scholarly journals Regulation of Ca2+sensitization by PKC and rho proteins in ovine cerebral arteries: effects of artery size and age

1998 ◽  
Vol 275 (3) ◽  
pp. H930-H939 ◽  
Author(s):  
Sergey E. Akopov ◽  
Lubo Zhang ◽  
William J. Pearce
Keyword(s):  
G Protein ◽  
Cerebral Arteries ◽  
Rho Kinase ◽  
Cerebrovascular Reactivity ◽  
Rho Proteins ◽  
Experimental Conditions ◽  
Fetal Sheep ◽  
Middle Cerebral Arteries ◽  
Near Term ◽  
Nonpregnant Adult

G protein-regulated Ca2+ sensitivity of vascular contractile proteins plays an important role in cerebrovascular reactivity. The present study examines the intracellular mechanisms that govern G protein-regulated Ca2+ sensitivity in cerebral arteries of different size and age. We studied β-escin-permeabilized segments of common carotid, basilar, and middle cerebral arteries from nonpregnant adult and near-term fetal sheep. Activation of protein kinase C (PKC) by (−)-indolactam V or a phorbol ester produced receptor-independent increases in Ca2+ sensitivity. Such increases were more marked in immature arteries and were inversely correlated with artery size in both mature and immature arteries. However, inhibitors of PKC did not significantly affect increases in Ca2+ sensitivity in responses to either serotonin (5-hydroxytryptamine, 5-HT) or guanosine 5′- O-(3-thiotriphosphate) (GTPγS). Alternatively, deactivation of rho p21, a small G protein associated with Rho kinase, by exotoxin C3 fully prevented increases in Ca2+ sensitivity in responses to 5-HT or GTPγS in both adult and fetal arteries of all types. Neither inhibitors of PKC nor exotoxin C3 altered baseline Ca2+ sensitivity. We conclude that patterns of receptor- and/or G protein-mediated modulation of Ca2+ sensitivity are dependent on an intracellular pathway that involves activation of small G proteins and Rho kinase. In contrast, PKC has little, if any, role in agonist-induced Ca2+ sensitization under the present experimental conditions.

Physiological variations in ovine cerebrovascular calcium sensitivity

1997 ◽  
Vol 272 (5) ◽  
pp. H2271-H2281 ◽  
Author(s):  
S. E. Akopov ◽  
L. Zhang ◽  
W. J. Pearce
Keyword(s):  
Biogenic Amines ◽  
G Protein ◽  
Calcium Sensitivity ◽  
Cerebrovascular Reactivity ◽  
Arterial Diameter ◽  
Fetal Sheep ◽  
Near Term ◽  
Nonpregnant Adult ◽  
Physiological Variations ◽  
Dependent Mechanism

Cerebrovascular reactivity to biogenic amines varies in relation to both arterial diameter and age. The present study examines the hypothesis that these patterns of reactivity are secondary to corresponding variations in the Ca2+ sensitivity of the contractile proteins. To test this hypothesis, we permeabilized segments of common carotid (Com), basilar, main branch middle cerebral, and second-branch middle cerebral (MCA-B) arteries from nonpregnant adult and near-term fetal sheep using beta-escin. Permeabilization methods were carefully validated and adjusted for each artery type. Baseline myofilament Ca2+ sensitivity in both adults and fetuses increased significantly from the Com to the MCA-B and was generally higher in fetuses than in adults. Serotonin dose dependently increased Ca2+ sensitivity via a G protein-dependent mechanism in all arteries. The magnitudes of this effect did not vary among artery types but were significantly greater in fetal than in adult arteries. This effect of serotonin was mimicked by guanosine 5'-O-(3-thiotriphosphate), a nonhydrolyzable analog of guanosine 5'-triphosphate, and its effects were also much greater in fetal than in adult arteries. We conclude that patterns of cerebrovascular reactivity to biogenic amines were determined, at least in part, by underlying variations in baseline myofilament Ca2+ sensitivity and/or its alteration by G protein-dependent mechanisms.

