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At least 19 recordsLinked to original sources
PubMed2004

Tachykinin and tachykinin receptor of an ascidian, Ciona intestinalis: evolutionary origin of the vertebrate tachykinin family.

Tachykinins (TKs) are the most prevalent vertebrate brain/gut peptides. In this study, we originally identified authentic TKs and their receptor from a protochordate, Ciona intestinalis. The Ciona TK (Ci-TK) precursor, like mammalian gamma-preprotachykinin A (gamma-PPTA), encodes two TKs, Ci-TK-I and -II, including the -FXGLM-NH(2) vertebrate TK consensus. Mass spectrometry of the neural extract revealed the production of both Ci-TKs. Ci-TK-I contains several Substance P (SP)-typical amino acids, whereas a Thr is exceptionally located at position 4 from the C terminus of Ci-TK-II. The Ci-TK gene encodes both Ci-TKs in the same exon, indicating no alternative generation of Ci-TKs, unlike the PPTA gene. These results suggested that the alternative splicing of the PPTA gene was established during evolution of vertebrates. The only Ci-TK receptor, Ci-TK-R, was equivalently activated by Ci-TK-I, SP, and neurokinin A at physiological concentrations, whereas Ci-TK-II showed 100-fold less potent activity, indicating that the ligand selectivity of Ci-TK-R is distinct from those of vertebrate TK receptors. Ci-TK-I, like SP, also elicited the typical contraction on the guinea pig ileum. The Ci-TK gene was expressed in neurons of the brain ganglion, small cells in the intestine, and the zone 7 in the endostyle, which corresponds to the vertebrate thyroid gland. Furthermore, the Ci-TK-R mRNA was distributed in these three tissues plus the gonad. These results showed that Ci-TKs play major roles in sexual behavior and feeding in protochordates as brain/gut peptides and endocrine/paracrine molecules. Taken together, our data revealed the biochemical and structural origins of vertebrate TKs and their receptors.

Alternative Splicing↗
PubMed2005

Functional and molecular characterization of tachykinins and tachykinin receptors in the mouse uterus.

The aim of this study was to analyze the function and expression of tachykinins, tachykinin receptors, and neprilysin (NEP) in the mouse uterus. A previous study showed that the uterotonic effects of substance P (SP), neurokinin A (NKA), and neurokinin B (NKB) in estrogen-treated mice were mainly mediated by the tachykinin NK1 receptor. In the present work, further contractility studies were undertaken to determine the nature of the receptors mediating responses to tachykinins in uteri of late pregnant mice. Endpoint and real-time quantitative RT-PCR were used to analyze the expression of the genes that encode the tachykinins SP/NKA, NKB, and hemokinin-1 (HK-1) (Tac1, Tac2, and Tac4); and the genes that encode tachykinin NK1 (Tacr1), NK2 (Tacr2), and NK3 (Tacr3) receptors in uteri from pregnant and nonpregnant mice. The data show that the mRNAs of tachykinins (particularly NKB and HK-1), tachykinin receptors, and NEP are locally expressed in the mouse uterus, and their expression changes during the estrous cycle and during pregnancy. The tachykinin NK1 receptor is the predominant tachykinin receptor in the nonpregnant and early pregnant mouse and may mediate tachykinin-induced uterine contractions in the nonpregnant mouse. The tachykinin NK2 receptor is predominant in the late pregnant mouse and is the main receptor mediating uterotonic responses to tachykinins at late pregnancy. The tachykinin NK3 receptor is expressed in considerable amounts only in uteri from nonpregnant diestrous animals, and its physiological significance remains to be clarified.

Animals↗
PubMed1999

Central tachykinin NK3 receptors in the inhibitory action on the rat colonic propulsion of a new tachykinin, PG-KII.

