effect of nerve stimulation on perfusion pressure, whereas the higher concentrations (10 .7 M) produced a marked potentiation [87].…”

Section: Presynaptic Effects Of Npymentioning

confidence: 97%

The role of neuropeptides in cardiovascular regulation

Ganten

Paul

Lang

1991

Cardiovasc Drug Ther

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During the past few years more than 30 novel, biologically active peptides have been discovered. Some are produced in endocrine glands and circulate as hormones in the blood; others are contained in the enterochromaffin cells of the gut and may be involved in the regulation of intestinal functions. The vast majority of new peptides, however, have been detected in the central and peripheral nervous systems, where they are synthesized in distinct neurons and stored in neurovesicles. Many of these neuropeptides may be involved in circulatory regulation. There is evidence supporting such a role, especially for centrally located angiotensin, opioid peptides, substance P, neuropeptide Y (NPY), vasopressin, atrial natriuretic peptide (ANP), kinins, corticotropin releasing factor, bombesin, and somatostatin. In this review we discuss the cardiovascular actions of angiotensin, neuropeptide Y, and calcitonin gene related peptide.

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Neuropeptide Y (NPY) reduces field stimulation-evoked release of noradrenaline and enhances force of contraction in the rat portal vein

Cited by 107 publications

References 18 publications

Effects of various neuropeptide Y/peptide YY fragments on electrically‐evoked contractions of the rat vas deferens

Effects of various neuropeptide Y/peptide YY fragments on electrically‐evoked contractions of the rat vas deferens

Plasma neuropeptide Y‐like immunoreactivity and catecholamines during various degrees of sympathetic activation in man

The role of neuropeptides in cardiovascular regulation

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