Cerebral artery KATP- and KCa-channel activity and contractility: changes with development

2000 ◽  
Vol 279 (6) ◽  
pp. R2004-R2014 ◽  
Author(s):  
Wen Long ◽  
Lubo Zhang ◽  
Lawrence D. Longo
Keyword(s):  
Channel Blocker ◽  
Cerebral Arteries ◽  
Dependent Manner ◽  
Channel Activity ◽  
Channel Opener ◽  
Channel Inhibition ◽  
Middle Cerebral Arteries ◽  
Intracellular Ca ◽  
Near Term ◽  
Nonpregnant Adult

The present study was designed to test the hypothesis that in cerebral arteries of the fetus, ATP-sensitive (KATP) and Ca2+-activated K+channels (KCa) play an important role in the regulation of intracellular Ca2+ concentration ([Ca2+]i) and that this differs significantly from that of the adult. In main branch middle cerebral arteries (MCA) from near-term fetal (∼140 days) and nonpregnant adult sheep, simultaneously we measured norepinephrine (NE)-induced responses of vascular tension and [Ca2+]i in the absence and presence of selective K+-channel openers/blockers. In fetal MCA, in a dose-dependent manner, both the KATP-channel opener pinacidil and the KCa-channel opener NS 1619 significantly inhibited NE-induced tension [negative logarithm of the half-maximal inhibitory concentration (pIC50) = 5.0 ± 0.1 and 8.2 ± 0.1, respectively], with a modest decrease of [Ca2+]i. In the adult MCA, in contrast, both pinacidil and NS 1619 produced a significant tension decrease (pIC50 = 5.1 ± 0.1 and 7.6 ± 0.1, respectively) with no change in [Ca2+]i. In addition, the KCa-channel blocker iberiotoxin (10−7 to 10−6 M) resulted in increased tension and [Ca2+]i in both adult and fetal MCA, although the KATP-channel blocker glibenclamide (10−7 to 3 × 10−5 M) failed to do so. Of interest, administration of 10−7 M iberiotoxin totally eliminated vascular contraction and increase in [Ca2+]i seen in response to 10−5M ryanodine. In precontracted fetal cerebral arteries, activation of the KATP and KCa channels significantly decreased both tension and [Ca2+]i, suggesting that both K+ channels play an important role in regulating L-type channel Ca2+ flux and therefore vascular tone in these vessels. In the adult, KATP and the KCa channels also appear to play an important role in this regard; however, in the adult vessel, activation of these channels with resultant vasorelaxation can occur with no significant change in [Ca2+]i. These channels show differing responses to inhibition, e.g., KCa-channel inhibition, resulting in increased tension and [Ca2+]i, whereas KATP-channel inhibition showed no such effect. In addition, the KCa channel appears to be coupled to the sarcoplasmic reticulum ryanodine receptor. Thus differences in plasma membrane K+-channel activity may account, in part, for the differences in the regulation of contractility of fetal and adult cerebral arteries.

Cerebral artery sarcoplasmic reticulum Ca2+ stores and contractility: changes with development

2000 ◽  
Vol 279 (3) ◽  
pp. R860-R873 ◽  
Author(s):  
Wen Long ◽  
Lubo Zhang ◽  
Lawrence D. Longo
Keyword(s):  
Plasma Membrane ◽  
Sarcoplasmic Reticulum ◽  
Cerebral Artery ◽  
Cerebral Arteries ◽  
Induced Responses ◽  
Adult Sheep ◽  
Middle Cerebral Arteries ◽  
Intracellular Ca ◽  
Near Term ◽  
Nonpregnant Adult

To test the hypothesis that sarcoplasmic reticulum (SR) Ca2+ stores play a key role in norepinephrine (NE)-induced contraction of fetal and adult cerebral arteries and that Ca2+ stores change with development, we performed the following study. In main branch middle cerebral arteries (MCA) from near-term fetal (∼140 days) and nonpregnant adult sheep, we measured NE-induced contraction and intracellular Ca2+ concentration ([Ca2+]i) in the absence and presence of different blockers. In adult MCA, after thapsigargin (10−6M), the NE-induced responses of tension and [Ca2+]i were 37 ± 5 and 47 ± 7%, respectively, of control values ( P < 0.01 for each). In the fetal artery, in contrast, this treatment resulted in no significant changes from control. When this was repeated in the absence of extracellular Ca2+, adult MCA increases in tension and [Ca2+]i were 32 ± 5 and 13 ± 3%, respectively, of control. Fetal cerebral arteries, however, showed essentially no response. Ryanodine (RYN, 3 × 10−6 to 10−5 M) resulted in increases in tension and [Ca2+]i in both fetal and adult MCA similar to that seen with NE. For both adult and fetal MCA, the increased tension and [Ca2+]i responses to RYN were essentially eliminated in the presence of zero extracellular Ca2+. These findings provide evidence that in fetal MCA, in contrast to those in the adult, SR Ca2+ stores are of less importance in NE-induced contraction, with such contraction being almost wholly dependent on Ca2+ flux via plasma membrane L-type Ca2+ channels. In addition, they suggest that in both adult and fetal MCA, the RYN receptor is coupled to the plasma membrane Ca2+-activated K+ channel and/or L-type Ca2+ channel.

