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Biomedical subjects

L Edvinsson

Publications and source records attributed to L Edvinsson.

At least 127 records · Page 7Linked to original sources
PubMed1997

Role of endothelium and nitric oxide in histamine-induced responses in human cranial arteries and detection of mRNA encoding H1- and H2-receptors by RT-PCR.

1. Histamine induces relaxation of human cranial arteries. Studies have revealed that the relaxant histamine H1-receptor predominates in human cerebral and the H2-receptor in temporal arteries, while H1- and H2-receptors are of equal importance in the middle meningeal artery. The purpose of the present study was to examine the role of the endothelium and nitric oxide in histamine-induced responses and to show the presence of mRNA encoding H1- and H2-receptors in human cranial arteries. 2. Electrophoresis of polymerase chain reaction (PCR) products from human cerebral, middle meningeal and temporal arteries, demonstrated products corresponding to mRNA encoding both H1- and H2-receptors in arteries with and without endothelium. The amplified PCR products were sequenced and showed 100% homology with the published sequences of these histamine receptors. 3. A sensitive in vitro system was used to study vasomotor responses to histamine. In precontracted cerebral, middle meningeal and temporal arteries with and without endothelium, histamine caused a concentration-dependent relaxation with Imax values between 87% and 81% and pIC50 values between 8.14 and 7.15. In arteries without endothelium the histamine-induced relaxation was significantly less potent (Imax values between 87% and 66% and pIC50 values between 7.01 and 6.67) than in cranial arteries with an intact endothelium. 4. This addition of histamine to arteries without endothelium and pretreated with the histamine H2-antagonist, cimetidine (10(-5) M), caused a concentration-dependent contraction of the cranial arteries with Emax values between 86% and 29% and pEC50 values between 7.53 and 6.77. This contraction was blocked by the histamine H1-receptor antagonist, mepyramine (10(-7) M), and even turned into a relaxation with Imax values between 84% and 14% and pIC50 values between 7.42 and 5.86. 5. The nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 3 x 10(-5) M) significantly inhibited the relaxant response to histamine in cerebral and temporal arteries (pIC50 values between 7.43 and 7.13). The combined treatment with L-NAME (3 x 10(-5) M) and cimetidine (10(-5) M) caused a further displacement of the concentration-response curve (pIC50 values between 7.14 and 6.57) and decreased the maximum relaxant responses in all three cranial arteries (Imax values between 62% and 39%). 6. In conclusion, this is the first study which show mRNA encoding histamine H1- and H2-receptors in human cranial arteries. The results indicate that histamine-induced relaxation of human cranial arteries is partially mediated via an endothelial H1-receptor coupled to the production of nitric oxide and partially via a H2-receptor associated with the smooth muscle cells. In addition, there is evidence for a contractile H1-receptor in the smooth muscle cells in these arteries.

Cerebral Arteries↗
PubMed1997

Release of histamine from dural mast cells by substance P and calcitonin gene-related peptide.

The aim of the present study was to examine if the neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) can stimulate histamine release from mast cells in the dura mater and thereby play a role in cranial vasoregulation and local neurogenic inflammation. Dura mater mast cells were compared with peritoneal mast cells in the rat. Histamine was released from dura mater mast cells by compound 48/80, SP and CGRP but from peritoneal mast cells only by compound 48/80 and SP. NPY and VIP released quite small amounts of histamine from dural mast cells. The release of SP and CGRP from rat dura mater mast cells was blocked by the receptor antagonists FK888 and CGRP8-37 respectively, suggesting receptor mediated release mechanisms. None of the stimuli released histamine from human or porcine dural mast cells, possibly because the sampling procedure injures and incapacitates the cells.

Animals↗
PubMed1997

Does the neuropeptide Y Y1 receptor contribute to blood pressure control in the spontaneously hypertensive rat?