The inhibitory action of the natural selective tachykinin NK3 receptor agonist, PG-KII, (pGlu-Pro-Asn-Pro-Asp-Glu-Phe-Val-Gly-Leu-Met-NH2), on colonic propulsion was studied in rats after central administration. Intracerebroventricular injection of PG-KII (0.1, 1, 10 and 100 ng/rat) produced a dose-related inhibition of colonic propulsion, measured as the increase in the mean expulsion time of a 5-mm glass bead placed in the distal colon. At the same doses as PG-KII, the selective tachykinin NK3 receptor agonist, senktide, (succ-[Asp6-MePhe8] substance P-(6-11)), induced a similar dose-related inhibition. Conversely, substance P (0.1, 1 and 10 microg/rat), a tachykinin NK1-preferring receptor agonist, had weaker antipropulsive effects, neurokinin A (0.1, 1 and 10 microg/rat), a tachykinin NK2-preferring receptor agonist, at the highest dose used only slightly inhibited colonic propulsion and neurokinin B (0.1, 1 and 10 microg/rat), a tachykinin NK3-preferring receptor agonist, left propulsion unchanged. Pretreatment with the selective tachykinin NK3 receptor antagonist, 3-indolycarbonyl-Hyp-Phg-N(me)-Bzl, referred as to R820 (6.2 microg/rat), prevented PG-KII-induced colonic antipropulsion, whereas the tachykinin NK1 receptor antagonist, (S)-1-(2-[3-(3,4-dichlorophenyl)-1-(3-isopropoxyphenylacetyl)pi peridin-3-yl] ethyl)-4-phenyl-1-azoniabicyclo[2.2.2] octane chloride, referred to as SR 140,333 (1 microg/rat), and the tachykinin NK2 receptor antagonist, ([Tyr5,D-Trp6,8,9, Arg10] neurokinin A-(4-10)), referred to as Men 10,376 (5 microg/rat), left it unchanged. These findings show that of the tachykinins tested, PG-KII and senktide are the most potent central inhibitors of colonic propulsion in the rat, suggesting that the central tachykinin NK3 receptor system plays an inhibitory role in modulating colonic transit. As well as confirming the selectivity of PG-KII for tachykinin NK3 receptors, we show that PG-KII provides useful information about the physiological role of central tachykinin NK3 receptors and that glass bead expulsion test is a reliable non-invasive in vivo method for evaluating the tachykinin NK3 receptor selectivity of new synthetic or natural tachykinins.

Animals↗
PubMed2003

Tachykinins and tachykinin receptors in human uterus.

(1) Studies were undertaken to determine the nature of the receptors mediating contractile effects of tachykinins in the uteri of nonpregnant women, and to analyse the expression of preprotachykinins (PPT), tachykinin receptors and the cell-surface peptidase, neprilysin (NEP), in the myometrium from pregnant and nonpregnant women. (2) The neurokinin B (NKB) precursor PPT-B was expressed in higher levels in the myometrium from nonpregnant than from pregnant women. Faint expression of PPT-A mRNA was detectable in the myometrium from nonpregnant but not pregnant women. PPT-C, the gene encoding the novel tachykinin peptide hemokinin-1 (HK-1), was present in trace amounts in the uteri from both pregnant and nonpregnant women. (3) Tachykinin NK(2) receptors were more strongly expressed in tissues from nonpregnant than from pregnant women. NK(1) receptor mRNA was present in low levels in tissues from both pregnant and nonpregnant women. A low abundance transcript corresponding to the NK(3) receptor was present only in tissues from nonpregnant women. (4) The mRNA expression of the tachykinin-degrading enzyme NEP was lower in tissues from nonpregnant than from pregnant women. (5) Substance P (SP), neurokinin A (NKA) and NKB, in the presence of the peptidase inhibitors thiorphan, captopril and bestatin, produced contractions of myometrium from nonpregnant women. The order of potency was NKA>>SP>/=NKB. The potency of NKA was unchanged in the absence of peptidase inhibitors. (6) The tachykinin NK(2) receptor-selective agonist [Lys(5)MeLeu(9)Nle(10)]NKA(4-l0) was approximately equipotent with NKA, but the tachykinin NK(1) and NK(3) receptor-selective agonists [Sar(9)Met(O(2))(11)]SP and [MePhe(7)]NKB were ineffective in the myometrium from nonpregnant women. (7) The uterotonic effects of [Lys(5)MeLeu(9)Nle(10)]NKA(4-10) were antagonized by the tachykinin NK(2) receptor-selective antagonist SR48968. Neither atropine, nor phentolamine nor tetrodotoxin affected responses to [Lys(5)MeLeu(9)Nle(10)]NKA(4-10). (8) These data are consistent with a role of tachykinins in the regulation of human uterine function, and reinforce the importance of NK(2) receptors in the regulation of myometrial contraction.