scholarly journals Effects of GV14 Acupuncture on Cerebral Blood Flow Velocity in the Basilar and Middle Cerebral Arteries and CO2 Reactivity during Hypercapnia in Normal Individuals

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Hyun Ku Lee ◽  
Sang-Kwan Moon ◽  
Chul Jin ◽  
Seung-Yeon Cho ◽  
Seong-Uk Park ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Arteries ◽  
Transcranial Doppler Sonography ◽  
Cerebrovascular Reactivity ◽  
Acupuncture Points ◽  
Co2 Reactivity ◽  
Middle Cerebral Arteries

The Governing Vessel 14 (GV14) (Dazhui) is one of the acupuncture points referred to as “seven acupoints for stroke.” Nevertheless, there is a scarcity of research on the effects of acupuncture treatment at GV14. This study investigated the effects of acupuncture at GV14 on cerebral blood flow (CBF), especially that in the basilar artery (BA) and the middle cerebral arteries (MCA). Sixteen healthy men aged 20 to 29 years were enrolled in this study. CBF velocity and cerebrovascular reactivity (CVR) were measured using transcranial Doppler sonography (TCD). The following were assessed: closed circuit rebreathing- (CCR-) induced carbon dioxide (CO2) reactivity, modified blood flow velocity at 40 mmHg (CV40) on BA and MCAs, blood pressure (BP), and heart rate (HR). Observed results were obtained after comparison with the baseline evaluation. Statistically significant elevations in CO2 reactivity were recorded in the BA (3.28 to 4.70, p < 0.001 ) and MCAs (right: 3.81 to 5.25, p = 0.001 ; left: 3.84 to 5.12, p = 0.005 ) after acupuncture at GV14. The CV40 increased statistically significantly only in the BA (45.49 to 50.41, p = 0.003 ). No change was observed in BP (106.83 to 107.08 (mmHg), p = 0.335 ) and HR (77 to 75 (bpm), p = 0.431 ). Acupuncture at GV14 improved CBF velocity. These results could be explained by the regulation of endothelium-dependent vessel dilation effected by acupuncture. This trial is registered with Korean Clinical Trial Registry (http://cris.nih.go.kr; registration number: KCT0004787).

Testosterone suppresses endothelium-dependent dilation of rat middle cerebral arteries

2004 ◽  
Vol 286 (2) ◽  
pp. H552-H560 ◽  
Author(s):  
Rayna J. Gonzales ◽  
Diana N. Krause ◽  
Sue P. Duckles
Keyword(s):  
Vascular Tone ◽  
Cerebral Arteries ◽  
Cerebrovascular Reactivity ◽  
Male Rats ◽  
Intraluminal Pressure ◽  
Vascular Effects ◽  
Additional Increase ◽  
Testosterone Treatment ◽  
Cox Inhibitor ◽  
Middle Cerebral Arteries