OBJECTIVE: To study the effects of the selective neuropeptide Y (NPY) Y1 receptor antagonist BIBP 3226 in spontaneously hypertensive rats (SHR) in order to elucidate whether NPY function may be altered in the SHR and whether the NPY Y1 receptor plays a specific role in the maintenance of high blood pressure in this genetic form of hypertension. METHODS: Pithed and conscious SHR were studied after intravenous administration of 0.125-1 mg/kg BIBP 3226. The cardiovascular effects were evaluated under baseline conditions, under acute stress and after exogenous administration of 20 microg/kg NPY. The potentiating effects of NPY on pressor responses to phenylephrine and tyramine were studied in the SHR. RESULTS: Intravenous administration of 0.125-1 mg/kg BIBP 3226 dose-dependently inhibited the pressor response to exogenous NPY in pithed SHR. At higher doses BIBP 3226 had an effect duration of 20-40 min. In the pithed SHR, a 0.5 mg/kg bolus injection of BIBP 3226 shifted the pressor response curve for exogenous NPY significantly to the right It also inhibited significantly the potentiating effects of NPY on pressor responses to phenylephrine and tyramine. In conscious SHR, 0.125-1 mg/kg BIBP 3226 did not reduce the basal blood pressure. In combination with a hypotensive dose of prazosin, administration of 0.5 mg/kg BIBP 3226 had no added effects lowering the basal blood pressure. A stressful stimulus, namely an air jet, caused a brief increase in blood pressure and heart rate in the conscious SHR. In this model, 0.5 mg/kg BIBP inhibited the heart rate response slightly but had no effect on the blood pressure response. CONCLUSIONS: Our results demonstrate that, although the selective NPY Y1 receptor antagonist BIBP 3226 may shift the pressor response to exogenous NPY potently, it does not influence basal blood pressure significantly in the SHR.

Animals↗
PubMed1997

Presence of contractile endothelin-A and dilatory endothelin-B receptors in human cerebral arteries.

OBJECTIVE: The aim of the present study was to elucidate the endothelin receptor subtypes responsible for the endothelin-induced vasomotor responses of human cerebral arteries. METHODS: Human cerebral arteries with endothelium were mounted in in vitro tissue baths, and the vascular responses to endothelin-1 (ET-1) and sarafotoxin 6c (a selective ETB agonist) were studied in the presence or absence of endothelin blockers, bosentan (Ro 47-0203), a novel nonpeptide ETA and ETB receptor antagonist, and FR139317, a selective ETA receptor antagonist. The presence of messenger ribonucleic acid encoding the human ETA and ETB receptors in human cerebral arteries with intact endothelium and in segments denuded of endothelium was studied by the use of reverse transcriptase-polymerase chain reaction. RESULTS: ET-1 induced concentration-dependent contraction of human cerebral arteries; the pEC50 value was 9.4 +/- 0.2. The vasoconstriction was significantly antagonized both by bosentan and by FR139317. The pA2 values were 7.2 +/- 0.4 and 7.4 +/- 0.4, respectively. Sarafotoxin 6c failed to cause contraction of human cerebral arteries. In precontracted vessels, however, sarafotoxin 6c induced dilatation that was significantly inhibited by bosentan (10 mumol/L), resulting in a pA2 value of 6.0 +/- 0.2. Furthermore, messenger ribonucleic acid encoding the human ETA and ETB receptors was detected in human cerebral arteries both with and without endothelium. CONCLUSION: The ET-1-induced vasoconstriction of human cerebral arteries is primarily mediated by the ETA receptor, whereas the sarafotoxin 6c-induced vasodilatation seems to be mediated via the ETB receptor.

Cerebral Arteries↗
PubMed1997

Innervation pattern of malformative cortical vessels in Sturge-Weber disease: an histochemical, immunohistochemical, and ultrastructural study.

OBJECTIVE: This study was undertaken to elucidate the pattern of vascular innervation in areas of pial angiomatosis in Sturge-Weber disease (SWD) and eventually correlating it with the pathophysiology of the disease, namely its chronic ischemic changes. METHODS: We processed part of a surgical specimen resected from a 3-year-old female patient who underwent functional hemispherectomy for SWD and characterized the pattern of innervation of the malformative cortical vessels using histochemical, immunohistochemical, and ultrastructural techniques. RESULTS: Cortical vessels were observed to be supplied with numerous varicose nerve fibers containing immunoreactivity for neuropeptide tyrosine and the catecholamine-synthesizing enzyme, tyrosine, tyrosine hydroxylase. In contrast, no nerve fibers containing acetylcholinesterase activity and immunoreactivity for Substance P, a calcitonin gene-related peptide and vasoactive intestinal peptide, were detected. Ultrastructural studies revealed the presence of numerous axon varicosities at the adventitial-medial border. Neuropeptide tyrosine immunoreactivity was localized in large granular vesicles in nerve varicosities that also contained numerous small granular vesicles. CONCLUSION: These results demonstrate that nerve supplying cortical vessels in SWD are arranged in a distribution pattern similar to the one observed in human normal cortical veins and suggest that these abnormal vessels are innervated only with noradrenergic sympathetic nerve fibers. This represents a clear difference from the pattern of innervation observed in both normal cortical arteries and veins, and is the consequence of the anatomic and functional dysangiogenic process characteristic of the affected cortical areas in SWD.

