Biomedical subjects

L Edvinsson

Publications and source records attributed to L Edvinsson.

At least 217 records · Page 12Linked to original sources

PubMed1993

Endothelin does not contribute to the vasospasm after balloon angioplasty in vitro.

The present study was undertaken in 43 rabbits to determine whether endothelin or potassium are mediating substances for vasospasm originating from the vessel wall after balloon angioplasty. Thirteen aortic segments were dilated and the luminal surfaces perfused. These perfusates were investigated for their vasomotor action per se and analyzed for their concentrations of potassium and endothelin-like immunoreactivity (ET-LI). The perfusates from angioplasty segments caused a contraction of 2.4 +/- 0.8 mN, while the perfusates from control segments only resulted in a contraction of 0.4 +/- 0.2 mN, (P = 0.004). There was no difference in the concentrations of potassium or ET-LI in the perfusates. Thirty aortic segments were used to measure the concentration of ET-LI in extractions of untreated, control, and angioplasty specimens. There was no statistically significant difference between the groups. Scanning electron microscopy demonstrated the angioplasty segments to be denuded of their endothelium. In conclusion, perfusates from rabbit aortic segments treated by angioplasty in vitro have a strong vasoconstricting effect, for which neither endothelin nor potassium seems to be responsible.

Angioplasty, Balloon↗

PubMed1993

Sympathetic activation after two weeks of nifedipine treatment in primary Raynaud's patients and controls.

The effect of a standardized cold pressor test on circulating noradrenaline and neuropeptide-Y-like immunoreactivity was investigated in 12 women with primary Raynaud's phenomenon and 12 healthy female controls before and after 2 weeks of treatment with the calcium antagonist, nifedipine. Measurement before treatment showed significant increase during the cold pressor test on circulating noradrenaline in both the primary Raynaud's phenomenon group and in the control group (from 0.29 +/- 0.15 ng/ml to 0.33 +/- 0.16 ng/ml, p < 0.05, and from 0.21 +/- 0.14 ng/ml to 0.29 +/- 0.16 ng/ml, p < 0.005, respectively). However, treatment with nifedipine resulted in significantly increased levels of circulating noradrenaline during the cold pressor test only in the control group (from 0.43 +/- 0.21 ng/ml to 0.50 +/- 0.20 ng/ml, p < 0.01). Plasma concentrations of neuropeptide-Y-like immunoreactivity were unchanged by the standardized cold pressor test, whether performed before or during nifedipine treatment in both groups. Nifedipine treatment per se significantly increased circulating noradrenaline in both the primary Raynaud's phenomenon patient group and in the control group (from 0.29 +/- 0.15 to 0.49 +/- 0.13 and 0.21 +/- 0.14 to 0.43 +/- 0.21 ng/ml, respectively, p < 0.001). Similarly, the circulating neuropeptide-Y-like immunoreactivity significantly increased in both the primary Raynaud's phenomenon group and in the control group (from 105 +/- 21 to 137 +/- 19 pmol/l and 107 +/- 17 to 147 +/- 13 pmol/l, respectively, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1993

Cortical blood flow during head-up postural change in subjects with orthostatic hypotension.

Regional cerebral blood flow was measured with the 133-Xenon inhalation method in seven healthy subjects with orthostatic hypotension not due to autonomic failure (i.e. non-neurogenic clinical disorder). Measurements were performed during supine rest and during head-up tilt (70 degrees). All subjects had a consistent drop in systolic blood pressure and the typical symptomatology of orthostatic hypotension. The results showed lower mean hemispheric blood flow during head-up tilt than during supine rest. In addition, a consistent and significant redistribution of the regional flow values was seen, with a reduction in frontal and an increase in postcentral areas. The frontal flow decrease during tilt was more marked than in subjects without orthostatic hypotension and was not related to variations in the level of PCO2 or to respiration. In contrast to the clinical symptoms of orthostatic hypotension (dizziness, nausea, visual disturbances, and in some cases syncope), the cortical blood flow reduction was, however, relatively moderate.

Adult↗

PubMed1993

Examination of the involvement of neuropeptide Y (NPY) in cerebral autoregulation using the novel NPY antagonist PP56.

