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Journal ArticleDOI

On the local reactions of the arterial wall to changes of internal pressure.

28 May 1902-The Journal of Physiology (Wiley/Blackwell (10.1111))-Vol. 28, Iss: 3, pp 220-231
TL;DR: My attention was first directed to these phenomena by the occurrence of curves like that reproduced in Fig. 11, which showed the effect of a fall of arterial pressure produced by exI citing the central end of the depressor nerve on the volume of the hind leg of the rabbit, the sciatic and the nerves accompanying the femoral artery having been cut.
Abstract: MY attention was first directed to these phenomena by the occurrence of curves like that reproduced in Fig. 11. In the course of experiments on vaso-dilator reflexes I sometimes observed what looked like a reflex of this kind, in a limb of which the nerves had been divided; the figure _ reproduced shows the effect of a fall of arterial pressure produced by exI citing the central end of the depressor nerve on the volume of the hind leg of the rabbit, the sciatic and the nerves accompanying the femoral artery having been cut. It will be noticed that as long as the fall of blood-pressure lasts there is a passive diminution of volume in the limb, but that as soon as the previous height of blood-pressure is attained, on cessation of the excitation, there is a considerable expansion of the limb lasting for some time. Such a curve would usually be explained by stating that Fig. 1. Effect of depressor excitation on there was present all through the volume of enervated leg. Upper curve blood-pressure, next below it volume of excitation a relaxration of the vessels, leg, upper of two chronographs-period but that it was prevented from showof excitation of depressor nerve, lower ing itself in an actual expansion of one-time in 10 sec. intervals. the limb by the simultaneous fall of blood-pressure; although it was
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Journal ArticleDOI
TL;DR: The main conclusions of this review are: 1) regulation of arterial smooth muscle membrane potential through activation or inhibition of K+ channel activity provides an important mechanism to dilate or constrict arteries; 2) KV, KCa, KIR, and KATP channels serve unique functions in the regulation of artery membrane potential
Abstract: This review examines the properties and roles of the four types of K+ channels that have been identified in the cell membrane of arterial smooth muscle cells. 1) Voltage-dependent K+ (KV) channels increase their activity with membrane depolarization and are important regulators of smooth muscle membrane potential in response to depolarizing stimuli. 2) Ca(2+)-activated K+ (KCa) channels respond to changes in intracellular Ca2+ to regulate membrane potential and play an important role in the control of myogenic tone in small arteries. 3) Inward rectifier K+ (KIR) channels regulate membrane potential in smooth muscle cells from several types of resistance arteries and may be responsible for external K(+)-induced dilations. 4) ATP-sensitive K+ (KATP) channels respond to changes in cellular metabolism and are targets of a variety of vasodilating stimuli. The main conclusions of this review are: 1) regulation of arterial smooth muscle membrane potential through activation or inhibition of K+ channel activity provides an important mechanism to dilate or constrict arteries; 2) KV, KCa, KIR, and KATP channels serve unique functions in the regulation of arterial smooth muscle membrane potential; and 3) K+ channels integrate a variety of vasoactive signals to dilate or constrict arteries through regulation of the membrane potential in arterial smooth muscle.

2,113 citations

Journal ArticleDOI
27 Oct 1995-Science
TL;DR: KCa channels activated by Ca2+ sparks appeared to hyperpolarize and dilate pressurized myogenic arteries because ryanodine and thapsigargin depolarized and constricted these arteries to an extent similar to that produced by blockers of KCa channels.
Abstract: Local increases in intracellular calcium ion concentration ([Ca2+]i) resulting from activation of the ryanodine-sensitive calcium-release channel in the sarcoplasmic reticulum (SR) of smooth muscle cause arterial dilation. Ryanodine-sensitive, spontaneous local increases in [Ca2+]i (Ca2+ sparks) from the SR were observed just under the surface membrane of single smooth muscle cells from myogenic cerebral arteries. Ryanodine and thapsigargin inhibited Ca2+ sparks and Ca(2+)-dependent potassium (KCa) currents, suggesting that Ca2+ sparks activate KCa channels. Furthermore, KCa channels activated by Ca2+ sparks appeared to hyperpolarize and dilate pressurized myogenic arteries because ryanodine and thapsigargin depolarized and constricted these arteries to an extent similar to that produced by blockers of KCa channels. Ca2+ sparks indirectly cause vasodilation through activation of KCa channels, but have little direct effect on spatially averaged [Ca2+]i, which regulates contraction.

1,364 citations

Journal ArticleDOI
TL;DR: It is likely that CYP metabolites of arachidonic acid contribute to the changes in renal function and vascular tone associated with some of these conditions and that drugs that modify the formation and/or actions of EETs and 20-HETE may have therapeutic benefits.
Abstract: Recent studies have indicated that arachidonic acid is primarily metabolized by cytochromeP-450 (CYP) enzymes in the brain, lung, kidney, and peripheral vasculature to 20-hydroxyeicosatetraenoic ac...

1,298 citations

Journal ArticleDOI
TL;DR: Even short durations of an intraoperative mean arterial pressure less than 55 mmHg are associated with AKI and myocardial injury, and Randomized trials are required to determine whether outcomes improve with interventions that maintain an intraoper MAP of at least 55mmHg.
Abstract: Background:Intraoperative hypotension may contribute to postoperative acute kidney injury (AKI) and myocardial injury, but what blood pressures are unsafe is unclear. The authors evaluated the association between the intraoperative mean arterial pressure (MAP) and the risk of AKI and myocardial inju

1,025 citations

Journal ArticleDOI
TL;DR: The purpose of this review is to summarize and synthesize information regarding the cellular mechanism(s) underlying the myogenic response in blood vessels, with particular emphasis on arterioles.
Abstract: The vascular myogenic response refers to the acute reaction of a blood vessel to a change in transmural pressure. This response is critically important for the development of resting vascular tone, upon which other control mechanisms exert vasodilator and vasoconstrictor influences. The purpose of this review is to summarize and synthesize information regarding the cellular mechanism(s) underlying the myogenic response in blood vessels, with particular emphasis on arterioles. When necessary, experiments performed on larger blood vessels, visceral smooth muscle, and even striated muscle are cited. Mechanical aspects of myogenic behavior are discussed first, followed by electromechanical coupling mechanisms. Next, mechanotransduction by membrane-bound enzymes and involvement of second messengers, including calcium, are discussed. After this, the roles of the extracellular matrix, integrins, and the smooth muscle cytoskeleton are reviewed, with emphasis on short-term signaling mechanisms. Finally, suggestions are offered for possible future studies.

994 citations


Cites background from "On the local reactions of the arter..."

  • ...Discovery of the myogenic response is credited to Bayliss in 1902, when he recorded large increases in the volume of the dog hindlimb following release of brief aortic occlusions (14)....

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