Regional and species differences in vascular reactivity to extracellular potassium

Ryman, Torsten; Brandt, Lennart; Andersson, Karl‐Erik; Mellergård, Pekka

doi:10.1111/j.1748-1716.1989.tb08647.x

Cited by 19 publications

(11 citation statements)

References 17 publications

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“…This is not surprising because human cerebral arteries are more sensitive to the vasoconstrictive effects of elevated [K ϩ ] o compared with rat and rabbit arteries (402). Altogether the data suggest a bidirectional relationship leading to a vicious cycle in injured brain: injury radically transforms the neurovascular response to SD, and in return the transformed neurovascular response exacerbates the tissue injury by both decreasing CBF and metabolic supply and by increasing the energy demand (364).…”

Section: B Brain Injurymentioning

confidence: 89%

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Ayata

Lauritzen

2015

Physiological Reviews

458

600

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Spreading depression (SD) is a transient wave of near-complete neuronal and glial depolarization associated with massive transmembrane ionic and water shifts. It is evolutionarily conserved in the central nervous systems of a wide variety of species from locust to human. The depolarization spreads slowly at a rate of only millimeters per minute by way of grey matter contiguity, irrespective of functional or vascular divisions, and lasts up to a minute in otherwise normal tissue. As such, SD is a radically different breed of electrophysiological activity compared with everyday neural activity, such as action potentials and synaptic transmission. Seventy years after its discovery by Leão, the mechanisms of SD and its profound metabolic and hemodynamic effects are still debated. What we did learn of consequence, however, is that SD plays a central role in the pathophysiology of a number of diseases including migraine, ischemic stroke, intracranial hemorrhage, and traumatic brain injury. An intriguing overlap among them is that they are all neurovascular disorders. Therefore, the interplay between neurons and vascular elements is critical for our understanding of the impact of this homeostatic breakdown in patients. The challenges of translating experimental data into human pathophysiology notwithstanding, this review provides a detailed account of bidirectional interactions between brain parenchyma and the cerebral vasculature during SD and puts this in the context of neurovascular diseases.

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Section: B Brain Injurymentioning

confidence: 89%

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Ayata

Lauritzen

2015

Physiological Reviews

458

600

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“…In the case of four compounds (aprikalim, nitrendipine, nitroglycerin and papaverine) that were representatives of the vasodilator classes studied, the potencies and efficacies were similar, regardless of whether the osmolarity of the preparation was normal or elevated. An increase in osmolarity of the medium reportedly attenuates contractile activity (Ryman et al 1989). On the other hand, if solutions are to remain isosmolar,, the reduction in [Na + ] required to maintain isosmolarity may reduce Ca 2+ efflux by inhibiting the Na + /Ca 2+ antiporter.…”

Section: Discussionmentioning

confidence: 99%

Influence of depolarization on vasorelaxant potency and efficacy of Ca2+ entry blockers, K+ channel openers, nitrate derivatives, salbutamol and papaverine in rat aortic rings

Magnon

Calderone

Floch

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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We examined the effects of various KCl concentrations on the actions of some vasodilators belonging to different pharmacological classes in rat aortic rings. In some experiments, tissues were precontracted with noradrenaline after blocking voltage-dependent channels to assess the effects of depolarisation unaccompanied by the entry of extracellular Ca2+ into the cytosol. Concentration/response curves for the vasorelaxant effect of calcium entry blockers (e.g. diltiazem), K+ channel openers (e.g. aprikalim), nitrate derivatives (e.g. nitroglycerin), a beta2-adrenergic agonist (salbutamol) and papaverine were obtained by using endothelium-denuded rat aortic rings precontracted with KC1 (20-60 mM) to determine the potencies and efficacies of the drugs. The efficacies and potencies of calcium entry inhibitors were virtually independent of the [KCl]. A reduction in the potency (up to 18-fold) of papaverine occurred without changes in efficacy when the [KCl] was raised from 20 to 60 mM. The decline in potency was even greater for nitrate-like compounds. The potency of K+ channel openers in aortic rings precontracted with 30 mM KCI decreased by three- to sixfold compared with those precontracted with 20 mM KCl. With the exception of pinacidil, the efficacy of these agents already started to decline in preparations precontracted with 25 mM KCI and was virtually zero in preparations precontracted with 60 mM KCI. In contrast to other K+ channel openers, the vasorelaxant action of pinacidil was relatively resistant to glibenclamide. Salbutamol produced only a slight relaxation even in preparations precontracted with 20 mM KCl. In nitrendipine-pretreated, noradrenaline-precontracted aortic rings, the vasorelaxant effects of aprikalim, but not those of linsidomine or papaverine, declined when the [KCl] of the bathing medium was increased. In conclusion, the vasorelaxant potency and efficacy of calcium entry blockers is independent of the [KCI] used to precontract rat aortic rings, and thus, of the degree of membrane depolarisation. In contrast, increasing the [KCl] strongly reduces the potency and the efficacy of K+ channel openers not only in this preparation but also in noradrenaline-precontracted rings in which the entry of extracellular Ca2+ was prevented with nitrendipine. This indicates that, with the exception of pinacidil, the vasorelaxant activity of K+ channel openers depends on the degree of membrane depolarisation. Finally, the vasorelaxant potency and efficacy of nitrate-like compounds and papaverine are independent of depolarisation per se but they are markedly affected by the influx of Ca2+ accompanying elevated [KCI]. Thus, the degree of vessel depolarisation should be taken into consideration when attempting to compare potencies and efficacies among vasorelaxant agents.

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“…vasoconstriction [2], and pretreatment with some vasodilating agents such as prostacyclin may be necessary to avoid incomplete perfusion [3, 4]. …”

Section: Introductionmentioning

confidence: 99%

Difference in the Effects of Low Temperatures on the Tension of Human Pulmonary Artery and Vein Ring Segments

Suzuki

Sugita²,

Ono³

et al. 2000

Respiration

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Background: Although limited data suggest that pulmonary flushing with organ preservation solutions should not be performed at too low temperatures, the influence of temperature on pulmonary vascular tone is unclear. Objective: The purpose of this study was to examine the effect of low temperatures of the tension of human pulmonary artery and vein ring segments and the vascular resistance of perfused rat lungs. Methods: 5 sets of human pulmonary artery and vein ring segments were suspended from a force displacement transducer at 37, 24 and 8°C, and the effect of 30 mM K⁺ on the tension was monitored. The effect of 30 mM K⁺ on vascular resistance was also examined at low temperatures in 5 perfused rat lungs. Results: Pulmonary artery segments dilated at 24°C, and more significant vasodilatation was observed at 8°C. In contrast, there was a significant constriction of pulmonary veins at 8°C. Vasoconstriction induced by 30 mM K⁺ at 37°C was significantly inhibited at low temperatures in both pulmonary arteries and veins. In rat lungs, perfusion at 8°C caused a significant increase in pulmonary vascular resistance, even though no further increase was observed in the presence of 30 mM K⁺. Conclusions: Our data indicate that pulmonary arteries dilate and the veins constrict at 8°C and may increase pulmonary vascular resistance. We conclude that the different effect of low temperatures between pulmonary arteries and veins may explain why pulmonary vascular flushing with organ preservation solutions at room temperature is more satisfactory.

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Regional and species differences in vascular reactivity to extracellular potassium

Cited by 19 publications

References 17 publications

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Influence of depolarization on vasorelaxant potency and efficacy of Ca2+ entry blockers, K+ channel openers, nitrate derivatives, salbutamol and papaverine in rat aortic rings

Difference in the Effects of Low Temperatures on the Tension of Human Pulmonary Artery and Vein Ring Segments

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