The contribution of neurotransmitters known to be present in the cervical sympathetic nervous system to cerebral autoregulation was evaluated in the anaesthetised cat using a continuous measurement of cerebral cortical perfusion with laser Doppler flowmetry and an in vitro pial vessel preparation. Autoregulation was tested by venesection and fluid administration to achieve changes in blood pressure from -40% of resting control levels to +80% and flow was monitored. Between -20% and +50% there was no significant alteration in cortical blood flow with perfusion following blood pressure passively outside these ranges. The non-competitive neuropeptide Y antagonist PP56 shifted the level at which the change in flow was passively dependent on blood pressure from +60% to +38%. The pial vessel study demonstrated that PP56 shifted the dose-response curve for the vasoconstrictor effect of NPY with a maximal reduction of 22 +/- 6%. These data suggest that the cervical sympathetic nerves with NPY play an active role in cerebral autoregulation. Furthermore in view of the longer time course of action of neuropeptide Y, it is an ideal transmitter candidate to be involved in cerebral autoregulation and any compound that blocks its action must be considered to potentially alter the normal cerebrovascular physiology.

Animals↗

PubMed1993

PACAP, a VIP-like peptide: immunohistochemical localization and effect upon cat pial arteries and cerebral blood flow.

Pituitary adenylate cyclase activating peptide (PACAP) is a vasoactive intestinal polypeptide (VIP)-like peptide recently isolated from ovine hypothalami. Nerve fibers containing PACAP immunoreactivity were present in the adventitia and the adventitia-media border of cat cerebral arteries. Double immunostaining revealed that PACAP-immunoreactive nerve fibers constituted a subpopulation of the VIP-containing fibers. PACAP effected a concentration-dependent relaxation of feline middle cerebral arteries that had been precontracted with prostaglandin F2 alpha. The maximum relaxation, 24 and 34% of precontraction, was achieved with PACAP-38 and PACAP-27, respectively, at a concentration of 10(-6) M. In cats anesthetized with alpha-chloralose, intracerebral microinjection of PACAP effected a moderate increase in cerebral blood flow. The maximal increase (18.6 +/- 6%) was observed following the injection of 5 micrograms PACAP.

Animals↗

PubMed1993

Cortical spreading depression does not result in the release of calcitonin gene-related peptide into the external jugular vein of the cat: relevance to human migraine.

There is circumstantial evidence that cortical spreading depression (SD) may account for the scotoma and the "spreading cortical oligemia" seen during migraine with aura. It has been shown that calcitonin gene-related peptide (CGRP) is increased in blood taken from the external jugular vein (EJV) in humans during migraine and after stimulation of the trigeminal ganglion. To test the hypothesis that cortical SD may elevate the concentration of this vasoactive peptide in the EJV during migraine, we have measured its concentration in the external jugular vein of cats during cortical SD. This study demonstrates that SD has no effect on the concentration of CGRP either during the passage of a wave of spreading depression across the cortex or, 60 min later, during the period of post-SD cortical oligemia.

Animals↗

PubMed1993

NOS neurones lie near branchings of cortical arteriolae.

We show that numerous neurones labelled for NADPH-diaphorase, which synthetize nitric oxide, lie near branching points of the arteriolae which descend through the cerebral cortex from its pial surface. This spatial relationship suggests the possibility of neural control of cortical blood flow by the NADPH-diaphorase neurones, possibly mediated by the rapid action of nitric oxide.

Amino Acid Oxidoreductases↗

PubMed1993

Characterization of endothelin-A receptors in the cerebral circulation.

Endothelin-1 (ET-1), a 21-amino acid peptide produced by the vascular endothelium, mediates contraction. In the present study we demonstrate that both ET-1 (Emax: 238 +/- 29% of potassium contraction) and ET-2 (Emax: 231 +/- 36%) produce strong concentration-dependent contractions of circular segments of guinea-pig middle cerebral artery, whereas ET-3 has only weak effects (Emax: 32 +/- 13%). FR 139317 (10(-6) M), a selective endothelinA (ETA) receptor antagonist, shifted the ET-1 response curve to the right (pD2:7.86 +/- 0.09 with and 8.76 +/- 0.09 without the antagonist) in a competitive manner (pA2 = 6.83). These findings are the first to show the presence of ETA receptors in cerebral vessels.

Animals↗

PubMed1993

Effects of vasoconstrictors on rabbit coronary arteries exposed to isotonic ionic and nonionic contrast media.

