Electrical conduction within the cerebrovasculature of stroke-prone spontaneously hypertensive rats

1998 ◽  
Vol 76 (2) ◽  
pp. 194-201 ◽  
Author(s):  
John S Smeda ◽  
Shelley R King
Keyword(s):  
Electrical Conductivity ◽  
Membrane Potential ◽  
Gap Junction ◽  
Electrical Conduction ◽  
Cerebral Arteries ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Middle Cerebral Arteries ◽  
Length Constant ◽  
Electrotonic Potential

Alterations in electrical conductivity between smooth muscle cells (SMCs) can alter the spread and effectiveness of electromechanical SMC contraction. We attempted to determine whether alterations in pressure-dependent constriction (PDC) occurring in relation to stroke development within the middle cerebral arteries (MCAs) of Wistar-Kyoto stroke-prone hypertensive rats (SHRsp) were associated with changes in electrical conductivity between the SMCs. Current was injected into nonpressurized MCAs, using a suction electrode. The conducting distance along the length of the MCA where the amplitude of the membrane potential deflection (electrotonic potential) produced by current injection declined to 1/e (length constant) was used to measure conductivity. PDC to a 100 mmHg pressure step was measured with a pressure myograph. A loss of PDC in the MCAs of SHRsp preceded stroke development. Heptanol (4 mM), a gap junction communication inhibitor, reversibly inhibited conductivity and PDC in the MCA of prestroke SHRsp. The ability of heptanol to reversibly inhibit PDC was likely not related to it's ability to alter electrical conduction. The length constant of electrical conduction in the MCAs was about 0.75 mm and didn't differ between MCA sampled from pre- versus post-stroke SHRsp or Sprague-Dawley rats. It was concluded that alterations in electrical conductivity along the MCA could modify the spread of PDC, but such changes do not contribute to the loss of PDC within the MCA of poststroke SHRsp.Key words: membrane potential, electrotonic potential, middle cerebral arteries, myogenic response, gap junction, stroke-prone hypertensive rats.

scholarly journals Angiotensin-(1-7) and low-dose angiotensin II infusion reverse salt-induced endothelial dysfunction via different mechanisms in rat middle cerebral arteries

2010 ◽  
Vol 299 (4) ◽  
pp. H1024-H1033 ◽  
Author(s):  
Matthew J. Durand ◽  
Gábor Raffai ◽  
Brian D. Weinberg ◽  
Julian H. Lombard
Keyword(s):  
Endothelial Dysfunction ◽  
Receptor Antagonist ◽  
Intravenous Infusion ◽  
Low Dose ◽  
Cerebral Arteries ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Mas Receptor ◽  
Middle Cerebral Arteries

The goals of this study were to 1) determine the acute effect of ANG-(1-7) on vascular tone in isolated middle cerebral arteries (MCAs) from Sprague-Dawley rats fed a normal salt (NS; 0.4% NaCl) diet, 2) evaluate the ability of chronic intravenous infusion of ANG-(1-7) (4 ng·kg−1·min−1) for 3 days to restore endothelium-dependent dilation to acetylcholine (ACh) in rats fed a high-salt (HS; 4% NaCl) diet, and 3) determine whether the amelioration of endothelial dysfunction by ANG-(1-7) infusion in rats fed a HS diet is different from the protective effect of low-dose ANG II infusion in salt-fed rats. MCAs from rats fed a NS diet dilated in response to exogenous ANG-(1-7) (10−10–10−5 M). Chronic ANG-(1-7) infusion significantly reduced vascular superoxide levels and restored the nitric oxide-dependent dilation to ACh (10−10–10−5 M) that was lost in MCAs of rats fed a HS diet. Acute vasodilation to ANG-(1-7) and the restoration of ACh-induced dilation by chronic ANG-(1-7) infusion in rats fed a HS diet were blocked by the Mas receptor antagonist [d-ALA( 7 )]-ANG-(1-7) or the ANG II type 2 receptor antagonist PD-123319 and unaffected by ANG II type 1 receptor blockade with losartan. The restoration of ACh-induced dilation in MCAs of HS-fed rats by chronic intravenous infusion of ANG II (5 ng·kg−1·min−1) was blocked by losartan and unaffected by d-ALA. These findings demonstrate that circulating ANG-(1-7), working via the Mas receptor, restores endothelium-dependent vasodilation in cerebral resistance arteries of animals fed a HS diet via mechanisms distinct from those activated by low-dose ANG II infusion.

scholarly journals Angiogenesis after Stroke is Correlated with Increased Numbers of Macrophages: The Clean-up Hypothesis

2001 ◽  
Vol 21 (10) ◽  
pp. 1223-1231 ◽  
Author(s):  
Panya S. Manoonkitiwongsa ◽  
Catherine Jackson-Friedman ◽  
Paul J. McMillan ◽  
Robert L. Schultz ◽  
Patrick D. Lyden
Keyword(s):  
Microvessel Density ◽  
Focal Cerebral Ischemia ◽  
Cerebral Arteries ◽  
Sprague Dawley ◽  
Regional Cerebral Blood ◽  
Ischemic Brain ◽  
Sprague Dawley Rats ◽  
Middle Cerebral Arteries ◽  
The Brain ◽  
Left Middle