Adult↗
PubMed2002

The human tachykinin NK1 (short form) and tachykinin NK4 receptor: a reappraisal.

Excessive secretion of placental neurokinin B into the circulation during the third trimester of pregnancy is seen in women with preeclampsia. To determine a role for neurokinin B, we have used a number of different animal models to ascertain the expression of the three tachykinin receptors (NK1--both short and long forms, NK2 and NK3) and the putative human tachykinin NK4 receptor in the placenta. Human and rat placenta express all three classical tachykinin receptors. However, we failed to reveal the expression of the short tachykinin NK1 receptor or the tachykinin NK4 receptor in any of 24 human tissues examined including the placenta. We conclude that the proposed short form of the tachykinin NK1 receptor is a truncated genomic clone and that the human tachykinin NK4 receptor is in fact, the guinea pig tachykinin NK3 receptor.

Animals↗
PubMed1997

Involvement of tachykinin NK1 receptors in plasma protein extravasation induced by tachykinins in the guinea pig upper airways.

Plasma protein extravasation in the upper airways of anesthetized guinea pigs was measured with the FITC (Fluorescein isothiocyanate)-dextran technique. The effect of selective tachykinin (NK1 and NK2) receptor agonists and antagonists, capsaicin or antigen was studied. The tachykinin NK1 receptor agonist, [Sar9]substance P sulfone, induced an increase in FITC-dextran extravasation which was blocked by the nasal application (30-100 nmol/kg) of the tachykinin NK1 receptor antagonist FK888, but not by 1 micromol/kg of the tachykinin NK2 receptor antagonist, MEN10,627. The tachykinin NK2 receptor agonist, [betaAla8]neurokinin A-(4-10), had no effect on dye leakage. FK888 (30 nmol/kg intranasal) abolished the increase in the tracer recovery induced both by antigen and capsaicin. Conversely, the intranasal administration of MEN10,627 (0.1-1.0 micromol/kg) significantly reduced capsaicin-induced and only marginally inhibited antigen-induced increase in plasma protein extravasation. Pretreatment with the neutral endopeptidase inhibitor, phosphoramidon, increased the effect of all inflammatory agents. These findings show that the plasma extravasation of the upper airways induced by exogenous or endogenous tachykinins is primarily mediated by tachykinin NK1 receptors. This inflammatory response could be controlled by locally applied tachykinin NK1 receptor antagonist.

Animals↗
PubMed2002

Tachykinins and tachykinin receptors in bone.

Tachykinins are neuropeptides that are widely distributed in the body and function as neurotransmitters and neuromodulators. Five tachykinin subtypes: substance P (SP), neurokinin A, neurokinin B, neuropeptide K, and neuropeptide gamma; and three receptor subtypes: neurokinin-1, -2, and -3 receptors, have been identified. SP was the first peptide of the tachykinin family to be identified. It is considered to be an important neuropeptide, and to function in the nervous system and intestine. However, recent advances in the analysis of SP receptors, particularly neurokinin-1 receptors (NK(1)-Rs) that have high affinity for SP, have demonstrated that NK(1)-Rs are distributed not only in neurons and immune cells, but also in other peripheral cells, including bone cells. This article reviews the current understanding of the distribution of SP and other tachykinins in bone, and the function of tachykinins, through neurokinin receptors. The distribution of tachykinin-immunoreactive axons and neurokinin receptors suggests that tachykinins may directly modulate bone metabolism through neurokinin receptors.

Animals↗
PubMed2004

Tachykinins and tachykinin receptors: a growing family.

The peptides of the tachykinin family are widely distributed within the mammalian peripheral and central nervous systems and play a well-recognized role as excitatory neurotransmitters. Currently, the concept that tachykinins act exclusively as neuropeptides is being challenged, since the best known members of the family, substance P, neurokinin A and neurokinin B, are also present in non-neuronal cells and in non-innervated tissues. Moreover, the recently cloned mammalian tachykinins hemokinin-1 and endokinins are primarily expressed in non-neuronal cells, suggesting a widespread distribution and important role for these peptides as intercellular signaling molecules. The biological actions of tachykinins are mediated through three types of receptors denoted NK(1), NK(2) and NK(3) that belong to the family of G protein-coupled receptors. The identification of additional tachykinins has reopened the debate of whether more tachykinin receptors exist. In this review, we summarize the current knowledge of tachykinins and their receptors.

