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Relevant bibliographies by topics / Vasodilatory peptides

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Academic literature on the topic 'Vasodilatory peptides'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Vasodilatory peptides"

1

Gosney, M. A., J. R. Gosney, and M. Lye. "Orthostatic hypotension and vasodilatory peptides in bronchial carcinoma." Journal of Clinical Pathology 48, no. 12 (December 1, 1995): 1102–5. http://dx.doi.org/10.1136/jcp.48.12.1102.

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Russ, R. D., T. C. Resta, and B. R. Walker. "Pulmonary vasodilatory response to neurohypophyseal peptides in the rat." Journal of Applied Physiology 73, no. 2 (August 1, 1992): 473–78. http://dx.doi.org/10.1152/jappl.1992.73.2.473.

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Experiments were performed on isolated salt-perfused rat lungs to determine the receptor type(s) responsible for the pulmonary vascular effects of the neurohypophyseal peptides arginine vasopressin (AVP) and oxytocin. Bolus administration of AVP to lungs preconstricted with the thromboxane mimetic U-46619 resulted in a dose-dependent vasodilatory response (approximately 65% reversal of U-46619-induced vasoconstriction at the highest dose tested) that was blocked by pretreatment with a selective V1- but not by a selective V2-vasopressinergic receptor antagonist. Administration of a selective V1-agonist to the preconstricted pulmonary vasculature resulted in a vasodilatory response similar to that observed with AVP (approximately 55% reversal of U-46619 vasoconstriction), which was blocked by prior administration of the selective V1-receptor antagonist. Administration of the selective V2-receptor agonist desmopressin to the preconstricted pulmonary vasculature resulted in a small (approximately 8% reversal of U-46619 vasoconstriction) vasodilatory response that was, nevertheless, greater than that produced by addition of vehicle alone and was attenuated by pretreatment with a selective V2-receptor antagonist. Finally, oxytocin also caused vasodilation in the preconstricted pulmonary vasculature; however, the potency of oxytocin was approximately 1% of AVP, and the vasodilation produced by oxytocin was blocked by prior administration of a selective V1-receptor antagonist, suggesting that oxytocin acts via V1-vasopressinergic receptor stimulation. We conclude from these experiments that AVP and oxytocin dilate the preconstricted pulmonary vasculature primarily via stimulation of V1-vasopressinergic receptors. V2-receptor stimulation results in a minor vasodilatory response, although its physiological significance is unclear.

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Kamiya, H., R. Saito, S. Nonaka, H. Konishi, Y. Takano, Y. Shimohigashi, H. Matsumoto, and M. Ohno. "Vasodilatory actions of tachykinin peptides in isolated vascular smooth muscle." European Journal of Pharmacology 183, no. 6 (July 1990): 2222–23. http://dx.doi.org/10.1016/0014-2999(90)93757-h.

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Faury, G., A. Chabaud, M. T. Ristori, L. Robert, and J. Verdetti. "Effect of age on the vasodilatory action of elastin peptides." Mechanisms of Ageing and Development 95, no. 1-2 (April 1997): 31–42. http://dx.doi.org/10.1016/s0047-6374(96)01842-8.

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Eto, Tanenao, and Willis K. Samson. "Adrenomedullin and proadrenomedullin N-terminal 20 peptide: vasodilatory peptides with multiple cardiovascular and endocrine actions." Trends in Endocrinology & Metabolism 12, no. 3 (April 2001): 91–93. http://dx.doi.org/10.1016/s1043-2760(01)00374-5.

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Forte, Madonna, Schiavon, Valenti, Versaci, Zoccai, Frati, and Sciarretta. "Cardiovascular Pleiotropic Effects of Natriuretic Peptides." International Journal of Molecular Sciences 20, no. 16 (August 8, 2019): 3874. http://dx.doi.org/10.3390/ijms20163874.