RATIONALE AND OBJECTIVES: Vasodilation is a well-known side effect of contrast media (CM) that is primarily explained by the hyperosmolality of the media. Few reports have dealt with the influences of chemotoxicity and ion toxicity on vessel tone. We compared the effects of solutions iso-osmolar to plasma of iohexol (nonionic monomer), ioxaglate (ionic dimer), diatrizoate (ionic monomer), and mannitol on responses to vasoconstrictors (potassium chloride [KCl], histamine, and endothelin-1). The aim of this study was to investigate if differences in chemotoxicity and ion toxicity could contribute to the changes in vessel tone seen clinically during arteriography. METHODS: Segments of rabbit coronary arteries were mounted between two L-shaped prongs in tissue baths with buffer solution or CM solutions. Their responses to increasing concentrations of a vasoconstrictor were measured. The maximal contraction of the vasoconstrictor (Emax) and the concentration of the vasoconstrictor causing half maximal contraction (EC50) were calculated. RESULTS: Iohexol caused the same changes as the nonionic solution of mannitol. The media reduced the actions of KCl, histamine, and endothelin-1 to 50% to 60% of their action in buffer. The ionic CM, ioxaglate and diatrizoate, caused a more pronounced inhibition of histamine and almost totally inhibited the action of KCl. The action of endothelin-1 was inhibited to a greater extent by iohexol and mannitol than by ioxaglate and diatrizoate. CONCLUSIONS: Different types of iso-osmolar CM interact differently with vasoconstrictors. These effects are caused by differences in chemo- and ion toxicity. These interactions might contribute to the differences in vasodilatation found clinically.

Animals↗

PubMed1993

Cardiovascular effects of alpha-trinositol in spontaneously hypertensive and normotensive Wistar-Kyoto rats.

OBJECTIVE: To investigate the cardiovascular effect of alpha-trinositol (D-myo-inositol-1,2,6-trisphosphate; PP56) in spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto (WKY) rats. alpha-Trinositol, a representative of a new group of pharmacological agents, is an inositol phosphate which seems to bind to a single population of binding sites, inhibiting, for example, agonist-induced vasoconstriction. In particular, alpha-trinositol seems to inhibit agonist-induced (e.g. neuropeptide Y-induced) elevations in intracellular Ca2+ levels in vascular smooth muscle cells. METHODS: alpha-Trinositol was administered as a bolus injection (2-40 mg/kg body weight), followed by a continuous infusion (20-400 mg/kg body weight per h) for 40 min in freely moving SHR and WKY rats. RESULTS: Acute intravenous bolus administration of alpha-trinositol reduced systolic and diastolic blood pressure, as well as heart rate, in a dose-dependent manner in SHR and WKY rats. After completion of the 40-min infusion the reduction in blood pressure was more pronounced in the SHR than in the WKY control rats. Heart rate did not change in the SHR, whereas it was significantly increased at the highest dosage (400 mg/kg) in the WKY rats. At this dosage, three out of eight SHR died from cardiac arrhythmias after completing the infusion. The lowest dose of alpha-trinositol administered (2 mg/kg bolus followed by 20 mg/kg per h infusion over 40 min) significantly inhibited the increase in mean arterial pressure induced by neuropeptide Y (2 micrograms/kg per min for 10 min) by approximately 30% in both the SHR and WKY rats. Furthermore, alpha-trinositol treatment completely inhibited the potentiation induced by neuropeptide Y (0.1 micrograms/min for 30 min) of the blood pressure responses to intravenous bolus injections of noradrenaline (20 ng), tyramine (40 micrograms) or angiotensin II (10 ng). CONCLUSIONS: Our results demonstrate that alpha-trinositol antagonizes the direct postsynaptic pressor response to exogenous neuropeptide Y, as well as the potentiating effects of neuropeptide Y on other vasoconstrictors in SHR and WKY rats. However, in the SHR alpha-trinositol lowered basal blood pressure only in the dose range which was non-specific for neuropeptide Y inhibition. Thus, the present study indicates that neuropeptide Y is involved only slightly in the maintenance of high blood pressure in SHR.