Amino Acid Sequence↗
PubMed2004

Tachykinins and tachykinin receptors: structure and activity relationships.

In addition to the classical neurotransmitters, acetylcholine and noradrenaline, a wide number of peptides with neurotransmitter activity have been identified in the past few years. Among them, the tachykinins substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) appear to act as mediators of nonadrenergic, noncholinergic (NANC) excitatory neurotransmission. Tachykinins interact with specific membrane proteins, belonging to the family of G protein-coupling cell membrane receptors. Until now, three tachykinin receptors termed NK1 (NK1R), NK2 (NK2R) and NK3 (NK3R) have been cloned in different species. A large amount of reports suggests that these peptides are involved in nociception and neuroimmunomodulation, and in the development of different diseases such as bronchial asthma, inflammatory bowel syndrome and psychiatric disorders. Tachykinin receptor antagonists are therefore promising, therapeutically relevant agents. However, and in spite of extensive research, the obtention of selective antagonists of tachykinin receptors have revealed very difficult. An understanding of how ligands interact with their receptors is essential to permit a rational design of compounds acting selectively at the tachykinin receptor level. The major aim of the present article is to review the structure-activity data that exist for tachykinins and their receptors, with the purpose of getting insight into basic structural requirements that determine ligand/receptor interaction.

Amino Acid Sequence↗
PubMed2001

Contractile responses to natural tachykinins and selective tachykinin analogs in normal and inflamed ileal and colonic muscle.

BACKGROUND: Tachykinins and acetylcholine are main physiological motility stimulators in the gut by their effects exerted through neurokinin and muscarinic receptors. METHODS: Longitudinal and circular muscle strips from normal ileum and colon or corresponding tissues from patients with inflammatory bowel disease were studied in organ baths. Contractile responses to the tachykinins substance P, neurokinin A, neurokinin B and neuropeptide gamma and specific analogs for their respective receptors were compared to acetylcholine. RESULTS: Acetylcholine caused concentration-dependent phasic contractions in longitudinal and circular muscle of normal ileum and colon (both P < 0.01). In inflamed tissues, contractile responses were reduced to 17%-33% in ileum (P < 0.05) and 3%-26% in colon (P < 0.01). Both natural tachykinins and their specific analogs caused concentration-dependent phasic, tonic and rhythmic contractions (each P < 0.01). Neuropeptide gamma was most potent in contracting the ileum and colon, followed by neurokinin A, substance P and neurokinin B, let alone longitudinal muscle of the ileum where neuropeptide gamma and neurokinin A were equipotent. Of the tachykinin analogs, Nle10-NKA(4-10) was more potent than substance P methyl ester and senktide, indicating neurokinin 2 receptors are predominant for contractile effects of tachykinins. In inflamed tissues, contractile responses to tachykinins were reduced to 0%-42% in ileum (P < 0.05) and 0%-17% in colon (P < 0.01) compared to controls. CONCLUSION: In humans, tachykinins exert gut contractile effects, of similar strength as acetylcholine, predominantly through activation of neurokinin 2 receptors. These responses are greatly reduced in inflamed tissues of ulcerative colitis and Crohn disease.

Acetylcholine↗
PubMed1987

Effect of the tachykinin antagonist, [D-Pro4, D-Trp7,9,10] substance P-(4-11), on tachykinin- and histamine-induced inositol phosphate generation in intestinal smooth muscle.

The effect of the tachykinin antagonist, [D-Pro4, D-Trp7,9,10] substance P-(4-11), on inositol phosphate accumulation produced by tachykinins and by histamine in strips of longitudinal muscle from the guinea-pig small intestine was investigated in the presence of 12 mM Li+. The two tachykinins substance P (SP) and kassinin (20 nM-20 microM) caused an accumulation of inositol phosphates in a concentration-dependent manner. This was seen with an agonist contact time of only 30 s. SP and kassinin were roughly equipotent in inducing inositol phosphate accumulation, which is consistent with their relative potencies in causing muscle contraction. The tachykinin antagonist (20 microM) produced a shift to the right of the dose-response curves for inositol phosphate accumulation caused by SP and kassinin. However, the effect of kassinin was inhibited much more than that of SP, which is consistent with a similar differential antagonism of the contractions induced by these agonists. The tachykinin antagonist also depressed histamine-induced accumulation of inositol phosphates whereas histamine-induced contractions had previously been found unaffected by the antagonist. These findings show that the tachykinin antagonist is not totally selective with regard to agonist-induced accumulation of inositol phosphates in intestinal smooth muscle. This may suggest that the antagonist not only acts on tachykinin receptors but also has another site of cellular action.

