Increased sensitivity of cat cerebral arteries to serotonin upon elevation of transmural pressure

1988 ◽  
Vol 411 (6) ◽  
pp. 698-700 ◽  
Author(s):  
David R. Harder
Keyword(s):  
Cerebral Arteries ◽  
Transmural Pressure ◽  
Increased Sensitivity

Ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage

1986 ◽  
Vol 64 (2) ◽  
pp. 292-297 ◽  
Author(s):  
Thomas A. Duff ◽  
Grayson Scott ◽  
John A. Feilbach
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Prolonged Exposure ◽  
Cerebral Arteries ◽  
Content Type ◽  
Ultrastructural Evidence ◽  
Experimental Subarachnoid Hemorrhage ◽  
Catecholamine Histofluorescence ◽  
Increased Sensitivity ◽  
The Media ◽  
Adult Cats

✓ Loss of catecholamine histofluorescence, increased sensitivity to norepinephrine, and changes in alpha1 receptor binding have led to the proposal that denervation hypersensitivity may play a role in cerebrovascular spasm. Because the significance of these alterations has remained unclear, the present study was undertaken to determine whether there was direct ultrastructural evidence of arterial denervation following experimental subarachnoid hemorrhage. Under general anesthesia, adult cats were subjected to pre-pontine injection of blood or serum (5 to 7 ml) via a transclival approach. The animals were sacrificed 4, 7, or 10 days later and basilar artery segments were prepared for electron microscopy. Control vessels appeared normal, whereas those bathed in blood revealed unequivocal changes in neural and supporting elements, including: 1) disintegration of both clear- and dense-core vesicles; 2) fragmentation of varicosities; 3) loss of Schwann cell cytoplasm; and 4) axonal degeneration. These changes were most pronounced 7 days after instillation of blood, and correlated in time with maximal injury of the media and endothelium. Although the development of smooth-muscle hypersensitivity remains unsettled, this study indicates that prolonged exposure to blood can cause extensive denervation of cerebral arteries.

scholarly journals Increased sensitivity to endothelin‐1 in posterior cerebral arteries from obstructive sleep apnea rats

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
David Joseph Durgan ◽  
Randy F. Crossland ◽  
Eric E. Lloyd ◽  
Sharon C. Phillips ◽  
Shawn P. Marrelli ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Cerebral Arteries ◽  
Endothelin 1 ◽  
Obstructive Sleep ◽  
Increased Sensitivity

Regulation of membrane potential and diameter by voltage-dependent K+ channels in rabbit myogenic cerebral arteries

1995 ◽  
Vol 269 (1) ◽  
pp. H348-H355 ◽  
Author(s):  
H. J. Knot ◽  
M. T. Nelson
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Cerebral Arteries ◽  
Muscle Cells ◽  
Transmural Pressure ◽  
Muscle Membrane ◽  
K Channels ◽  
Wide Range ◽  
Voltage Dependent

The hypothesis that voltage-dependent K+ channels are involved in the regulation of arterial smooth muscle membrane potential and blood vessel diameter was tested by examining the effects of inhibitors [4-aminopyridine (4-AP) and 3,4-diaminopyridine (3,4-DAP)] of voltage-dependent K+ channels on the membrane potential and diameter of pressurized small (100- to 300-microns diam) cerebral arteries from rabbit. In response to graded elevations in transmural pressure (20-100 mmHg), the membrane potential of smooth muscle cells in these arteries depolarized and the arteries constricted. 4-AP (1 mM) and 3,4-DAP (1 mM) depolarized cerebral arteries by 19 and 21 mV, respectively, when they were subjected to a transmural pressure of 80 mmHg. 3-Aminopyridine (3-AP, 1 mM), which is a relatively poor inhibitor of voltage-dependent K+ channels, depolarized smooth muscle cells in the arteries by 1 mV. 4-AP and 3,4-DAP constricted pressurized (to 80 mmHg) cerebral arteries. 3-AP had little effect on arterial diameter. 4-AP increased the arterial constriction to transmural pressure over a wide range of pressures (40-90 mmHg). The effects of 4-AP and 3,4-DAP on membrane potential and diameter were not prevented by inhibitors of calcium channels, calcium-activated K+ channels, ATP-sensitive K+ channels, inward rectifier K+ channels, blockers of adrenergic, serotonergic, muscarinic, and histaminergic receptors, or removal of the endothelium. These results suggest that voltage-dependent K+ channels are involved in the regulation of membrane potential and response of small cerebral arteries to changes in intravascular pressure.

Abstract 208: Altered Cerebrovascular Reactivity Following One Month of Obstructive Sleep Apnea

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
David J Durgan ◽  
Randy F Crossland ◽  
Eric E Lloyd ◽  
Sharon C Phillips ◽  
Robert Bryan
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Cerebral Arteries ◽  
Significant Risk ◽  
Fold Increase ◽  
Cerebrovascular Reactivity ◽  
No Production ◽  
No Donor ◽  
Obstructive Sleep ◽  
Increased Sensitivity