Animals↗

PubMed1993

Effects of cold pressor test on circulating atrial natriuretic peptide 99-126 (ANP) in patients with Raynaud's phenomenon and influence of treatment with magnesium sulphate and nifedipine.

The effect of a standardized cold pressure test (CPT) on the venous concentration of immunoreactive atrial natriuretic peptide (irANP) was studied in 12 females with primary Raynaud's phenomenon (PRP) and 12 female age-matched controls. The test was performed at the end of three stages. During the first stage no medication was given. During the second stage a magnesium infusion was given. After fourteen days of medication with a calcium antagonist (Nifedipine) the third stage of the study was performed. The venous irANP increased significantly (P < 0.05) 10 min after the start of the CPT both in the PRP group and in the control group (136 +/- 39 to 159 +/- 54 and 153 +/- 45 to 179 +/- 40 pg ml-1, given as mean and SD). Baseline irANP did not change in the PRP group after treatment with magnesium or nifedipine. In the control group nifedipine treatment significantly (P < 0.01) lowered venous irANP compared to the no treatment or magnesium sulphate infusion stages (128 +/- 31 vs. 153 +/- 45 and 160 +/- 41 pg ml-1). After the CPT in both PRP group and control group the venous irANP did not increase either during magnesium sulphate infusion or nifedipine treatment. In conclusion the study has demonstrated that a standardized CPT results in a delayed increase in irANP in venous plasma and that magnesium sulphate infusion and nifedipine treatment prevent this increase. Furthermore, our data do not suggest a role for irANP in the symptomatology of primary Raynaud's phenomenon.

Adult↗

PubMed1993

A novel ETA-receptor antagonist, FR 139317, inhibits endothelin-induced contractions of guinea-pig pulmonary arteries, but not trachea.

1. The effects of a proposed endothelin-receptor antagonist, FR 139317, on the contraction induced by endothelin-1, endothelin-2 and endothelin-3, were analysed on isolated circular segments of pulmonary arteries and rings of trachea from the guinea-pig. 2. The pharmacological profiles of endothelin-1 and endothelin-2 were almost identical in the guinea-pig pulmonary artery, whereas endothelin-3 demonstrated a weaker and less potent contractile effect. The contractions induced by endothelin-1 and endotheliln-2 were competitively antagonized by FR 139317. Schild plot analysis revealed a straight line with a slope that did not differ from unity. The pA2 value was 6.65. In contrast, the endothelin-3 induced contractile response was unaffected by FR 139317. 3. In tracheal segments endothelin-1, endothelin-2 and endothelin-3 evoked contractions of similar magnitude and sensitivity. FR 139317 had no effect on the endothelin-induced contractions in tracheal segments. 4. In ring segments of pulmonary artery and trachea, potassium, noradrenaline and histamine caused concentration-dependent contractile effects. These contractions were not modified by FR 139317 in the concentration range 10(-7) to 3 x 10(-6)M. 5. FR 139317 seems to be a selective ETA-receptor antagonist which competitively antagonizes the endothelin-1- and endothelin-2-induced contractions of guinea-pig isolated pulmonary arteries. Thus, the guinea-pig pulmonary artery appears to be endowed with one receptor type (ETA) which is antagonized by FR 139317 and with another endothelin-receptor subtype which responds to endothelin-3, but is not antagonized by FR 139317. In the trachea, all three peptides act on a homogeneous population of receptors which is unaffected by FR 139317. This suggests an ETA-receptor in the guinea-pig pulmonary artery and another receptor, probably of ETB-type, in the guinea-pig trachea.

Animals↗

PubMed1993

Interactions between cultured bovine arterial endothelial and smooth muscle cells: studies on uptake and degradation of low density lipoproteins by smooth muscle cells.

This study was designed to investigate the effects of substances released from non-injured and injured bovine arterial endothelial cells on 125I-low density lipoprotein uptake and degradation by smooth muscle cells in culture. It was demonstrated that endothelial cell-released non-dialysable (molecular weight cut off 12-14000) substances significantly stimulated 125I-low density lipoprotein uptake and degradation by smooth muscle cells. Endothelial cell-released dialysable substances and endothelin-1 did not cause this stimulation. The increase in 125I-low density lipoprotein uptake and degradation by smooth muscle cells could be dissociated from cell proliferation. However, in endothelial cell-smooth muscle cell co-culture 125I-low density lipoprotein uptake and degradation by smooth muscle cells were not stimulated. Injury to endothelial cells by lipid-soluble smoke particles or ultraviolet light, which reduced total cellular protein by 15-25%, enhanced the endothelial cell release of the substances stimulating 125I-low density lipoprotein uptake. The results are discussed in relation to atherogenesis.