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Atrial natriuretic peptide (ANP) is a cardiac hormone belonging to the family of natriuretic peptides (NPs). ANP exerts diuretic, natriuretic, and vasodilatory effects that contribute to maintain water–salt balance and regulate blood pressure. Besides these systemic properties, ANP displays important pleiotropic effects in the heart and in the vascular system that are independent of blood pressure regulation. These functions occur through autocrine and paracrine mechanisms. Previous works examining the cardiac phenotype of loss-of-function mouse models of ANP signaling showed that both mice with gene deletion of ANP or its receptor natriuretic peptide receptor A (NPR-A) developed cardiac hypertrophy and dysfunction in response to pressure overload and chronic ischemic remodeling. Conversely, ANP administration has been shown to improve cardiac function in response to remodeling and reduces ischemia-reperfusion (I/R) injury. ANP also acts as a pro-angiogenetic, anti-inflammatory, and anti-atherosclerotic factor in the vascular system. Pleiotropic effects regarding brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) were also reported. In this review, we discuss the current evidence underlying the pleiotropic effects of NPs, underlying their importance in cardiovascular homeostasis.

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Rodríguez-pérez, Federico, Carlos M. Isales, and Roberto J. Groszmann. "Platelet cytosolic calcium, peripheral hemodynamics, and vasodilatory peptides in liver cirrhosis." Gastroenterology 105, no. 3 (September 1993): 863–67. http://dx.doi.org/10.1016/0016-5085(93)90906-s.

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Kakumanu, Rahini, Wayne C. Hodgson, Ravina Ravi, Alejandro Alagon, Richard J. Harris, Andreas Brust, Paul F. Alewood, Barbara K. Kemp-Harper, and Bryan G. Fry. "Vampire Venom: Vasodilatory Mechanisms of Vampire Bat (Desmodus rotundus) Blood Feeding." Toxins 11, no. 1 (January 8, 2019): 26. http://dx.doi.org/10.3390/toxins11010026.

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Animals that specialise in blood feeding have particular challenges in obtaining their meal, whereby they impair blood hemostasis by promoting anticoagulation and vasodilation in order to facilitate feeding. These convergent selection pressures have been studied in a number of lineages, ranging from fleas to leeches. However, the vampire bat (Desmondus rotundus) is unstudied in regards to potential vasodilatory mechanisms of their feeding secretions (which are a type of venom). This is despite the intense investigations of their anticoagulant properties which have demonstrated that D. rotundus venom contains strong anticoagulant and proteolytic activities which delay the formation of blood clots and interfere with the blood coagulation cascade. In this study, we identified and tested a compound from D. rotundus venom that is similar in size and amino acid sequence to human calcitonin gene-related peptide (CGRP) which has potent vasodilatory properties. We found that the vampire bat-derived form of CGRP (i.e., vCGRP) selectively caused endothelium-independent relaxation of pre-contracted rat small mesenteric arteries. The vasorelaxant efficacy and potency of vCGRP were similar to that of CGRP, in activating CGRP receptors and Kv channels to relax arteriole smooth muscle, which would facilitate blood meal feeding by promoting continual blood flow. Our results provide, for the first time, a detailed investigation into the identification and function of a vasodilatory peptide found in D. rotundus venom, which provides a basis in understanding the convergent pathways and selectivity of hematophagous venoms. These unique peptides also show excellent drug design and development potential, thus highlighting the social and economic value of venomous animals.

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De Plater, G. M., R. L. Martin, and P. J. Milburn. "A C-Type Natriuretic Peptide from The Venom of The Platypus (Ornithorhynchus anatinus) - Structure and Pharmacology." Australian Mammalogy 20, no. 2 (1998): 301. http://dx.doi.org/10.1071/am98302.

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A peptide which relaxes rat uterine smooth muscle and exhibits homology with the mammalian C-type natriuretic peptide (CNP) has previously been identified in platypus venom. In this study we describe detailed structural and pharmacological characteristics of this peptide, which has been labelled ONP-39 (Ornithorhynchus Natriuretic Peptide). Elucidation of its 39-residue primary sequence confirms the substantial homology it shares with mammalian CNPs. These peptides exhibit natriuretic, diuretic and hypotensive activities in vivo and relax smooth muscle in vitro but are poorly characterised in terms of physiological function. ONP-39 is equipotent with CNP in causing cGMP elevation in cultured vascular smooth muscle cells, suggesting that, like CNP, it acts through ANPB receptors. The direct elevation of cGMP in vascular smooth muscle by ONP-39 may underlie vasodilatory effects of platypus venom.

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Sridharan, Sindhuja, and R. Manjunatha Kini. "Decoding the molecular switches of natriuretic peptides which differentiate its vascular and renal functions." Biochemical Journal 475, no. 2 (January 23, 2018): 399–413. http://dx.doi.org/10.1042/bcj20170690.

