Neuropeptide Y in sympathetic co-transmission—Recent advances in the search for neuropeptide Y antagonists

Edvinsson, Lars; Erlinge, David

doi:10.1016/0143-4179(94)90165-1

Cited by 3 publications

(4 citation statements)

References 26 publications

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“…Neuropeptide Y, which was originally isolated from porcine brain, is a 36 amino acid peptide (Tat-emoto 1982). Neuropeptide Y can induce numerous physiological responses, including contraction of blood vessels (Michel 1991;Edvinsson et al 1990Edvinsson et al & 1994Jansen et al 1994). In the present work, we found that in relatively high concentration (1 O-'-lOWM) neuropeptide Y not only induced elevation in the basal concentration of cGMP but also induced a transient relaxation (1 0-6M) of precontracted basilar artery segments with endothelium.…”

Section: Discussionsupporting

confidence: 57%

“…a-Trinositol is an isomer of inositol-l,4,5-trisphosphate and has been demonstrated to block selectively neuropeptide Y-induced contraction of different vessels in vitro and in situ (Edvinsson et al 1990;Sun et al 199 1 ;Adamsson & Edvinsson 1991;Adamsson et al 1992). a-Trinositol significantly decreased the maximum contraction induced by neuropeptide Y in guinea pig basilar arteries by about 60% without any significant alteration of the sensitivity (pD2 value) (Edvinsson et al 1994). Relaxation induced by acetylcholine or substance P was markedly attenuated by neuropeptide Y whose antagonistic effect on the vasomotor…”

Section: Discussionmentioning

confidence: 89%

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Relation between Cyclic GMP Generation and Cerebrovascular Reactivity: Modulation by NPY and α‐Trinositol

You

Zhang

Jansen‐Olesen

et al. 1995

Pharmacology & Toxicology

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It is considered that cyclic guanosine monophosphate (cGMP) plays a pivotal role in mediating the relaxation of vascular and nonvascular smooth muscles. cGMP steady state levels are regulated by guanylyl cyclase, cGMP phosphodiesterases and its flux from cells. The present study examines the possible relation between cerebrovascular vasodilator agents and generation of cGMP in guinea pig cerebral vessels. Acetylcholine, substance P, nitroglycerine and sodium nitroprusside significantly increased the generation of cGMP. The application of acetylcholine, substance P, nitroglycerine and sodium nitroprusside elicited concentration-dependent relaxation of basilar artery segments. Neuropeptide Y increased the generation of cGMP by 2%-46% of control levels (at 10(-7)-10(-6)M of neuropeptide Y; *P < 0.05). In addition, neuropeptide Y (10(-6)M) induced a transient relaxation of the precontracted guinea pig basilar arteries with endothelium. This transient relaxation was blocked by nitro-L-arginine (10(-4)M). alpha-Trinositol does not alter the formation of cGMP nor the neuropeptide Y-induced relaxation. In the presence of alpha-trinositol neuropeptide Y (10(-7)-10(-6)M) did not significantly elevate the production of cGMP as compared with controls. The rise in cGMP induced by acetylcholine, substance P and nitroglycerine was slightly increased by the addition of neuropeptide Y (3 x 10(-7) M). Acetylcholine and substance P induced an endothelium-dependent relaxation of the precontracted guinea pig basilar arteries, while sodium nitroprusside and nitroglycerine induced an endothelium-independent relaxation. Acetylcholine, substance P and nitroglycerine induced concentration-dependent relaxations of basilar artery, respectively. The relaxation elicited by acetylcholine or substance P, but not nitroglycerine, was markedly attenuated by neuropeptide Y (3 x 10(-7) M).(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 89%

Relation between Cyclic GMP Generation and Cerebrovascular Reactivity: Modulation by NPY and α‐Trinositol

You

Zhang

Jansen‐Olesen

et al. 1995

Pharmacology & Toxicology

View full text Add to dashboard Cite

show abstract

“…NPY-induced vasoconstriction in general and elevations in mean arterial pressure occur predominantly via postjunctional Y1-receptors in the arterial vascular smooth muscles [15][16][17][18]. Therefore, the aim of our study was to determine whether in experimental portal hypertension (a) NPY-evoked vasoconstriction and/ or NPY-induced facilitation of adrenergic vasoconstriction are altered and (b) if so whether this is mediated by Y1-receptors.…”

Section: Introductionmentioning

confidence: 99%

Enhanced Y1-receptor-mediated vasoconstrictive action of neuropeptide Y (NPY) in superior mesenteric arteries in portal hypertension

Wiest

Jurzik

Moleda

et al. 2006

Journal of Hepatology

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“…The cellular actions of 1,2,6-IP 3 could be mediated through specific receptors located in the cell membrane of different tissues (20). This is supported by data showing that 1,2,6-IP 3 interferes with the intracellular formation of inositol phosphate that is induced by neuropeptide Y without entering the cell (5,9).…”

Section: Discussionmentioning

confidence: 63%

Inhibition of Plasma Extravasation After Burns by D-Myo-Inositol-1,2,6-Trisphosphate Using Digital Image Colour Analysis

Tarnow

Jönsson²,

Mattsson³

et al. 1998

Scandinavian Journal of Plastic and Reconstructive Surgery and

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D-myo-inositol-1,2,6-triphosphate (1,2,6-IP3) has beneficial effects in experimental, progressive burn-induced ischaemia and oedema. A 1 cm2 full-thickness burn was made in the skin of 20 rats with a hot aluminium rod followed by infusion of 1,2,6-IP3 (60 mg.kg.-1 h-1) or isotonic saline (n = 10 in each group). One hour later Evans blue was injected intravenously. Colour photographs of the area of the burn were taken in a standard manner before the burn and at intervals for three hours afterwards. The photographs were analysed by digital image colour analysis using normalised red-green-blue values. The increase in normalised blue values between 60 and 180 minutes after the burn was significantly reduced in animals treated with 1,2,6-IP3 compared with control animals (p < 0.001). Spectrophotometric analysis of extravasated Evans blue in the skin 180 minutes after the burn showed that it had been significantly inhibited by treatment with 1,2,6-IP3 (p < 0.001). In conclusion, digital image analysis allowed repeated evaluation over time and confirmed previous data about the ability of 1,2,6-IP3 to inhibit extravasation of plasma after burns.

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Neuropeptide Y in sympathetic co-transmission—Recent advances in the search for neuropeptide Y antagonists

Cited by 3 publications

References 26 publications

Relation between Cyclic GMP Generation and Cerebrovascular Reactivity: Modulation by NPY and α‐Trinositol

Relation between Cyclic GMP Generation and Cerebrovascular Reactivity: Modulation by NPY and α‐Trinositol

Enhanced Y1-receptor-mediated vasoconstrictive action of neuropeptide Y (NPY) in superior mesenteric arteries in portal hypertension

Inhibition of Plasma Extravasation After Burns by D-Myo-Inositol-1,2,6-Trisphosphate Using Digital Image Colour Analysis

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