Animals↗

PubMed1993

5-Hydroxytryptamine receptor characterization of human cerebral, middle meningeal and temporal arteries: regional differences.

We have studied the regional distribution of 5-hydroxytryptamine (5-HT) receptor subtypes in fresh circular segments of human cerebral, middle meningeal, and temporal arteries. Vasomotor responses induced by a series of 5-HT agonists and antagonists with some degree of selectivity were studied by using a sensitive in vitro system. Nine 5-HT agonists were examined for contractile effects on the arteries. In cerebral and meningeal arteries 5-carboxamidotryptamine (5-CT) was more potent than 5-HT. The opposite order of potency (5-HT-5-CT) was found in temporal arteries. In the cerebral arteries 5-methoxytryptamine (5-MeOHT) was more potent than sumatriptan while sumatriptan was more potent than 5-MeOHT in meningeal and temporal arteries. The 5-HT1 receptor antagonist, methiothepin, competitively antagonized 5-CT-induced contractions in cerebral arteries, with a pA2 value of 9.05. 5-HT-induced contractions were competitively antagonized by ketanserin (5-HT2) in the temporal arteries pA2 value of 9.06). Methiothepin and ketanserin had non-competitive antagonistic effects in the middle meningeal arteries. The 5-HT3 selective antagonist ondansetron did not cause any shift of the contractions induced by 2-methyl-5-HT in the temporal, cerebral and middle meningeal arteries. These results suggest that the cerebral arteries mainly contain 5-HT1D or 5-HT1-like receptors, and the temporal artery 5-HT2 receptors; the data further indicate the presence of both receptor subtypes in the middle meningeal artery.

5-Methoxytryptamine↗

PubMed1993

In-vivo effects of endothelin-1 and ETA receptor blockade on arterial, venous and capillary functions in skeletal muscle.

Results from in vitro studies have indicated that endothelin-1 is a main candidate for endothelium-derived contracting factors. The aim of this in vivo study was to describe in quantitative terms the effects of endothelin-1 (ET-1), and of ETA receptor blockade, on vascular tone (resistance) in large-bore arterial resistance vessels (> 25 microns), small arterioles (< 25 microns) and the veins, as well as on capillary pressure and fluid exchange in cat gastrocnemius muscle. Endothelin-1 (100-1600 ng kg-1 min-1, i.a.) elicited, after an initial transient dilation, a strong dose-dependent constrictor response in all three consecutive vascular sections, yet with a preferential action on the small arterioles and the veins. The vasoconstriction developed very slowly over about 1 h and was also long-lasting after cessation of the infusion. Our main quantitative analysis refers to effects elicited by 20 min long i.a. infusions of ET-1 at a dose of 400 ng kg-1 min-1. At the end of this period, the peptide caused, on average, a three-fold increase in total regional vascular resistance, in turn explained by a 70% increase in large-bore arterial resistance, a 280% increase in arteriolar resistance and a 220% increase in venous resistance. The latter effect was also manifested as a pronounced capacitance response, and as a decrease in the pre- to post-capillary resistance ratio leading regularly to a rise in capillary pressure, net transcapillary fluid filtration and oedema formation which is unusual for a vasoconstrictor. The new specific competitive ETA receptor antagonist FR 139317 was found to be fully effective in vivo, insofar as it abolished the constrictor response to endothelin-1. ETA receptor blockade, or administration of phosphoramidon, an inhibitor of ET-1 production, did not influence the level of basal vascular tone, indicating no significant endogenous release of ET-1 under resting conditions. This contrasts to the established pronounced endogenous release of endothelium-derived nitric oxide. Finally, vascular myogenic regulation was found not to be mediated by ET-1. The results, taken together, suggest a possible role of ET-1 in long-term, rather than short-term, regulation of vascular tone in vivo, perhaps especially during pathophysiological conditions.

Animals↗

PubMed1993

Mitogenic effects of ATP on vascular smooth muscle cells vs. other growth factors and sympathetic cotransmitters.