Brain cells manufacture and secrete angiogenic peptides after focal cerebral ischemia, but the purpose of this angiogenic response is unknown. Because the maximum possible regional cerebral blood flow is determined by the quantity of microvessels in each unit volume, it is possible that angiogenic peptides are secreted to generate new collateral channels; other possibilities include neuroprotection, recovery/regeneration, and removal of necrotic debris. If the brain attempts to create new collaterals, microvessel density should increase significantly after ischemia. Conversely, if angiogenic-signaling molecules serve some other purpose, microvessel densities may increase slightly or not at all. To clarify, the authors measured microvessel densities with quantitative morphometry. Left middle cerebral arteries of adult male Sprague–Dawley rats were occluded with intraluminal nylon suture for 4 hours followed by 7, 14, 19, or 30 days of reperfusion. Controls received no surgery or suture occlusion. Changes in microvessel density and macrophage numbers were measured by light microscopic morphometry using semiautomated stereologic methods. Microvessel density increased only in the ischemic margin adjacent to areas of pannecrosis and was always associated with increased numbers of macrophages. Ischemic brain areas without macrophages displayed no vascularity changes compared with normal animals. These data suggest that ischemia-induced microvessels are formed to facilitate macrophage infiltration and removal of necrotic brain.

scholarly journals Effect of Nearby Construction Activity on Endothelial Function, Sensitivity to Nitric Oxide, and Potassium Channel Activity in the Middle Cerebral Arteries of Rats

2020 ◽  
Author(s):  
Maia N Terashvili ◽  
Kaleigh N Kozak ◽  
Debebe Gebremedhin ◽  
Linda A Allen ◽  
Alison L Gifford ◽  
...  
Keyword(s):  
Single Channel ◽  
Cerebral Arteries ◽  
High Sensitivity ◽  
Vibration Monitoring ◽  
Raspberry Pi ◽  
Sprague Dawley ◽  
Film Sensor ◽  
No Donor ◽  
Middle Cerebral Arteries ◽  
Construction Activity

The present study assessed the effect of nearby construction activity on the responses of rat middle cerebral arteries (MCA)to the endothelium-dependent vasodilator acetylcholine and the NO donor sodium nitroprusside (SNP) and the activity of MaxiK potassium channels in MCA smooth muscle cells from male Sprague–Dawley rats. Two monitoring systems were used to assess vibrations in the animal rooms during and immediately after construction activities near the research building where the animal facility is located. One was a commercially available system; the other was a Raspberry-Pi (RPi)–based vibration monitoring system designed in our laboratory that included a small computing unit attached to a rolling sensor (low sensitivity) and a piezoelectric film sensor (high sensitivity). Both systems recorded increased levels of vibration during construction activity outside the building. During the construction period, vasodilator responses to acetylcholine and SNP were abolished, and MaxiK single-channel current opening frequency and open-state probability in cell-attached patches of isolated MCA myocytes were dramatically decreased. Recovery of acetylcholine- and SNP-induced dilation was minimal in MCA from rats studied after completion of construction but housed in the animal facility during construction, whereas responses to acetylcholine and SNP were intact in rats purchased, housed, and studied after construction. Baseline levels of vibration returned after the completion of construction, concomitant with the recovery of normal endothelium-dependent vasodilation to acetylcholine and of NO sensitivity assessed by using SNP in MCA from animals obtained after construction. The results of this study indicate that the vibration associated with nearby construction can have highly disruptive effects on crucial physiologic phenotypes.

Abstract 357: Cerebral Arterial Endothelial Dysfunction in the Post-Cardiac Arrest Period

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Frederik B Hansen ◽  
Goncalo Esteves ◽  
Niels Secher ◽  
Bo Lofgren ◽  
Ulf Simonsen ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Endothelial Dysfunction ◽  
Cerebral Arteries ◽  
Channel Blockers ◽  
Sprague Dawley ◽  
No Donor ◽  
Sprague Dawley Rats ◽  
Middle Cerebral Arteries ◽  
Cerebral Vasodilation ◽  
Synthase Inhibitor