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Heart failure (HF) is associated with high morbidity and mortality. Dysfunction of blood pressure and/or volume homeostatic processes result in lower perfusion and/or congestion. Treatment strategies exerting differential effects on pressure and volume mechanisms are critical in handling patients with HF. Atrial natriuretic peptides (ANPs) are a key hormone in maintaining circulation. It binds to NP receptor-A (NPR-A) on vasculature, kidneys and nervous system to lowers blood pressure and volume. It exerts a concentration-dependent pharmacological activity, and only increased renal excretion of water and sodium at low doses and vasodilation along with renal effects at slightly higher doses. Recently, we showed that K-Ring (conserved ring of krait venom NP) elicited only vasodilatory properties despite its ability to evoke NPR-A. Through systematic analysis of the structure–function relationships of K-Ring, we have delineated the molecular switches that control vasodilatory and diuretic properties of NPs in anesthetized rats. In the process, we have identified residues that — (a) differentiate vascular and renal functions, (b) affect heart rate and pulse pressure, (c) exhibit sustained effect on vasodilatory function and (d) forceful diuresis switches. Furthermore, we have shown these residues to have equivalent effects on ANP scaffold, thereby introducing modularity in designing function-based ANP analogs. By comparing the ability of designed NPs to evoke cGMP levels, we propose a hypothetical mechanism for the observed tissue-specific effects. The present study opens new avenues in the development of suitable therapeutic agents for personalized care for HF patients.

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Dissertations / Theses on the topic "Vasodilatory peptides"

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Drake, W. M. "Desensitisation of calcitonin gene-related peptide of adrenomedullin receptors in vascular smooth muscle of SK-N-MC cells." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275192.

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McLeod, Janet Leigh, and janet mcleod@deakin edu au. "The natriuretic peptides and their receptors in the brain of the amphibian, Bufo marinus." Deakin University. School of Biological and Chemical Sciences, 1999. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20071024.112730.

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The natriuretic peptides, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) are members of a family of hormones that play an important role in mammalian fluid and electrolyte balance. In the periphery, natriuretic peptides reduce blood volume and subsequently blood pressure by increasing renal natriuresis and diuresis and relaxation of vascular smooth muscle. The actions of natriuretic peptides are mediated via two membrane-linked guanylate cyclase receptors (NPR-GC); natriuretic peptide receptor-A (NPR-A) which has a high affinity for ANP and BNP; and natriuretic peptide receptor-B (NPR-B)which has the greatest affinity for CNP. A third receptor not linked to guanylate cyclase, natriuretic peptide receptor-C (NPR-C) also exists, which binds to ANP, BNP and CNP with a relatively equal affinity, and is involved with clearance of the peptides from the circulation and tissues. The natriuretic peptides are present in the brain and are particularly predominant in cardiovascular and fluid and electrolyte regulating areas such as the anteroventral third ventricle (AV3V) region. This distribution has led to the suggestion natriuretic peptides play a neuromodulatory role in the central control of fluid homeostasis. Natriuretic peptides in the brain have been observed to inhibit the release of other fluid and electrolyte regulating hormones such as arginine vasopressin (AVP) and angiotensin II (AII). Natriuretic peptides have also been identified in the non-mammalian vertebrates although information regarding the distribution of the peptides and their receptors in the non-mammalian brain is limited. In amphibians, immunohistochemical studies have shown that natriuretic peptides are highly concentrated in the preoptic region of the brain, an area believed to be analogous to the A\T3\ region in mammals, which suggests that natriuretic peptides may also be involved in central fluid and electrolyte regulation in amphibians. To date, CNP is the only natriuretic peptide that has been isolated and cloned from the lower vertebrate brain, although studies on the distribution of CNP binding sites in the brain have only been performed in one fish species. Studies on the distribution of ANP binding sites in the lower vertebrate brain are similarly limited and have only been performed in one fish and two amphibian species. Moreover, the nature and distribution of the natriuretic peptide receptors has not been characterised. The current study therefore, used several approaches to investigate the distribution of natriuretic peptides and their receptors in the brain of the amphibian Bufo marinus. The topographical relationship of natriuretic peptides and the fluid and electrolyte regulating hormone arginine vasotocin was also investigated, in order to gain a greater understanding of the role of the natriuretic peptide system in the lower vertebrate brain. Immunohistochemical studies showed natriuretic peptides were distributed throughout the brain and were highly concentrated in the preoptic region and interpeduncular nucleus. No natriuretic peptide-like immunoreactivity (NP-IR) was observed in the pituitary gland. Arginine vasotocin-like immunoreactivity (AvT-IR) was confined to distinct regions, particularly in the preoptic/hypothalamic region and pituitary gland. Double labelling studies of NP-JR and AvT-IR showed the peptides are not colocalised in the same neural pathways. The distribution of natriuretic peptide binding sites using the ligands 125I-rat ANP (125I-rANP) and 125I-porcine CNP (125I-pCNP) showed different distributions in the brain of B. marinus. The specificity of binding was determined by displacement with unlabelled rat ANP, porcine CNP and C-ANF, an NPR-C specific ligand. 125I-rANP binding sites were broadly distributed throughout the brain with the highest concentration in pituitary gland, habenular, medial pallium and olfactory region. Minimal 125I-rANP binding was observed in the preoptic region. Residual 125I-rANP binding in the presence of C-ANF was observed in the olfactory region, habenular and pituitary gland indicating the presence of both NPR-GC and NPR-C in these regions. 125I-pCNP binding was limited to the olfactory region, pallium and posterior pituitary gland. All 125I-pCNP binding was displaced by C-ANF which suggests that CNP in the brain of B. marinus binds only to NPR-C. Affinity cross-linking and SDS-PAGB demonstrated two binding sites at 136 kDa and 65 kDa under reducing conditions. Guanylate cyclase assays showed 0.1 µM ANP increased cGMP levels 50% above basal whilst a 10-fold higher concentration of CNP was required to produce the same result. Molecular cloning studies revealed a 669 base pair fragment showing 91% homology with human and rat NPR-A and 89% homology with human, rat and eel NPR-B. A 432 base pair fragment showing 67% homology to the mammalian NPR-C and 58% homology with eel NPR-D was also obtained. The results show natriuretic peptides and their receptors are distributed throughout the brain of B. marinus which indicates that natriuretic peptides may participate in a range of regulatory functions throughout the brain. The potential for natriuretic peptides to regulate the release of the fluid and electrolyte regulating hormone AVT also exists due to the high number of natriuretic peptide binding sites in the posterior pituitary gland. At least two populations of natriuretic peptide receptors are present in the brain of B. marinus, one linked to guanylate cyclase and one resembling the mammalian clearance receptor. Furthermore, autoradiography and guanylate cyclase studies suggest ANP may be the major ligand in the brain of B. marinus, even though CNP is the only natriuretic peptide that has been isolated from the lower vertebrate brain to date.