Little is known about vascular effects of testosterone. We previously reported chronic testosterone treatment increases vascular tone in middle cerebral arteries (MCA; 300 μm diameter) of male rats. In the present study, we investigated the hypothesis that physiological levels of circulating testosterone affect endothelial factors that modulate cerebrovascular reactivity. Small branches of MCA (150 μm diameter) were isolated from orchiectomized (ORX) and testosterone-treated (ORX+T) rats. Intraluminal diameters were recorded after step changes in intraluminal pressure (20–100 Torr) in the absence or presence of NG-nitro-l-arginine-methyl ester (l-NAME), a nitric oxide synthase (NOS) inhibitor; indomethacin, a cyclooxygenase (COX) inhibitor; and/or apamin and charybdotoxin (CTX); and KCa channel blockers used to inhibit endothelium-derived hyperpolarizing factors (EDHF). At intraluminal pressures ≥60 Torr, arteries from ORX+T developed greater tone compared with ORX arteries. This difference was abolished by removal of the endothelium but remained after treatment of intact arteries with indomethacin or l-NAME. In addition, testosterone treatment had no effect on cerebrovascular production of endothelin-1 or prostacyclin nor did it alter protein levels of endothelial NOS or COX-1. Endothelium removal after l-NAME/indomethacin exposure caused an additional increase in tone. Interestingly, the latter effect was smaller in arteries from ORX+T, suggesting testosterone affects endothelial vasodilators that are independent of NOS and COX. Apamin/CTX, in the presence of l-NAME/indomethacin, abolished the difference in tone between ORX and ORX+T and resulted in vessel diameters similar to those of endothelium-denuded preparations. In conclusion, testosterone may modulate vascular tone in cerebral arteries by suppressing EDHF.

scholarly journals Intracellular Acidification Alters Myogenic Responsiveness and Vasomotion of Mouse Middle Cerebral Arteries

2013 ◽  
Vol 34 (1) ◽  
pp. 161-168 ◽  
Author(s):  
Axel BK Thomsen ◽  
Sukhan Kim ◽  
Filip Aalbaek ◽  
Christian Aalkjaer ◽  
Ebbe Boedtkjer
Keyword(s):  
Knockout Mice ◽  
Kinase Inhibitor ◽  
Cerebral Arteries ◽  
Rho Kinase ◽  
Vascular Wall ◽  
Mesenteric Arteries ◽  
Myogenic Tone ◽  
No Production ◽  
Wild Type ◽  
Middle Cerebral Arteries

Intracellular pH (pHi) in the vascular wall modulates agonist-induced vasocontractile and vasorelaxant responses in mesenteric arteries, whereas effects on myogenic tone have been unsettled. We studied the role of Na+,HCO3− cotransporter NBCn1 in mouse isolated middle cerebral arteries and the influence of pHi disturbances on myogenic tone. Na+,HCO3− cotransport was abolished in arteries from NBCn1 knockout mice and steady-state pHi ∼0.3 units reduced compared with wild-type mice. Myogenic tone development was low under control conditions but increased on treatment with the NO-synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME). This effect of L-NAME was smaller in arteries from NBCn1 knockout than wild-type mice. Myogenic tone with L-NAME present was significantly lower in arteries from NBCn1 knockout than wild-type mice and was abolished by rho-kinase inhibitor Y-27632. The arteries displayed vasomotion, and this rhythmic contractile pattern was also attenuated in arteries from NBCn1 knockout mice. No differences in membrane potential or intracellular [Ca2+] were seen between arteries from NBCn1 knockout and wild-type mice. We propose that NO production and rho-kinase-dependent Ca2+ sensitivity are reduced at low pHi in pressurized mouse middle cerebral arteries. This likely impedes the ability to adjust to changes in perfusion pressure and regulate cerebral blood flow.

scholarly journals Effects of Kininase II Inhibitors on the Vasomotor Response to Bradykinin of Feline Intracranial and Extracranial Arteries in vitro and in situ

1983 ◽  
Vol 3 (3) ◽  
pp. 339-345 ◽  
Author(s):  
Michael Wahl ◽  
Alan R. Young ◽  
Lars Edvinsson ◽  
Franz Wagner
Keyword(s):  
Cerebral Arteries ◽  
Surrounding Tissue ◽  
Experimental Conditions ◽  
Pial Arteries ◽  
Simultaneous Application ◽  
Kininase Ii ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F