Introduction: Cardiac arrest (CA) has a poor prognosis due to brain injury that progresses over time. Endothelial dysfunction may play an important role in the impairment of the cerebral circulation after CA. Aims: To investigate 1) whether endothelial dysfunction is present in cerebral arteries, and 2) if the altered endothelial function is caused by increased activity of calcium-activated potassium (K ca ) channels. Methods: Male Sprague-Dawley rats (403g±24g) were anaesthetized, intubated and ventilated. Four groups were examined; two CA groups observed for either 2 hours (2h-CA, n=10) or 4 hours (4h-CA, n=10) and two corresponding sham groups (2h-sham, n=10; 4h-sham, n=10). Following 7 minutes of asphyxial CA, the rats were resuscitated using adrenaline, ventilation, and chest compressions. Middle cerebral arteries were isolated and examined in wire-myographs. Results: Cerebral vasodilation was significantly enhanced in response to bradykinin in arteries from 4h-CA rats when compared to 4h-sham rats (4h-sham: E max 58% (5.57 of 9.69) ± 6% vs 4h-CA: E max 84% (6.16 of 7.32) ± 4%, p=0.007). Likewise, vasodilation induced by NS309 (K Ca -channel activator) was increased in CA rats when compared to sham rats. In the presence of L-NAME (NO synthase inhibitor), bradykinin induced vasodilation was significantly augmented in 4h-CA rats when compared to 4h-sham rats, whereas SNP (NO donor) induced vasodilation was similar between groups. In the presence of L-NAME and K Ca -channel blockers (UCL1684 and ICA-17043), bradykinin induced vasodilation was abolished in cerebral arteries in all four groups. Conclusion: Our findings demonstrate an enhanced endothelial-dependent vasodilation in cerebral arteries in the post-cardiac arrest period. The increased vasodilatory response may be explained by increased endothelial K Ca -channel activity and bioavailability of NO, and may contribute to dysregulation of cerebral blood flow after CA.

scholarly journals Loss of cerebrovascular Shaker-type K+ channels: a shared vasodilator defect of genetic and renal hypertensive rats

2009 ◽  
Vol 297 (1) ◽  
pp. H293-H303 ◽  
Author(s):  
Ann A. Tobin ◽  
Biny K. Joseph ◽  
Hamood N. Al-Kindi ◽  
Sulayma Albarwani ◽  
Jane A. Madden ◽  
...  
Keyword(s):  
Cerebral Arteries ◽  
Chronic Hypertension ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Western Blots ◽  
Spontaneously Hypertensive ◽  
Rat Models ◽  
Middle Cerebral Arteries ◽  
Wistar Kyoto ◽  
Renal Hypertensive Rats

The cerebral arteries of hypertensive rats are depolarized and highly myogenic, suggesting a loss of K+ channels in the vascular smooth muscle cells (VSMCs). The present study evaluated whether the dilator function of the prominent Shaker-type voltage-gated K+ (KV1) channels is attenuated in middle cerebral arteries from two rat models of hypertension. Block of KV1 channels by correolide (1 μmol/l) or psora-4 (100 nmol/l) reduced the resting diameter of pressurized (80 mmHg) cerebral arteries from normotensive rats by an average of 28 ± 3% or 26 ± 3%, respectively. In contrast, arteries from spontaneously hypertensive rats (SHR) and aortic-banded (Ao-B) rats with chronic hypertension showed enhanced Ca2+-dependent tone and failed to significantly constrict to correolide or psora-4, implying a loss of KV1 channel-mediated vasodilation. Patch-clamp studies in the VSMCs of SHR confirmed that the peak K+ current density attributed to KV1 channels averaged only 5.47 ± 1.03 pA/pF, compared with 9.58 ± 0.82 pA/pF in VSMCs of control Wistar-Kyoto rats. Subsequently, Western blots revealed a 49 ± 7% to 66 ± 7% loss of the pore-forming α1.2- and α1.5-subunits that compose KV1 channels in cerebral arteries of SHR and Ao-B rats compared with control animals. In each case, the deficiency of KV1 channels was associated with reduced mRNA levels encoding either or both α-subunits. Collectively, these findings demonstrate that a deficit of α1.2- and α1.5-subunits results in a reduced contribution of KV1 channels to the resting diameters of cerebral arteries from two rat models of hypertension that originate from different etiologies.

scholarly journals Sex differences in the structure and function of rat middle cerebral arteries

2020 ◽  
Vol 318 (5) ◽  
pp. H1219-H1232 ◽  
Author(s):  
Shaoxun Wang ◽  
Huawei Zhang ◽  
Yedan Liu ◽  
Longyang Li ◽  
Ya Guo ◽  
...  
Keyword(s):  
Cerebral Arteries ◽  
Structure And Function ◽  
Sprague Dawley ◽  
Sd Rats ◽  
Middle Cerebral Arteries ◽  
Structural Differences ◽  
Males And Females ◽  
Physiological Pressure ◽  
Perfusion Fixation ◽  
And Function

Using perfusion fixation of the middle cerebral artery (MCA) in calcium-free solution at physiological pressure and systematically randomly sampling the sections prepared from the same M2 segments of MCA, we found that there are structural differences that are associated with altered cerebral blood flow (CBF) autoregulation but not neurovascular coupling and cognition in young, healthy Sprague-Dawley (SD) rats. Understanding the intrinsic differences in cerebrovascular structure and function in males and females is essential to develop new pharmaceutical treatments for cerebrovascular disease (CVD).

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