Axons↗
PubMed1997

Effects of dihydroergotamine and sumatriptan on isolated human cerebral and peripheral arteries and veins.

BACKGROUND: Pharmacological cerebral vasoconstriction has recently been suggested as treatment for patients with increased intracranial pressure (ICP) after severe traumatic brain lesions. Hypothetically, a moderate constriction of precapillary resistance vessels might be advantageous since it decreases intracapillary blood pressure, and a contraction of cerebral veins might effectively reduce intracranial blood volume and ICP. This report examines the in vitro effects of two vasoconstrictors, dihydroergotamine (DHE) and sumatriptan, which may be considered for treatment of increased ICP. METHODS: The reactivity of isolated small human cerebral subcutaneous and omental arteries and veins were studied during exposure to different concentrations of DHE and sumatriptan. RESULTS: Both sumatriptan and DHE induced concentration-dependent contractions in human cerebral arteries and veins and 50% of maximum contractions were obtained at significantly lower concentrations of DHE than of sumatriptan. The maximum contraction of cerebral arteries was significantly higher with sumatriptan than with DHE. Both drugs caused contractions of subcutaneous arteries at concentrations of 10(-7)-10(-6)M, which is within the therapeutic concentration range of sumatriptan, while no effect was obtained in omental vessels. CONCLUSIONS: Both DHE and sumatriptan cause contraction of isolated human cortical arteries and veins at very low concentrations. The differences observed between the two drugs may be explained by the fact that DHE is an alpha-adrenergic as well as a 5-HT agonist while sumatriptan acts specifically on 5-HT receptors. The study supports the hypothesis underlying the use of DHE for the treatment of increased ICP in patients with severe traumatic brain lesions.

Cerebral Arteries↗
PubMed1997

Differential effects of increasing doses of alpha-trinositol on cerebral blood flow autoregulation.

The effect of neuropeptide Y inhibition with alpha-trinositol on the cerebral blood flow autoregulation was studied in Wistar Kyoto rats. alpha-Trinositol was tested in two doses: one dose (5 mg kg-1 hr-1) selectively affecting neuropeptide Y and one higher dose (50 mg kg-1 hr-1) affecting both neuropeptide Y and the adrenergic response. The cerebral blood flow was measured with the intracarotid 133xenon injection method in halothane nitrous oxide-anaesthetized animals. Blood pressure was raised by norepinephrine infusion and lowered by controlled haemorrhage in separate groups of rats. In addition we examined the effect of alpha-trinositol on neuropeptide Y-induced contraction of cerebral vessels in vitro. The in vitro study demonstrated inhibition of neuropeptide Y-induced contraction with a alpha-trinositol dose selective of neuropeptide Y. The in vivo study demonstrated that cerebral blood flow autoregulation was preserved after both doses of alpha-trinositol. alpha-Trinositol in the low neuropeptide Y-selective dose (5 mg kg-1 hr-1) did not affect the blood pressure limits of cerebral blood flow autoregulation, but the higher dose (50 mg kg-1 hr-1) of alpha-trinositol shifted the upper blood pressure limit of cerebral blood flow autoregulation towards lower blood pressures, an effect probably due to inhibition of both the adrenergic and neuropeptide Y systems.

Animals↗
PubMed1996

Neuropeptide Y potentiates noradrenaline-induced contraction through the neuropeptide Y Y1 receptor.