Animals↗
PubMed2006

Tachykinins are involved in local reflex modulation of vagally mediated striated muscle contractions in the rat esophagus via tachykinin NK1 receptors.

The objective of the present study was to investigate the hypothesis of the presence of a local neural reflex modulating the vagally mediated contractions of striated muscle in the rat esophagus and to determine the possible involvement of tachykinins in such a local neural reflex. Electrical stimulation of the vagus nerve evoked twitch contractile responses that were abolished by d-tubocurarine (5 microM). Capsaicin (1-100 microM) inhibited the vagally mediated twitch contractions o f the normal rat esophageal preparations concentration-dependently but not those of the neonatally capsaicin-treated ones. NG-nitro-L-arginine methyl ester (100 microM), a nitric oxide synthase inhibitor, blocked the inhibitory effect of capsaicin and exogenous application of a nitric oxide donor (1 mM) inhibited the vagally mediated twitch contractions. Capsaicin suppressed acetylcholine release from the normal rat esophageal segments evoked by vagus nerve stimulation but not that from the neonatally capsaicin-treated ones. A selective tachykinin NK1 receptor antagonist (0.1 or 1 microM) attenuated the inhibitory effect of capsaicin. However, antagonists of tachykinin NK2, tachykinin NK3 and calcitonin gene-related peptide receptors (1 microM) did not have any effect. A tachykinin NK1 receptor agonist (1 or 5 microM) inhibited the vagally mediated twitch contractions, which was prevented by NG-nitro-L-arginine methyl ester (100 microM). These data suggest that the rat esophagus might have a local neural reflex inhibiting the vagally mediated striated muscle motility, which consists of capsaicin-sensitive sensory neurons and myenteric nitrergic neurons, and that tachykinins might be involved in the neural reflex through tachykinin NK1 receptors.

Acetylcholine↗
PubMed1991

Tachykinin receptor subtypes involved in the central effects of tachykinins on water and salt intake.

The present study was aimed at investigating which tachykinin receptor subtypes mediate the inhibitory effects of tachykinins a) on salt intake induced by sodium depletion, b) on water intake induced by subcutaneous hypertonic NaCl administration and c) on water intake induced by central angiotensin II injection. The study was carried out by evaluating the potency of action, following intracerebroventricular injection, of several peptides, including both naturally occurring tachykinins and synthetic peptides selective for a given receptor subtype. The results obtained show different rank orders of potency of the agonists in the different behavioral tests, thus suggesting that different receptor subtypes are involved in the effects of tachykinins on water and salt intake. NK-3 receptors appear to be involved in the inhibitory effect of tachykinins on depletion-induced salt appetite. NK-2 receptors apparently mediate the inhibitory effect of tachykinins on drinking induced by hyperosmotic NaCl administration, while NK-1 receptors are probably involved in the inhibition of angiotensin II-induced drinking.

Amino Acid Sequence↗
PubMed2001

Airway inflammation and tachykinins: prospects for the development of tachykinin receptor antagonists.

The tachykinins substance P and neurokinin A are contained within sensory airway nerves. Immune cells form an additional source of tachykinins in inflamed airways. Elevated levels of tachykinins have been recovered from the airways of patients with asthma and chronic obstructive pulmonary disease. Airway inflammation leads to an upregulation of tachykinin NK(1) and NK(2) receptors. Preclinical studies have indicated a role for the tachykinin NK(1), NK(2) and NK(3) receptors in bronchoconstriction, airway hyperresponsiveness and airway inflammation caused by allergic and nonallergic stimuli. Compounds that are able to block two or three tachykinin receptors hold promise for the treatment of airways diseases such as asthma and/or chronic obstructive pulmonary disease.

Animals↗
PubMed1988

A tachykinin receptor antagonist inhibits and an inhibitor of tachykinin metabolism potentiates toluene diisocyanate-induced airway hyperresponsiveness in guinea pigs.

