Influence of transmural pressure on myogenic responses of isolated cerebral arteries of the rat

1985 ◽  
Vol 13 (3-4) ◽  
pp. 287-293 ◽  
Author(s):  
Wiliam Halpern ◽  
George Osol
Keyword(s):  
Cerebral Arteries ◽  
Transmural Pressure ◽  
Myogenic Responses

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)

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.

Specific Mechanotransduction Signaling Involved in Myogenic Responses of the Cerebral Arteries

2009 ◽  
pp. 453-481 ◽  
Author(s):  
Koichi Nakayama ◽  
Kazuo Obara ◽  
Tomohisa Ishikawa ◽  
Shigeru Nishizawa
Keyword(s):  
Cerebral Arteries ◽  
Myogenic Responses

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.

Traumatic Brain Injury Reduces Myogenic Responses in Pressurized Rodent Middle Cerebral Arteries

1999 ◽  
Vol 16 (12) ◽  
pp. 1177-1186 ◽  
Author(s):  
BABU P. MATHEW ◽  
DOUGLAS S. DeWITT ◽  
ROBERT M. BRYAN ◽  
RICHARD D. BUKOSKI ◽  
DONALD S. PROUGH
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Arteries ◽  
Middle Cerebral Arteries ◽  
Myogenic Responses

scholarly journals Modulation of p66Shc impairs cerebrovascular myogenic tone in low renin but not low nitric oxide models of systemic hypertension

2021 ◽  
Author(s):  
William E. Hughes ◽  
Joe Hockenberry ◽  
Bradley Miller ◽  
Andrey Sorokin ◽  
Andreas M. Beyer
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Adaptor Protein ◽  
Transmural Pressure ◽  
Systemic Hypertension ◽  
Myogenic Tone ◽  
Loss Of Function ◽  
Cerebrovascular Function ◽  
Myogenic Responses

Cerebral blood flow and perfusion are tightly maintained through autoregulation despite changes in transmural pressure. Oxidative stress impairs cerebral blood flow, precipitating cerebrovascular events. Phosphorylation of the adaptor protein p66Shc increases mitochondrial-derived oxidative stress. The effect of p66Shc gain or loss of function in non-hypertensive rats is unclear. We hypothesized that p66Shc gain of function would impair autoregulation of cerebral microcirculation under physiological and pathological conditions. Three previously established transgenic (salt-sensitive background; SS) p66Shc rats were utilized, p66-Del/SS (express p66Shc with a 9-amino acid deletion), p66Shc-KO/SS (frameshift premature termination codon), and p66Shc-S36A/SS (substitution of Ser36Ala). The p66Shc-Del were also bred on Sprague-Dawley backgrounds (p66-Del/SD), and a subset was exposed to a hypertensive stimulus (L-NAME) for 4 weeks. Active and passive diameters to increasing transmural pressure were measured and myogenic tone was calculated. Myogenic responses to increasing pressure were impaired in p66Shc-Del/SS rats relative to WT/SS and knock-in substitution of S36A (P<0.05). p66-Del/SD rats did not demonstrate changes in active/passive diameters or myogenic tone relative to WT/SD, but did demonstrate attenuated passive diameter responses to higher transmural pressure relative to p66-Del/SS. 4 weeks of a hypertensive stimulus (L-NAME) did not alter active or passive diameter responses to increasing transmural pressure (P=0.86-0.99), but increased myogenic responses relative to p66-Del/SD (P<0.05). Collectively, we demonstrate the functional impact of modulation of p66Shc within the cerebral circulation and demonstrate that the genetic background of p66Shc rats largely drives changes in cerebrovascular function.

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