To elucidate which neuropeptide Y receptor subtype is responsible for the neuropeptide Y-induced potentiation of the noradrenaline-evoked contraction in human omental arteries we used antisense oligodeoxynucleotide (Antisense), the new selective neuropeptide Y Y1 receptor antagonist, BIBP3226 {(R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl) methyl]-D-arginine-amide} and the reverse transcriptase-polymerase chain reaction (RT-PCR). Neuropeptide Y significantly potentiated the noradrenaline-induced contraction in non-incubated vessels (pEC50 6.4 +/- 0.2 vs. 5.9 +/- 0.2) and in vessels incubated with 1 microM Sense oligodeoxynucleotide (Sense) (pEC50 6.0 +/- 0.1 vs. 5.6 +/- 0.2). In vessels incubated with 1 microM Antisense the potentiating effect of neuropeptide Y was completely abolished. BIBP3226 (1 microM) inhibited the neuropeptide Y-induced potentiation in human omental arteries (pEC50 5.8 +/- 0.3 vs. 6.4 +/- 0.2). Finally, messenger RNA for the neuropeptide Y Y1 receptor was detected using RT-PCR. On the basis of our results we conclude that the neuropeptide Y-induced potentiation of the noradrenaline-induced contraction is mediated by the neuropeptide Y Y1 receptor.

Adrenergic alpha-Agonists↗
PubMed1996

Endothelin-A and -B receptors in human coronary arteries and veins.

Using reverse transcriptase-polymerase chain reaction, products corresponding to mRNA encoding endothelin-A and -B (ETA and ETB) receptors were demonstrated in human coronary arteries and veins with intact endothelium and in endothelium-denuded human coronary arteries. Vasomotor responses were studied on isolated segments of human epicardial coronary arteries and veins at resting tension and after precontraction with U46619. In both arteries and veins, endothelin-1 (ET) induced strong and potent contractions, and preincubation with different concentrations of the non-selective ETA/ETB receptor antagonist PD 145065 caused a rightward shift of the concentration-response curves without significantly changing maximum responses (pA2 value 6.7 arteries, 7.4 veins). The ETB receptor agonist IRL 1620 induced no contraction of arteries or veins at resting tension, but induced weak relaxation of all arteries and most precontracted veins, the relaxation being endothelium-dependent in arteries. ET at low concentrations induced weak relaxations of most precontracted arteries, but no veins. In conclusion, mRNA encoding ETA and ETB receptors is present in human coronary arteries and veins, ETA receptors mediating contraction and ETB receptors mediating relaxation. In arteries, mRNA for both receptor types was detected in the media, but ETB receptor-mediated relaxation was endothelium-dependent.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

Nitroxidergic innervation of guinea pig cerebral arteries.

The presence and distribution of nitric oxide synthase (NOS)-immunoreactive nerve fibers associated with the guinea pig major cerebral arteries was studied by means of immunohistochemical, histochemical and ultrastructural techniques. Anterior arteries of the circle of Willis received a rich supply of perivascular nerve fibers containing NOS immunoreactivity while posteriorly localized arteries presented a moderate to sparse innervation. A double immunofluorescence staining technique revealed that NOS was localized in nerve fibers distinct from those displaying substance P or tyrosine hydroxylase. Combined immunofluorescence and histochemical staining of the same preparation indicated that NOS immunoreactivity was localized in putative cholinergic nerve fibers (identified by their acetylcholinesterase content) and that NADPH-diaphorase activity (a marker for NOS-containing neurons) was found in nerves which also possessed VIP immunoreactivity. The ultrastructural study revealed that NOS immunoreactivity was present in numerous nerve varicosities at the adventitial-medial border. These results suggest that NO and VIP co-exist in putative parasympathetic nerve fibers supplying the guinea pig cerebral arteries and may be release together in response to nervous stimulation.

Acetylcholinesterase↗
PubMed1996

Presence of neuropeptide Y Y1 receptor mediating vasoconstriction in human cerebral arteries.

The neuropeptide Y-induced vasoconstriction of human cerebral arteries is mediated by the neuropeptide Y Y1 receptor. We conclude this on the basis of our results from: (1) in vitro studies on neuropeptide Y agonists. Neuropeptide Y and pro34NPY caused potent and long-lasting contractions of human cerebral arteries, while NPY 13-36 had no contractile effect at all on the vessels tested; (2) in vitro studies using the selective Y1 receptor antagonist BIBP3226 which in increasing concentrations (10(-9)-10(-6)M) caused a parallel shift to the right of the neuropeptide Y concentration-response curve without change of the maximum contractile response (pA2 value 8.38 +/- 0.10); and (3) with reverse transcriptase-polymerase chain reaction (RT-PCR) we detected specific mRNA for a neuropeptide Y Y1 receptor in human pial and human middle cerebral arteries using three forward primers and one reverse primer.