Obstructive sleep apnea (OSA) has been identified as a significant risk factor for stroke. However, little is known regarding the effects of OSA on the cerebrovascular wall. Using a novel rodent model of OSA we assessed the hypothesis that (1) OSA augments endothelin (ET-1) induced constrictions of cerebral arteries and (2) OSA attenuates dilations of cerebral arteries by agonist-induced nitric oxide (NO) release from the cerebrovascular endothelium. The repetitive airway closures associated with OSA lead to intermittent hypoxia/hypercapnia and reoxygenation, increased negative intrathoracic pressures, and arousals. In order to model the physiological consequences of OSA, we have chronically instrumented rats with inflatable endotracheal obstruction devices. Unanesthetized freely-ranging rats underwent 30 apneas/ hour for 8 hours/ day (sleep phase) for 1 month. During apnea pO 2 decreased from 122±3 to 67±3 mm Hg; pCO 2 increased from 43±1 to 51±1 mm Hg; pH decreased from 7.46±0.00 to 7.38±0.01; and hemoglobin O 2 saturation decreased from 94±1 to 82±1 % (n=5 and p<0.05 for each). Following 1 month of OSA blood pressure, plasma ET-1 and NO levels were similar in sham and OSA rats. Using the pressurized cerebral artery preparation, we observed a 17.5-fold increase in sensitivity to ET-1 (n=5-6, p<0.05) after 1 month of OSA. The increased sensitivity of OSA cerebral arteries to ET-1 was abolished by the ET-B receptor antagonist BQ-788 (n=6, NS). Additionally, constrictions to the ET-B specific agonist IRL-1620 were significantly greater in OSA, versus sham, cerebral arteries (n=6, p<0.05). Dilations to ATP (a P2Y 2 agonist which stimulates NO production in the endothelium) were attenuated in cerebral arteries from OSA rats by 40% (n=5-8, p<0.05). However dilations to the NO-donor MAHMA-NOnoate were similar between groups. In conclusion, 1 month of OSA results in (1) increased sensitivity of cerebral arteries to ET-1, likely through upregulation of ET-B receptors on the vascular smooth muscle and (2) decreased endothelial-derived NO production. These data suggest that OSA results in significant alterations to the cerebrovascular wall in the absence of hypertension.

Myogenic properties of cerebral blood vessels from normotensive and hypertensive rats

1985 ◽  
Vol 249 (5) ◽  
pp. H914-H921 ◽  
Author(s):  
G. Osol ◽  
W. Halpern
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Cerebral Arteries ◽  
Physiological Saline ◽  
Transmural Pressure ◽  
Hypertensive Rats ◽  
Pressure Step ◽  
Wide Range ◽  
Myogenic Responses ◽  
Wistar Kyoto

Myogenic properties of posterior cerebral arteries from normotensive and hypertensive rats were analyzed in vitro and quantified in terms of both pressure range limits and degree of myogenic activity. Spontaneously hypertensive rat (SHR) vessels were significantly narrower in a fully relaxed state, and both wall thickness and wall-to-radius ratios were increased. After equilibration in 1.6 mM calcium physiological saline solution a substantial tone developed which resulted in average diameter decreases of 34 and 37% in Wistar-Kyoto (WKY) and SHR, respectively; average lumen diameters were approximately 125 micron. Rapid changes in transmural pressure (delta P 10-25 mmHg/s) were applied and diameter responses measured continuously. Myogenic responses began 1-3 s after a change in transmural pressure, and arteries regained their initial diameters after a pressure step in about 2 min; a final, steady-state diameter was achieved in 4-5 min. Myogenic pressure ranges were 49-145 mmHg in WKY and 64-181 in SHR; when responses were segregated according to positive and negative pressure steps, more myogenic responses were observed at lower pressures for pressure step decreases when compared with pressure step increases. Thus myogenic ranges for increasing pressure steps were 71-151 (WKY) and 72-188 mmHg (SHR) and for decreasing steps 45-117 (WKY) and 57-148 mmHg (SHR). Myogenic responses in SHR were weaker than in WKY rats: the former maintained essentially a constant diameter over a wide range of pressures, whereas arteries from the latter decreased diameter with increasing pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased sensitivity to ET-1 in rat cerebral arteries following organ culture

Neuroreport ◽  
2000 ◽  
Vol 11 (3) ◽  
pp. 649-652 ◽  
Author(s):  
Jacob Hansen-Schwartz ◽  
Lars Edvinsson
Keyword(s):  
Organ Culture ◽  
Cerebral Arteries ◽  
Increased Sensitivity

Interaction of myogenic mechanisms and hypoxic dilation in rat middle cerebral arteries

2002 ◽  
Vol 283 (6) ◽  
pp. H2276-H2281 ◽  
Author(s):  
Yanping Liu ◽  
David R. Harder ◽  
Julian H. Lombard
Keyword(s):  
Transmembrane Potential ◽  
Cerebral Arteries ◽  
Vessel Diameter ◽  
Transmural Pressure ◽  
Sprague Dawley ◽  
Pressure Elevation ◽  
Sprague Dawley Rats ◽  
Middle Cerebral Arteries ◽  
Arterial Dilation ◽  
Myogenic Responses

The goal of this study was to determine how myogenic responses and vascular responses to reduced Po 2 interact to determine vascular smooth muscle (VSM) transmembrane potential and active tone in isolated middle cerebral arteries from Sprague-Dawley rats. Stepwise elevation of transmural pressure led to depolarization of the VSM cells and myogenic constriction, and reduction of the O2concentration of the perfusion and superfusion reservoirs from 21% O2 to 0% O2 caused vasodilation and VSM hyperpolarization. Myogenic constriction and VSM depolarization in response to transmural pressure elevation still occurred at reduced Po 2. Arterial dilation in response to reduced Po 2 was not impaired by pressure elevation but was significantly reduced at the lowest transmural pressure (60 mmHg). However, the magnitude of VSM hyperpolarization was unaffected by transmural pressure elevation. This study demonstrates that myogenic activation in response to transmural pressure elevation does not override hypoxic relaxation of middle cerebral arteries and that myogenic responses and hypoxic relaxation can independently regulate vessel diameter despite substantial changes in the other variable.

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