The effect of local changes in potassium and bicarbonate concentration on hypothalamic blood flow in the rabbit.

Cameron, I. R.; Caronna, J.

doi:10.1113/jphysiol.1976.sp011602

Cited by 36 publications

(16 citation statements)

References 27 publications

(41 reference statements)

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“…Smaller increases in [K+]o also occur during physiological changes in neuronal activity (Somjen, 1979). Conclusions In summary, elevated [K+]O is associated with vasodilatation and increased blood flow in heart and brain under physiological and pathophysiological conditions (Buenger et al 1976;Cameron & Caronna, 1976;Paulson & Newman, 1987). K+ efflux from tissue is indicative of its metabolic state or activity and has been proposed as a local regulator of blood flow in the brain (Kuschinsky et al 1972).…”

Section: Methods Preparationmentioning

confidence: 99%

Extracellular K(+)‐induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K(+) channels.

Knot

Zimmermann

Nelson

1996

The Journal of Physiology

302

261

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1. The hypothesis that inward rectifier K+ channels are involved in the vasodilatation of small coronary and cerebral arteries (100-200 ,um diameter) in response to elevated [K+]. was tested. The diameters and membrane potentials of pressurized arteries from rat were measured using a video-imaging system and conventional microelectrodes, respectively. 2. Elevation of [K+]o from 6 to 16 mm caused the membrane potential of pressurized (60 mmHg) arteries to hyperpolarize by 12-14 mV. Extracellular Ba2P (Ba20+) blocked K+-induced membrane potential hyperpolarizations at concentrations (IC50, 6 uM) that block inward rectifier K+ currents in smooth muscle cells isolated from these arteries. 5. These findings suggest that K+ dilates small rat coronary and cerebral arteries through activation of inward rectifier K+ channels. Furthermore, these results support the hypothesis that inward rectifier K+ channels may be involved in metabolic regulation of coronary and cerebral blood flow in response to changes in [K+]0.

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Section: Methods Preparationmentioning

confidence: 99%

Extracellular K(+)‐induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K(+) channels.

Knot

Zimmermann

Nelson

1996

The Journal of Physiology

302

261

View full text Add to dashboard Cite

show abstract

“…The normal extracellular ionic response to neuronal activity is a rise in K+ and a fall in H+ and Ca 2 + (Nicolson et aI ., 1977;Cameron, 1977;Purves, 1978). Like other vascular smooth muscle , isolated cerebral arteries and pial arterioles contract when the extracellular potassium concentration is reduced from 10 to 0 mM (Kuschinsky et aI ., 1972;Toda, 1974Toda, , 1976Betz et aI ., 1975;Pickard et aI ., 1975bPickard et aI ., , 1976Cameron and Caronna, 1976). This behaviour is attributed to the operation of an electrogenic sodium pump that is inhibited at 0 mM K+ and near maximally active at 10 mM K. Siegel et ai .…”

Section: Clinical Significance Of Cerebral Arachidonate Metabolismmentioning

confidence: 99%

“…This phenomenon has been used as an indicator of Na+-K+ ATPase activ ity in extracranial vascular smooth muscle (Webb and Bohr, 1978). It explains the high concentration of potassium required to produce pial and paren chymal arteriolar constriction in vivo (Kuschinsky et aI ., 1972;Betz et aI ., 1975 ;Cameron and Caronna, 1976) ; a large depolarization is required to over come the hyperpolarizing effect of fully activating the electrogenic sodium pump. A fall in extracellu lar fluid (ECF) pH is well documented as a cerebral vasodilator, and the effects of carbon dioxide have been attributed completely to the change in ECF pH (Cameron , 1977, for review).…”

Section: Clinical Significance Of Cerebral Arachidonate Metabolismmentioning

confidence: 99%

Role of Prostaglandins and Arachidonic Acid Derivatives in the Coupling of Cerebral Blood Flow to Cerebral Metabolism

Pickard

1981

J Cereb Blood Flow Metab

174

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“…The activity of the Na + -K + pump may be assessed with tension studies using a phenomenon first described by Barr et al (1962) and subse quently refined by Webb and Bohr (1978). Like other vascular smooth muscle, isolated cerebral ar-teries and pial arterioles contract when the extra cellular potassium concentration is reduced from 10 to 0 mM (Kuschinsky et ai., 1972;Toda, 1974Toda, , 1976Betz et ai., 1975;Pickard et ai., 1975;Cameron and Caronna, 1976). This behaviour is attributed to the operation of an electrogenic Na + -K + pump that is inhibited by 0 mM potassium and near maximally active at 10 mM potassium.…”

mentioning

confidence: 99%

Spectrum of Altered Reactivity of Isolated Cerebral Arteries following Subarachnoid Haemorrhage—Response to Potassium, pH, Noradrenaline, 5-Hydroxytryptamine, and Sodium Loading

Pickard

Perry

1984

J Cereb Blood Flow Metab

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Summary:The circular contractile responses to various stimuli have been measured in segments of cerebral ar teries (both middle cerebral and basilar) taken from dogs either 3 or 7 days following the cisternal injection of au tologous blood under anaesthesia. The maximum con tractile response to 5-hydroxytryptamine was increased significantly 7 days following subarachnoid haemorrhage; the response to noradrenaline also increased but not sig nificantly at 7 days. The contractile response to a raised extracellular potassium concentration (25 and 100 mM) was slightly depressed by 7 days, and the response to a fall in extracellular pH was depressed by 43% both 3 and 7 days following subarachnoid haemorrhage. The ability of these arteries to handle a sodium load was also as sessed. The arteries were sodium loaded for various pe riods of time in mock cerebrospinal fluid with a zero po-The ability of the cerebral circulation to respond to changes either in arterial blood pressure or in arterial blood gases may be impaired in both hu mans and animals following a recent subarachnoid haemorrhage (Heilbrun et aI., 1972; Nornes et aI., 1977; Symon, 1978; Pickard et aI., 1979). The greater the impairment of the cerebrovascular reac tivity, the greater may be the risk of developing late neurological deficits (Pickard et aI., 1980; Farrar et aI., 1981). To study the mechanism of this change in reactivity, we have first sought to establish that this altered reactivity persists in vitro by examining the contractile responses to a variety of stimuli of 599tassium concentration. On transfer to 25 mM potassium solution, the duration but not the magnitude of the initial relaxation phase prior to a final contraction was greater with increasing time spent in the zero potassium solution. Both the magnitude and the duration of this relaxation phase, which reflect in part the ability of the vascular smooth muscle to extrude the sodium load, were in creased in arteries following subarachnoid haemorrhage when compared with control arteries. These results dem onstrate that the altered reactivity of cerebrovascular smooth muscle following subarachnoid haemorrhage per sists in vitro and is more than simply an enhanced re sponse to biogenic amines.

show abstract

The effect of local changes in potassium and bicarbonate concentration on hypothalamic blood flow in the rabbit.

Abstract: [HCO-]. The changes in blood flow in the brain which accompany neuronal activity could be mediated by variation in local [K+].

Cited by 36 publications

References 27 publications

Extracellular K(+)‐induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K(+) channels.

Extracellular K(+)‐induced hyperpolarizations and dilatations of rat coronary and cerebral arteries involve inward rectifier K(+) channels.

Role of Prostaglandins and Arachidonic Acid Derivatives in the Coupling of Cerebral Blood Flow to Cerebral Metabolism

Spectrum of Altered Reactivity of Isolated Cerebral Arteries following Subarachnoid Haemorrhage—Response to Potassium, pH, Noradrenaline, 5-Hydroxytryptamine, and Sodium Loading

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