Arginine↗
PubMed1996

Cerebral vasodilatation in the cat involves nitric oxide from parasympathetic nerves.

The recent description of the synthesis of nitric oxide (NO) in vivo and its putative role in endothelial-dependent vasodilatation has led to considerable interest in possible roles for the molecule. In this study the distribution, origin and some aspects of the physiology of NO found in the cerebral circulation is examined. A rich supply of nerve fibres displaying immunoreactivity against nitric oxide synthase (NOS) could be seen in the adventitia of the cat cerebral vessels. There was a large number of NOS-positive cells in the sphenopalatine ganglion and these constituted a sub-population of the vasoactive intestinal polypeptide (VIP) positive cells. Blockade of NOS activity with NG-nitro-L-arginine methyl ester (L-NAME) significantly attenuated the cerebral vasodilator response to facial nerve stimulation when applied locally to the cortex. Intravenous administration of L-NAME did not affect the VII-elicited cerebral vasodilator response. It may be concluded that the parasympathetic nerves innervating the cerebral circulation contain NOS and furthermore, since blockade of NOS reduces parasympathetic vasodilatation, that NO is one of the transmitters in this system.

Animals↗
PubMed1996

Orthostatic hypotension in organic dementia: relationship between blood pressure, cortical blood flow and symptoms.

Regional cerebral blood flow was measured in 35 patients with organic dementia (Alzheimer's disease, n = 13, vascular dementia, n = 17, frontotemporal dementia, n = 5) and orthostatic hypotension. Measurements were performed during supine rest and during head-up tilt (60 degrees). Despite marked blood pressure falls, few patients had symptoms of orthostatic hypotension. All three dementia groups had a decrease in regional cerebral blood flow in the frontal lobes during head-up tilt, but no change in mean hemispheric flow. All patients had a consistent drop in their systolic blood pressure upon head-up tilt, with a wide variation over time. The findings suggest that orthostatic hypotension needs to be considered, and actively sought for, in organic dementia as many patients may lack the typical symptoms of orthostatic hypotension, despite a marked fall in blood pressure.

Aged↗
PubMed1996

Relaxation of human temporal artery by endothelin ETB receptors.

Endothelin receptors have been characterized in human temporal artery by molecular biological methods and in vitro pharmacology. Reverse transcriptase-polymerase chain reaction was used to detect mRNA encoding ETA and ETB receptors in normal and endothelium-denuded arteries. Vasomotor response experiments with a specific ETA antagonist (FR 139317) suggested the presence of ETA subtypes. Marked ETB-mediated relaxation was obtained with ET-3 when ETA activity was blocked in precontracted arteries. Relaxation was significantly reduced by bosentan, indomethacin, and a nitric oxide synthase inhibitor. It may be speculated that the relaxant activity is mediated through ETB1 receptors.

Azepines↗
PubMed1996

Pharmacological characterization of the ETA receptor in the vascular smooth muscle comparing its analogous distribution in the rat mesenteric artery and in the arterial mesenteric bed.