The sympathetic nervous system has been shown to exert a trophic influence on vascular smooth muscle cells (VSMC). Therefore, we studied the growth-regulating effects of the sympathetic cotransmitters ATP, neuropeptide Y (NPY), and norepinephrine (NE). ATP in concentrations of 1-100 microM greatly increased the incorporation of [3H]thymidine in VSMC from rat aorta and vena cava. ATP also increased cell number and total protein content. The maximal effect on [3H]thymidine incorporation was greater than for epidermal growth factor (20 ng/ml) or insulin (1 microgram/ml) and approximately one-half that of 10% fetal calf serum. The potency series of other nucleotides and analogues of ATP was ATP > beta, gamma-methyleneATP (AMP-PCP) > ADP > adenosine > alpha, beta- methyleneATP (AMP-CPP) > 2-methylthioATP, indicating involvement of a P2 receptor, however, it does not meet proposed pharmacological criteria of either the P2x or P2y subclass. Several proposed P2 receptor antagonists were without effect. The effect of ATP could be mediated by a "nucleotide receptor," since UTP also stimulated [3H]thymidine incorporation. In our model, there was a strong correlation between the mitogenic effects of ATP, AMP-CPP, AMP-PCP, and UTP and their ability to stimulate influx of extracellular Ca2+ (Ca2+o). Moreover, the mitogenic effect of ATP was increased by high concentrations of Ca2+o. Taken together with data showing the lack of involvement of several other second-messenger systems, this indicates a critical role for Ca2+o in mediating the mitogenic effects of ATP. Amiloride, known to inhibit the action of several growth factors, also inhibited ATP-induced mitogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1993

Peptidergic innervation of human epicardial coronary arteries.

The peptidergic innervation of proximal (internal diameter, > 0.8 mm) and distal (internal diameter, < 0.8 mm) regions of human epicardial coronary arteries was investigated by means of immunohistochemical, chromatographic, radioimmunological, and in vitro pharmacological techniques. The use of an antiserum to the general neuronal marker protein gene product 9.5 revealed that the proximal part of epicardial arteries possessed a relatively sparse supply of nerve fibers forming a loose network in the adventitia. The perivascular network increased in density as the vessels were followed distally. In both proximal and distal regions, the majority of nerve fibers possessed neuropeptide Y and tyrosine hydroxylase immunoreactivity. Calcitonin gene-related peptide (CGRP)- and substance P-immunoreactive nerve fibers were very sparse in the proximal region of the arteries and increased in number distally. Only a few scattered vasoactive intestinal peptide (VIP)-immunoreactive nerve fibers were detected in both arterial regions. The use of high-performance liquid chromatography and radioimmunoassay revealed that the immunoreactive material present in coronary artery extracts closely resembled synthetic peptides. An in vitro pharmacological method demonstrated that neuropeptide Y elicited no detectable response in either proximal or distal arterial segments. In contrast, CGRP, substance P, and VIP all produced a concentration-dependent relaxation of both arterial regions. CGRP and substance P were stronger and more potent than VIP. CGRP and substance P induced a more potent response in distal compared with proximal regions of the arteries. These results suggest that the peptidergic nerves supplying human large epicardial coronary arteries may be predominantly involved in mediating vasodilation.

Adult↗

PubMed1993

Endothelial influence on vessel wall induced vasospasm after balloon angioplasty.

Aortic segments from 47 New Zealand rabbits were used, of which 14 were denuded of endothelium. Balloon angioplasty was performed on the aortic segments in vitro. The inner surfaces were perfused and the perfusates then given to vessel segments with or without endothelium. The contraction evoked was then counteracted by adding either vasoactive intestinal polypeptide (VIP), substance P (SP), acetylcholine (ACh), or nitroglycerin (NTG) in increasing concentrations. Perfusates from aortic segments with or without endothelium and previously treated with angioplasty induced vasoconstriction of similar magnitude in the segments used for vasomotor investigation irrespective of whether the endothelium was intact in these or not. Endothelial dependent dilators (ACh, SP) did not counteract the contraction whereas endothelial independent dilators did (NTG, VIP). Neither the induction nor the reversal of vessel wall induced vasoconstriction after balloon angioplasty seems to depend on the presence of endothelial cells.

Acetylcholine↗