Bradykinin is known to effect a vasodilatation of feline cerebral arteries in situ and of both human and feline pial arteries in vitro. In order to demonstrate whether kininase II (localized within the vessel wall or in the surrounding tissue or fluid) influences the response to bradykinin, two different inhibitors of this bradykinin degradation enzyme were tested. Perivascular microapplication of potentiator C (10−10–10−4 M) or captopril (10−10–10−3 M) did not, by itself, change the diameter of feline pial arteries (87–305 μm) in situ. In a similar investigation, the dilating action of bradykinin (10−8–10−5 M) was not modified by the simultaneous application of potentiator C or captopril (10−5 M). Furthermore, the relaxing effect of bradykinin (10−10–10−4 M) on isolated feline middle cerebral arteries (preconstricted with 5-hydroxytryptamine or prostaglandin F2α) was not influenced by the presence of captopril (10−7 M). In contrast, when studied on isolated extracranial vessel segments (feline sublingual artery), bradykinin caused a concentration-dependent constriction of the artery. This constriction was completely reversed to dilatation in the presence of captopril (10−7 M). Moreover, the characteristic effect of kininase II inhibition was demonstrated in the isolated guinea pig ileum preparation. In this instance, bradykinin induced a concentration-dependent contraction that was enhanced by potentiator C or captopril. We conclude, therefore, that bradykinin exerts variable responses on vascular smooth muscle, depending on the species used, the muscle location and experimental conditions. Finally, the in situ and in vitro findings for pial and middle cerebral arteries demonstrate that kininase II does not modify the dilating effect of bradykinin under our experimental conditions.

Neurologic Manifestations of In Utero Cocaine Exposure in Near-Term and Term Infants

PEDIATRICS ◽  
1995 ◽  
Vol 96 (2) ◽  
pp. 259-264
Author(s):  
Terri A. King ◽  
Jeffrey M. Perlman ◽  
Abbot R. Laptook ◽  
Nancy Rollins ◽  
Gregory Jackson ◽  
...  
Keyword(s):  
Flow Velocity ◽  
Intraventricular Hemorrhage ◽  
Anterior Cerebral Artery ◽  
Drug Withdrawal ◽  
Cerebral Arteries ◽  
In Utero ◽  
Neurologic Examination ◽  
Term Infants ◽  
Middle Cerebral Arteries ◽  
Near Term

Objective. To determine whether the incidence of neurosonographic and neurologic abnormalities is higher in cocaine-exposed infants at birth. Methods. In utero exposure to cocaine was investigated in 39 term and near-term infants with positive urine screens for cocaine only and 39 matched control infants without drug exposure admitted to the regular term newborn nursery. Serial evaluations were performed on each infant on postnatal days 1 and 2 and included a cranial sonogram, a neurologic and behavioral assessment for drug withdrawal, and Doppler interrogation of the anterior and middle cerebral arteries. Results. There were no differences between groups in neurosonographic abnormalities. Grade I or II intraventricular hemorrhage occurred in 11% of cocaine-exposed and 11% of control infants. There were no cases of grade III intraventricular hemorrhage, cystic periventricular leukomalacia, or neonatal stroke. Head size was smaller in cocaine-exposed infants, ie, 32.7 ± 0.1 cm versus 33.8 ± 0.1 cm. The neurologic examination was similar between groups with regard to tone, reflexes, and cranial nerves. Behavioral scores were higher on both days, in cocaine-exposed versus control infants, ie, 4.4 ± 0.5 versus 2.7 ± 0.3 on day 1 and 5.0 ± 0.5 versus 1.71 ± 0.31 on day 2. Cerebral blood flow velocity measurements in the anterior cerebral artery were similar between groups on both days of examination. However, cocaine-exposed infants demonstrated a significant increase in flow velocity from day 1 to day 2, ie, 0.48 ± 0.03 to 0.57 ± 0.04. There was a concomitant decrease in the pulsatility index from day 1 to day 2 in the cocaine-exposed, ie, 0.74 ± 0.02 to 0.69 ± 0.02, but not in the control infants. No differences were noted in the flow velocities in the middle cerebral arteries between groups. Conclusions. Term and near-term infants admitted to a regular nursery who are exposed to cocaine in utero: (1) do not exhibit an increased incidence of neurosonographic abnormalities; (2) do exhibit altered behavior consistent with drug withdrawal; and (3) do demonstrate changes in flow velocity in the anterior cerebral artery consistent with the vasoconstrictive effects of the drug. However, these changes were not accompanied by changes in the neurologic examination or altered care. The long-term neurodevelopmental implications of these subtle abnormalities in the neonatal period remain to be determined.

scholarly journals Effects of Pentobarbital on Contractile Responses of Feline Cerebral Arteries