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Coppock, Hedley Alan. "Investigation of the receptors and mechanisms of action of the novel vasodilator peptide, adrenomedullin." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327028.

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4

Buckley, Theresa. "The release and activity of the neuropeptide vasodilator calcitonin gene-related peptide (CGRP) in rabbit skin." Thesis, Imperial College London, 1991. http://hdl.handle.net/10044/1/46689.

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Tan, Keith Kwan Cheuk. "Application of monoclonal antibodies to the investigation of the role of calcitonin gene-related peptide as a vasodilatory neurotransmitter." Thesis, University of Cambridge, 1994. https://www.repository.cam.ac.uk/handle/1810/283698.

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6

Cureton, Natalie. "Development of nanocarriers for targeted drug delivery to the placenta." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/development-of-nanocarriers-for-targeted-drug-delivery-to-the-placenta(696cfc4f-0bd7-4fbe-9b23-d2b83a7fec7d).html.

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Pregnancy complications such as fetal growth restriction (FGR) are often attributed to poor uteroplacental blood flow, but the risk of systemic side-effects hinders therapeutic intervention. We have utilised novel placental-specific homing peptides to overcome this and have conjugated these to biocompatible liposomes. Peptide-conjugated liposomes were found to selectively bind to the outer syncytiotrophoblast layer of the human placenta and to the uteroplacental vasculature and labyrinth region of the mouse placenta. The novel vasodilator SE175 was selected as a nitric oxide donor with a favourable stability and release profile, to encapsulate in peptide-conjugated liposomes in an attempt to restore impaired uteroplacental blood flow in a mouse model of FGR, the endothelial nitric oxide synthase knockout mouse. Liposomes containing SE175 or PBS were prepared by lipid film hydration and targeting peptides coupled to the liposomal surface. Vehicle control, free SE175, PBS- or SE175-containing liposomes were intravenously injected on embryonic (E) days 11.5, 13.5, 15.5 and 17.5. Animals were sacrificed at E18.5 and fetal and placental weights recorded. Targeted delivery of SE175 significantly increased fetal weight compared to vehicle control but no other treatment groups, whilst significantly decreasing placental weight, indicating improved placental efficiency. Treatment was well tolerated, having no impact on litter size or resorptions. Targeted delivery of SE175, but no other treatment group, reduced a marker of lipid peroxidation in the placenta, indicating a reduction in oxidative stress. These data suggest that selective delivery of SE175 to the uteroplacental vasculature in peptide decorated liposomes may represent a novel treatment for FGR.