We have previously shown that tachykinin depletion or antagonism prevented the increase in airway responsiveness to inhaled acetylcholine caused by exposure to toluene diisocyanate (TDI) in awake guinea pigs. To insure that the effects of tachykinins were not limited to the extrathoracic airways and were not dependent on effects of TDI on baseline airway caliber, we determined airway responsiveness to acetylcholine inhaled through a tracheostomy in anesthetized and ventilated guinea pigs that were exposed to TDI or air after treatment with the tachykinin antagonist spantide, the tachykinin metabolism inhibitor phosphoramidon, or the vehicles for each drug. When these drugs were administered before and during TDI exposure, spantide significantly inhibited the TDI-induced increase in acetylcholine responsiveness and phosphoramidon significantly potentiated this effect, whereas neither drug altered acetylcholine responsiveness in air-exposed animals. To determine whether tachykinins were exerting their effect primarily during TDI exposure or during the subsequent acetylcholine challenge, we also examined the effect of each drug on acetylcholine responsiveness when the drugs were given after TDI exposure. At that time, spantide did not inhibit TDI-induced acetylcholine hyperresponsiveness and phosphoramidon did not potentiate it. Neither drug nor TDI increased pulmonary resistance measured through a tracheostomy in these anesthetized and ventilated animals. These results suggest that the TDI-induced increase in acetylcholine responsiveness is mediated by release of tachykinins into the intrathoracic airways during exposure to TDI.

Acetylcholine↗
PubMed2000

NK1, NK2 and NK3 tachykinin receptor localization and tachykinin distribution in the ileum of the mouse.

Tachykinin receptors NK1r, NK2r and NK3r bind tachykinins with different affinities and share pharmacological and molecular differences among animal species. NK1r, NK2r, NK3r and tachykinin (SP/NKA) distribution was studied by immunohistochemistry in the ileum of mouse since no data are available for this species. The results were then compared to those obtained in the rat and guinea pig either by us or by others to ascertain interspecies similarities and/or differences. NK1r- and NK3r-immunoreactivity (IR) were detected in neurons and NK1r-IR in the interstitial cells of Cajal at the deep muscular plexus. At variance with rat and guinea pig, NK1r-IR was also found in the myoid cells of the villi, while NK2r-IR was never detected in nerve varicosities. This latter datum suggests that the NK2r does not play a presynaptic role in the mouse. Unexpectedly, a high NK2r-IR and the presence of NK3r-IR were observed at the inner portion of the circular muscle layer in the mouse as well as in the rat and guinea pig, demonstrating a subregional distribution of these receptors. Tachykinin distribution did not show noticeable species-related differences. The present findings show species-related differences in the tachykinin receptor distribution that might be related to a different tachykinin control of intestinal motility.

Animals↗
PubMed2004

Newly discovered tachykinins raise new questions about their peripheral roles and the tachykinin nomenclature.

The tachykinin family has recently been extended by the discovery of a third tachykinin gene encoding previously unknown mammalian tachykinins (hemokinin 1, endokinin A and endokinin B) that have a widespread peripheral distribution and a tachykinin NK(1) receptor selectivity. This and the identification of other tachykinin-like peptides such as C14TKL-1 and virokinin raise many questions about the roles played by tachykinins in peripheral tissues and render terms such as 'neurokinins' and 'SP receptor' inappropriate.

Animals↗
PubMed2004

mRNA expression of tachykinins and tachykinin receptors in different human tissues.

The tachykinins substance P, neurokinin A and neurokinin B are involved in many pathophysiological processes. A reverse transcription-polymerase chain reaction (RT-PCR) assay was used to analyse the expression of TAC1 and TAC3, the genes that encode substance P/neurokinin A and neurokinin B, respectively, and the genes encoding the tachykinin NK(1), NK(2) and NK(3) receptors in different human tissues. The data show that tachykinins and their receptors mRNAs are broadly distributed in different human tissues being present in neuronal and non-neuronal types of cells. The presence of TAC3 and the tachykinin NK(3) receptor (TACR3) in a wide variety of peripheral tissues argue for a still unexplored role of this ligand-receptor pair in mediating visceral effects of tachykinins. We found, for the first time, that TAC3 and TACR3 mRNAs are expressed in human airways and pulmonary arteries and veins, providing further evidence for the involvement of this system in lung physiopathology.

Actins↗