1981 ◽  
Vol 1 (4) ◽  
pp. 437-440 ◽  
Author(s):  
L. Edvinsson ◽  
J. McCulloch
Keyword(s):  
Anaesthetic Agent ◽  
Cerebral Arteries ◽  
Cerebrovascular Reactivity ◽  
Contractile Responses ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F

The effects of pentobarbital on the contractile responses of isolated feline middle cerebral arteries have been examined. In the presence of pentobarbital (3 × 10−4 M), the maximum contractions effected by potassium, noradrenaline, and prostaglandin F2α were reduced by 37 ± 3, 69 ± 3, and 10 ± 6%, respectively. The results caution against the use of pentobarbital as an anaesthetic agent in investigations of cerebrovascular reactivity.

Role of Ca2+ channels in NE-induced increase in [Ca2+]iand tension in fetal and adult cerebral arteries

1999 ◽  
Vol 277 (1) ◽  
pp. R286-R294 ◽  
Author(s):  
Wen Long ◽  
Yu Zhao ◽  
Lubo Zhang ◽  
Lawrence D. Longo
Keyword(s):  
Plasma Membrane ◽  
Cerebral Arteries ◽  
Channel Blockers ◽  
Developmental Age ◽  
Intracellular Ca ◽  
Lanthanum Ion ◽  
Near Term ◽  
Dose Dependent Decrease ◽  
Nonpregnant Adult

In vascular smooth muscle, elevation of agonist-induced intracellular Ca2+ concentration ([Ca2+]i) occurs via both Ca2+ release from intracellular stores and Ca2+influx across the plasma membrane. In the cerebral vasculature of the fetus and adult the relative roles of these mechanisms have not been defined. To test the hypothesis that plasma membrane L-type and receptor-operated Ca2+ channels play a key role in NE-induced vasoconstriction via alterations in plasma membrane Ca2+ flux and that this may change with developmental age, we performed the following study. In main branch middle cerebral arteries (MCA) from near-term fetal (∼140 days) and nonpregnant adult sheep, we quantified NE-induced responses of vascular tension and [Ca2+]i(by use of fura 2) under standard conditions in response to several Ca2+ channel blockers and in response to zero extracellular Ca2+. In fetal and adult MCA, maximal NE-induced tensions (g) were 0.91 ± 0.12 ( n = 10) and 1.61 ± 0.13 ( n = 12), respectively. The pD2 values for NE-induced tension were both 6.0 ± 0.1, whereas the fetal and adult maximum responses (%Kmax) were 107 ± 16 and 119 ± 7, respectively. The fetal and adult pD2 values for NE-induced increase of [Ca2+]iwere 6.2 ± 0.1 and 6.4 ± 0.1, respectively, whereas maximum [Ca2+]iresponses were 81 ± 9 and 103 ± 15% of Kmax, respectively. After 10−5 M NE-induced contraction, nifedipine resulted in dose-dependent decrease in vessel tone and [Ca2+]iwith pIC50 values for fetal and adult tensions of 7.3 ± 0.1 and 6.6 ± 0.1, respectively ( P < 0.01; n = 4 each), whereas pIC50 for [Ca2+]iresponses were 7.2 ± 0.1 and 6.9 ± 0.1, respectively. The pIC50 values for tension for diltiazem and verapamil were somewhat lower but showed a similar relationship. The receptor-operated Ca2+ channel blocker 2-nitro-4 carboxyphenyl- N,N-diphenyl carbamate showed little effect on NE-induced vessel contractility or [Ca2+]i. In the absence of extracellular Ca2+ for 2 min, 10−5 M NE resulted in markedly attenuated responses of adult MCA tension and [Ca2+]ito 39 ± 7 and 73 ± 8% of control values ( n = 4). For fetal MCA, exposure to extracellular Ca2+concentration resulted in essentially no contractile or [Ca2+]iresponse ( n = 4). Similar blunting of NE-induced tension and [Ca2+]iwas seen in response to 10−3M lanthanum ion. These findings provide evidence to suggest that especially in fetal, but also in adult, ovine MCA, Ca2+ flux via L-type calcium channels plays a key role in NE-induced contraction. In contrast, Ca2+ flux via receptor-operated Ca2+ channels is of less importance. This developmental difference in the role of cerebrovascular plasma membrane Ca2+ channels may be an important association with increased Ca2+sensitivity of the fetal vessels.

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