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Yang, Yang. "Vascular KATP Channel Modulation by S-Glutathionylation: A Novel Mechanism for Cellular Response to Oxidative Stress." Digital Archive @ GSU, 2011. http://digitalarchive.gsu.edu/biology_diss/97.

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The KATP channels play an important role in the membrane excitability and vascular tone regulation. Previous studies indicate that the function of KATP channels is disrupted in oxidative stress seen in a variety of cardiovascular diseases, while the underlying mechanism remains unclear. Here, we demonstrate S-glutathionylation to be a modulation mechanism underlying the oxidant-mediated vascular KATP channel inhibition, the molecular basis for the channel inhibition and the alleviation of the channel inhibition by vasoactive intestinal peptide (VIP). We found that an exposure of isolated mesenteric rings to H2O2 impaired the KATP channel-mediated vascular dilation. In whole-cell recordings and inside-out patches, micromolar H2O2 or diamide caused a strong inhibition of the vascular KATP channel (Kir6.1/SUR2B) in the presence, but not in the absence, of glutathione (GSH), indicating S-glutathionylation. By co-expressions of Kir6.1 or Kir6.2 with SUR2B subunits, we found that the oxidant sensitivity of the KATP channel relied on the Kir6.1 subunit. Systematic mutational analysis revealed three cysteine residues (Cys43, Cys120 and Cys176) to be important. Among them, Cys176 was prominent, contributing to >80% oxidant sensitivity. Biochemical pull-down assay with biotinylated glutathione ethyl ester (BioGEE) showed that mutations of Cys176 impaired the oxidant-induced incorporation of GSH to the Kir6.1 subunit. Simulation modeling of Kir6.1 S-glutathionylation revealed that after incorporation to residue 176, the GSH moiety occupied a space between slide helix and two transmembrane helices. This prevented the necessary conformational change of the inner helix for channel gating, and retained the channel in its closed state. VIP is a potent vasodilator, and is shown to have protective role against oxidative stress. We found that the channel was strongly augmented by VIP and the channel activation relied on PKA phosphorylation. These results therefore indicate that 1) the vascular KATP channel is strongly inhibited in oxidative stress, 2) S-glutathionylation underlies the oxidant-mediated KATP channel inhibition, 3) Cys176 in the Kir6.1 subunit is the major site for S-glutathionylation, and 4) the Kir6.1/SUR2B channel is activated in a PKA-dependent manner by VIP that has been previously shown to alleviate oxidative stress.

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Books on the topic "Vasodilatory peptides"

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1962-, Martínez Alfredo, and Cuttitta Frank, eds. Adrenomedullin. Amsterdam: IOS Press, 1998.

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Frank, Cuttitta, and Martínez Alfredo, eds. Adrenomedulin. Amsterdam: IOS Press, 1998.

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M, Vanhoutte Paul, Shepherd John T. 1919-, International Union of Physiological Sciences. Congress, and International Symposium on Mechanisms of Vasodilatation (4th : 1986 : Rochester, Minn.), eds. Vasodilatation: Vascular smooth muscle, peptides, autonomic nerves, and endothelium. New York: Raven Press, 1988.

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Book chapters on the topic "Vasodilatory peptides"

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Nokihara, Kiyoshi, Yoshihiro Nakata, Ethan Lerner, Tadashi Yasuhara, and Victor Wray. "Structural Requirements of Non-Mammalian Vasodilatory Peptide Maxadilan, an Excellent Agonist of PACAP Type 1 Receptors." In Peptides: The Wave of the Future, 793–94. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0464-0_371.

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Watson, Ralph E., Donald J. DiPette, Scott C. Supowit, Khurshed A. Katki, and Huawei Zhao. "Vasodilator Peptides: CGRP, Substance P, and Adrenomedullin." In Hypertension, 193–202. Elsevier, 2005. http://dx.doi.org/10.1016/b978-0-7216-0258-5.50109-5.

