Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood flow in salivary glands is regulated mainly by sympathetic and parasympathetic nerve activity. This study was carried out to determine the relative contributions of cholinergic, adrenergic and peptidergic neurotransmitters to the control of submandibular blood flow in the rat using laser-Doppler flowmetry. Parasympathetic impulses caused a rapid atropine-sensitive vasodilation followed by a maintained increase in blood flow, a portion of which remained in the presence of both atropine and L-NAME. In contrast, continuous sympathetic stimulation caused an intense vasoconstriction that was followed by a prolonged after-vasodilation. The same number of impulses delivered in bursts resulted in a cyclic vasoconstriction followed by a rapid vasodilation. Alpha-adrenoceptor blockade largely abolished the vasoconstriction, and the duration and magnitude of the after-vasodilation were reduced. Inhibition of nitric oxide (NO) synthase by L-NAME reduced the vasodilation. The addition of a beta-adrenoceptor antagonist eliminated the sympathetic vasodilator response, but in the presence of complete alpha- and beta-adrenoceptor blockade and L-NAME a small vasoconstriction remained. We conclude that the vasoconstrictor effects of sympathetic stimulation of the rat submandibular gland are due to alpha-adrenergic receptor activation and probably also NPY, and the vasodilator effects are due to NO and beta-adrenergic activity. Parasympathetic vasodilation was due to NO-independent mechanisms mediated by acetylcholine and substance P, and NO-dependent mechanisms mediated by VIP.
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PMID:Neural regulation of blood flow in the rat submandibular gland. 982 25

The effects of five neuropeptides (CGRP, SOM, SP, NPY, VIP), L-NAME (nitric oxide synthase inhibitor), and adrenaline on the contractile tone of the aortic anastomosis in the estuarine crocodile, Crocodylus porosus, were investigated. None of the neuropeptides, which had previously been found to be present in the aortic anastomosis, had any direct effect on the tension developed by ring preparations. L-NAME itself significantly increased the basal tone of the vascular ring preparations, suggesting a tonic release of nitric oxide in the preparation. Adrenaline produced concentration-dependent vasoconstrictions that were counteracted by profound reflex vasodilatations that were susceptible to blockade by L-NAME. Immunohistochemistry revealed the presence of nitric oxide synthase and tyrosine hydroxylase-containing (indicating the presence of a adrenergic innervation) nerve fibres in the adventitia and adventitio-medial border of the aortic anastomosis. These data demonstrate opposing actions of adrenaline and nitric oxide on the vascular smooth muscle in the anastomosis of the C. porosus. The morphology of the anastomosis, with the extremely thick muscular vessel wall, suggests a sphincter-like function for this vessel that could be controlled mainly by adrenergic and nitrergic mechanisms.
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PMID:Nitric oxide, a potent vasodilator of the aortic anastomosis in the estuarine crocodile, Crocodylus porosus. 1131 25

The present study investigated the mechanisms of vasodilatation of the human pancreatic polypeptide [cPP(1-7), NPY(19-23),Ala(31),Aib(32),Gln(34)]hPP (hPP) in mesenteric small arteries from Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). The arteries were isolated and mounted in microvascular myographs for isometric tension recording. In vasopressin-contracted preparations with endothelium from WKY rats, hPP evoked concentration-dependent relaxations with maximal responses of 50+/-2% (n=5). hPP relaxation was reduced by endothelial cell removal and abolished in the presence of a nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine-methylester (L-NAME). hPP relaxation was blunted in segments with endothelium, and absent in segments without endothelium from SHR. The combined neuropeptide Y(1)- and Y(4)-receptor antagonist, GR23118 (Ile-Glu-Pro-Dpr-Tyr-Arg-Leu-Arg-Tyr-CONH(2)), and the neuropeptide Y(1) receptor antagonist, BIBP3226 ((R) -N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)-methyl]-arginineamide), inhibited hPP-induced vasodilatation. Calcitonin gene-related peptide (CGRP) relaxation was reduced in arteries from SHR compared to WKY. The CGRP receptor antagonist, CGRP (8-37), antagonized vasodilatation induced by CGRP and rightward shifted concentration-response curves for hPP in arteries from WKY rats. There were no differences in nerves immunoreactive for CGRP in arteries from SHR compared to WKY rats. In contrast to neuropeptide Y which evokes contraction by activation of neuropeptide Y(1) and Y(2) receptors, the present results suggest hPP evokes relaxation of mesenteric small arteries by activation of prejunctional neuropeptide Y(1)-like receptors localized in CGRP-containing nerves followed by release of CGRP and of endothelium-derived NO. hPP relaxation is blunted in arteries from SHR probably as a consequence of endothelial cell dysfunction leading to reduced efficacy of CGRP.
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PMID:Blunted pancreatic polypeptide-induced vasodilatation in mesenteric resistance vessels from spontaneously hypertensive rats. 1885 59

Numerous data indicate that Rho kinase inhibitors, such as Fasudil, may constitute a novel therapy for cardiovascular and metabolic diseases. We evaluated long-term effects of exposure to Fasudil during late gestation (10 mg/day) in male rat offspring from birth until 9 months. We also analyzed its effects in offspring from hypertensive mothers treated with a nitric oxide synthesis inhibitor (L-NAME; 50 mg/day). Prenatal exposure to Fasudil did not affect birth weight, but increased body weight from postnatal day 7 (P7) to 9 months. In intrauterine growth-restricted (IUGR) fetuses exposed to L-NAME, maternal Fasudil treatment increased birth weight. At P42 and P180, rats exposed to Fasudil and L-NAME showed alterations of their food intake as well as an increased basal glycemia associated with mild glucose intolerance at 6 months which was also observed in Fasudil-exposed rats. In 9 month-old rats, exposure to Fasudil increased the daily food intake as well as hypothalamic mRNA level of the orexigenic NPY peptide without modulation of the anorexigenic POMC gene expression. Altogether, our data suggest that prenatal Fasudil exposure alleviates fetal growth in IUGR rats, but programs long-term metabolic disturbances including transient perturbations of glucose metabolism, a persistent increase of body weight gain, hyperphagia and an augmented expression of hypothalamic NPY orexigenic gene. We postulate that Fasudil treatment during perinatal periods may predispose individuals to the development of metabolic disorders.
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PMID:Prenatal fasudil exposure alleviates fetal growth but programs hyperphagia and overweight in the adult male rat. 2268 67