The potency of ET-1, ET-2, and ET-3 to contract the isolated perfused rat arterial mesenteric bed was 2.73 +/- 0.57, 1.63 +/- 0.32, and 144 +/- 30 nM, respectively. The vasomotor effect of the ETs was slow in onset, persistent but reversible. Sarafotoxin S6b mimicked the ETs with a potency twofold lower than ET-1; sarafotoxin S6c and the C-terminal hexapeptide of ET-1 was inactive. ETH agonists such as IRL-1620 and AGETB-89 were inactive as vasoconstrictors within the range of concentrations examined. Minor chemical modifications of ET-1 amino acids residues in position 7 or 21 decreased significantly the peptide potency; ET-1 analogues with one or none of the disulfide bonds resulted inactive. The vasomotor effect of ETs was blocked in a competitive, reversible, and selective manner by FR 139317 and BQ-123, the latter being about threefold less potent than the former antagonist. The potency of FR 139317 was 20-fold higher to antagonize ET-3 than ET-1, and threefold higher to block ET-2 than ET-1. In strict analogy to FR 139317, BQ-123 was 12-fold more potent to antagonize ET-3 than ET-1, and fourfold more potent to antagonize ET-2 than ET-1. Upon removal of the endothelial cell layer, the vasomotor potency of ET-1 or the antagonist potency of FR 139317 remained unaltered, suggesting that the vasomotor receptors are localized in the arterial smooth muscles. The ET-1-induced vasomotor responses desensitized, an effect not crossed to noradrenaline (NA); perfusion with 10 microM indomethacin did not alter the vasomotor potency of ET-1, excluding the participation of eicosanoids in the arteriolar effects of ET-1. In isolated rings of the rat mesenteric artery, set to record isometric contractions of the circular muscular layer, the potency of the ETs and their structural analogues was as follows; ET-2 = ET-1 = sarafotoxin S6b > ET-3 > sarafotoxin S6c. The C-terminal hexapeptide of ET-1 and [Ala 1,3,11,15]ET-1 were inactive. The ET-1-induced vasoconstriction was antagonized in a concentration-dependent fashion by FR 139317. These results allow to conclude that the ETA receptors present in the arterial mesenteric circulation are localized in the vascular smooth muscle of the large-sized arteries as well as the smaller arterioles and precapillary vessels of the rat arterial mesenteric bed.

Animals↗
PubMed1996

Vasoactivity mediated by endothelin ETA and ETB receptors in isolated porcine ophthalmic artery.

Endothelin isopeptides and sarafotoxin S6b induced strong contractions in isolated porcine ophthalmic artery at basal tension, which were antagonized in a concentration-dependent manner by the specific ETA antagonist FR 139317. The maximum contraction and potency of endothelin-1 and sarafotoxin S6b were similar, whereas endothelin-3 was significantly less potent and induced weaker contractions. Schild plot analysis was only obtained for endothelin-1 and sarafotoxin S6b, but indicated competitive binding at the same ETA receptor site for these peptides. However, the slope obtained for endothelin-1 was significantly less than unity, suggesting more than one receptor. FR 139317 was a more potent antagonist of contractions induced by endothelin-3 than the other peptides. In arteries pre-contracted by prostaglandin F2 alpha high endothelin-3 concentrations induced additional contraction, except in the presence of FR 139317 when a marked relaxation was observed, an ability which was otherwise marked by the strong contractile activity. The relaxation was significantly reduced in endothelin-denuded segments. Both contraction and relaxation were abolished by the ETA/B antagonist bosentan. The results suggest the presence of ETB as well as ETA receptors in this artery type, though ETB receptor activity is only demonstrated at an unusually high concentration of endothelin in this preparation in vitro.

Animals↗
PubMed1996

Calcitonin gene-related peptide is released from capsaicin-sensitive nerve fibres and induces vasodilatation of human cerebral arteries concomitant with activation of adenylyl cyclase.

The vasomotor effects of calcitonin gene-related peptide (CGRP) analogues have been studied in circular segments of fresh human cerebral arteries obtained at neurosurgical operations using a sensitive in vitro system. Human alpha-CGRP, human beta-CGRP, rat alpha-CGRP and rat beta-CGRP induced strong and potent relaxation of precontracted circular vessel segments. The Imax (maximum relaxant effect) to human calcitonin was low and the pD2 (concentration for half maximum effect) 7.7 was much lower than that of CGRP. The CGRP-1, antagonist human alpha-CGRP8-37 blocked the response to human alpha-CGRP but not to human beta-CGRP, while the putative antagonist [Tyr]CGRP28-37 did not. Capsaicin (10(-15)-10(-8)M) caused relaxation of the cerebral arteries by 22% of precontraction. Pre-treatment with 10(-6)M human alpha-CGRP8-37 inhibited this relaxation. Human alpha-CGRP increased the cyclic AMP content of human cerebral arteries in a concentration-dependent manner. This increase in adenylyl cyclase activity was blocked by human alpha-CGRP8-37. The results suggest that CGRP-1 receptors coupled to adenylyl cyclase are present in human cerebral arteries.

1-Methyl-3-isobutylxanthine↗