Intracelluläre Potentialmessungen zur normalen Spontanaktivität der isolierten Portalvene des Meerschweinchens

Golenhofen, K.; D, von Loh

doi:10.1007/bf00586430

Cited by 34 publications

(8 citation statements)

References 27 publications

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“…Therefore, most authors used other methods, for example, the sucrose-gap technique [e.g. C uthbert et al, 1965; A xelsson et al, 1967; J ohansson et al, 1967; H olman et al, 1968], In recent intracellular measurements of spontaneous activity [G olenhofen and von Loh, 1970a], we have seen differences from the results obtained by the sucrose-gap method. There fore, it appeared necessary to verify reactive behaviour of the portal vein by microelectrode technique as well, first of all investigating responses to adrenergic drugs.…”

mentioning

confidence: 49%

The Effect of Adrenergic Drugs on Spontaneously Active Vascular Smooth Muscle Studied by Long-Term Intracellular Recording of Membrane-Potential

Loh¹

1971

J Vasc Res

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mentioning

confidence: 49%

The Effect of Adrenergic Drugs on Spontaneously Active Vascular Smooth Muscle Studied by Long-Term Intracellular Recording of Membrane-Potential

Loh¹

1971

J Vasc Res

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“…Isometric mechanical changes were measured using a mechano-electrical transducer and a potentiometric recorder. Extracellular electrical activity was measured using a perfused glass capillary [Golenhofen and v. Loh, 1970a] whilst intracellular electrical changes were measured with the technique of partial fixation as described by G olenhofen and v. Loh [1970b] using glass microelectrodes (resistance 30-100 ML?) containing 3 M potassium chloride solution.…”

Section: Methodsmentioning

confidence: 99%

Comparison of the Excitatory and Inhibitory Effects of Angiotensin and Vasopressin on Mammalian Portal Vein

Weston¹,

Golenhofen²

1976

J Vasc Res

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Angiotensin produced inhibitory and excitatory responses in guinea pig portal vein and excitatory responses in rabbit and rat portal vein. Vasopressin produced inhibitory responses in guinea pig and rabbit portal vein and excitatory and inhibitory responses in rat portal vein. In guinea pig portal vein, inhibition by angiotensin and vasopressin was associated with an increase in membrane potential which was, on average, smaller than that produced by isoprenaline, and with a suppression of spike discharges. Tachyphylaxis of the responses to angiotensin and vasopressin in portal vein was not observed and their effects were unaffected by tetrodotoxin, atropine and phentolamine plus propranolol.

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“…For microelectrode experiments, a longitudinal segment (8-12 mm) distal to the hepatic bifurcation was mounted on a truncated plcxiglas cone according to the method described by Golenhofen and Loh [ 15]. The hepatic end of the vein was fixed to the cone by 6 x 0 suture silk tied in a groove around the circumference of the cone, while the mesenteric end, extending beyond the cut top of the cone, was ligated.…”

Section: Microelectrode Measurementsmentioning

confidence: 99%

Effect of Glibenclamide on Membrane Response to Metabolic Inhibition in Smooth Muscle of Rat Portal Vein

Lydrup

Swärd²,

Hellstrand³

1994

J Vasc Res

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Vascular smooth muscle tone is dependent on oxidative metabolism, a phenomenon of potential importance for the metabolic regulation of blood flow to tissues. The response of the rat portal vein to inhibition of cell respiration by cyanide (0.1-1 mM) is a reduction of its spontaneous myogenic activity. The trains of action potentials triggering phasic contractions are reduced in duration, while the frequency of trains is often somewhat increased as the resting membrane potential in the intervals between spike trains is less negative by 6.5 mV. Glibenclamide (10^-7 M) did not affect the resting membrane potential or spontaneous mechanical activity of oxygenated portal veins, but partly restored the depressed myogenic activity in the presence of cyanide (0.5 mM). The spike trains were longer, while the membrane was depolarized by 3 mV compared with the effects of cyanide alone. Inhibition of both oxidative and glycolytic metabolism by 2 mM NaCN in a medium where glucose was replaced by β-hydroxybutyrate caused a hyperpolarization which was abolished by 10^–7M glibenclamide. The relaxing effect of the K⁺ channel opener cromakalim (5· 10^–9 to 6.25· 10^–7M)was partly antagonized by glibenclamide. Basal cytosolic [Ca²⁺] was increased by cyanide, while the Ca²⁺ transients associated with phasic contractions were reduced in duration. This latter effect was partially reversed by glibenclamide. The effect of cyanide on high-K⁺ contractures, which are associated with sustained membrane depolarization and not dependent on repetitive spike activity, was not influenced by 10^–7 M glibenclamide. The effects of inhibited cell respiration on spontaneous electrical activity seem to reflect a depolarizing drive caused by inhibited active ion exchange mechanisms, modified by a repolarizing drive, possibly from ATP-regulated K⁺ channels, causing reduced duration of the spike trains. While glibenclamide affects spontaneous activity at all levels of oxidative blockade, glibenclamide-sensitive hyperpolarization is seen only when both oxidative and glycolytic metabolism is inhibited.

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Intracelluläre Potentialmessungen zur normalen Spontanaktivität der isolierten Portalvene des Meerschweinchens

Cited by 34 publications

References 27 publications

The Effect of Adrenergic Drugs on Spontaneously Active Vascular Smooth Muscle Studied by Long-Term Intracellular Recording of Membrane-Potential

The Effect of Adrenergic Drugs on Spontaneously Active Vascular Smooth Muscle Studied by Long-Term Intracellular Recording of Membrane-Potential

Comparison of the Excitatory and Inhibitory Effects of Angiotensin and Vasopressin on Mammalian Portal Vein

Effect of Glibenclamide on Membrane Response to Metabolic Inhibition in Smooth Muscle of Rat Portal Vein

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