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Conference papers on the topic "Vasodilatory peptides"

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Thom, S., A. Hughes, G. Martin, P. Goldberg, and P. Server. "VASODILATOR PEPTIDES - CGRP AND VIP." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643720.

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The two peptides calcitonin gene related peptide (C6RP) and vasoactive intestinalpeptide (VIP) are widely distributed in animal species including man and a number ofdiverse actions of the peptides have been described [1,2]. They share vasoactive properties [3,4] and may have important functions as neurotransmitters in a non-adrenergic, non-cholinergic nervous system [5]. VIP has been located in perivascular nerves supplying several tissues and is co-stored with acetylcholine in the parasympathetic system [6]. CGRP has also been widely identified in the nervous system, the cardiovascular system and perivascular nerves, where it is located with substance P[7]. Our studies have assessed the activity of these peptides in a human vascular resistance bed -the forearm, and on isolated human blood vessels.Forearm studies were performed by infusingCGRP (10,30,100 ng/min) or ViP (10,30,100 ng/min) via the brachial artery for 5 min at each dose level and measuring blood flow by venous occlusion plethysmography. In vitro studies were performed using ringsegments of pulmonary, gastric, coronary, radial, and transverse cervical arteries freshly obtained from surgical resection specimens and cerebral arteries obtained from autogsy tissue within 4 hours of death. Vessels were mounted in organ baths containing Krebs buffer aerated with 95% 02, 5% C02 at 37C, and preconstricted using a submaximal concentration of noradrenaline (1-3 μM) or prostaglandin F2a (I-IO11μ7.CGRP or VIP was added to the tissue bath in a cumulative fashion. All arterial segments used for these studies relaxed in response to acetylcholine (0.1-3μM)or A23187 (0.1-3μM) and this was regarded as indicative of functional endothelial integrity. Studies were performed in the presence of indomethacin (lOμM). The endothelium was deliberately removed from some rings and in others haemoglobin (5μM) ormethylene blue (lOμM) were added to the tissue bath after the arterialrings were effectively relaxed by CGRP orVIP. Both peptides produced marked dose dependent increases in forearm blood flow; at 100 ng/min the mean net increase was 174 ± 24% (mean ±s.e.m.) with CGRP, and 223 + 34% (mean +s.e.m.) with VIP. In vitro CGRP (InM-lμM) relaxed preconstricted segments ofradial Tn=2), coronary (n=4), gastric (n=5) and cerebral (n=3) arteries in an endothelium dependent manner. VIP (1 nM - 1pm) also relaxed human gastric (n=2), splenic (n=2), cervical (n=3) and pulmonary (n=5) arteries VIP relaxation of the gastric and cervical arteries was dependent on the presence of endothelium; however, VIP inducedrelaxation of pulmonary artery was not dependent on functional endothelium. The endothelium dependent relaxations could be abolished either by luminal rubbing, additionor haemoglobin or methylene blue. Together these results might be taken to imply that the forearm vasodilatation response is mediated by EDRF. However, caution is necessary in extrapolating from in vitro observations of large vessels to the in vivo response of a resistance vascular bed.Others have demonstrated that the CGRPand VIP relaxatory responses of smaller human pial arteries (ID 250-600 pm) are endothelium independent [8] and preliminary work in our department supports this. The EDRF mechanism is cyclic GMP linked, but most of the studied functions of VIP and CGRP seem to be linked to a rise in cyclic AMP-. A further paradox is that the blood flow response to infused acetylcholine, the archetypal releaser of EDRF, is evanescent, and yet the vasodilator response to CGRP is persistent.

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Wang, Liming, Jun Yin, Ning Yin, Gerhard Wolff, and Wolfgang M. Kuebler. "Vasodilatory Effect Of The Vasoactive Intestinal Peptide Analog RO 25-1553 In The Pulmonary Circulation: A New Therapy For COPD?" In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2277.

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Toba, Michie, Abdallah Alzoubi, Kohtaro Abe, Takeo Urakami, Masanobu Komatsu, Yuri Matsumoto, Diego Alvarez, et al. "The Cell-Penetrating Homing Peptide CAR Selectively Enhances Pulmonary Effects Of Systemically Co-Administered Vasodilators In A Preclinical Model Of Severe Pulmonary Arterial Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1239.

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