Untersuchungen zur Acetylcholin-Wirkung auf die Vena portae des Meerschweinchens

Loh, D. v.

doi:10.1007/bf00588737

Cited by 8 publications

(3 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, ACh caused a contraction of non-innervated veins after a-adrenoceptor blockade. Therefore, a direct action of ACh was also postulated (Ehinger, Gennser, Owman, Persson & Sjoberg, 1968;Vanhoutte & Lorenz, 1970;Loh, 1971;Altura, Malaviya, Reich & Orkin, 1972).…”

Section: Introductionmentioning

confidence: 99%

The Effects of Acetylcholine on the Membrane and Contractile Properties of Smooth Muscle Cells of the Rabbit Superior Mesenteric Artery

Kuriyama

Suzuki

1978

British J Pharmacology

View full text Add to dashboard Cite

1 Effects of acetylcholine (ACh) on the membrane potential and mechanical properties of rabbit superior mesenteric artery were investigated by the use of microelectrode and isometric tension recording methods. The membrane potential was -62.5 + 3.0 mV (s.d. [K]o depolarized the membrane and produced contraction (contracture). The minimum depolarization to produce contraction was 10 mV. 2 Low concentrations (10 and 100 ng/ml) of ACh hyperpolarized the membrane. Increased concentrations of ACh (1 and 10 gg/ml) hyperpolarized the membrane further in adult rabbit, while increased concentrations of ACh produced a smaller hyperpolarization in young rabbit. These potential changes produced by ACh in immature and adult rabbits were suppressed by treatment with atropine (0.1 tg/ml). 3 ACh (10 ng to 1 ,ug/ml) consistently generated contraction in Krebs solution. However, ACh relaxed the contraction induced by either K+ or noradrenaline in the adult rabbit, and it enhanced contraction produced by this treatment in the immature rabbit. In Ca-free EGTA solution, the action of ACh on the mechanical response was markedly suppressed, although high concentrations of ACh still evoked contraction. However, treatment with atropine (1 ,ug/ml) completely prevented these actions of ACh. 4 ACh-induced relaxation during either K+-induced or noradrenaline-induced contraction was not caused by the hyperpolarization of the membrane. 5 It is concluded that ACh possesses dual actions on smooth muscle cells of the rabbit superior mesenteric artery in Krebs solution, i.e. ACh hyperpolarizes the membrane, while it consistently generates contraction. These ACh actions on the muscle cells were modified by aging.

show abstract

Section: Introductionmentioning

confidence: 99%

The Effects of Acetylcholine on the Membrane and Contractile Properties of Smooth Muscle Cells of the Rabbit Superior Mesenteric Artery

Kuriyama

Suzuki

1978

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…In the venous system, this direct constrictor effect has been observed in isolated cutaneous (3)(4)(5)(6)(7)(8), jugular (9), mesenteric (9)(10)(11)(12), portal (9,(13)(14)(15)(16), pulmonary (17,18), and umbilical (19) veins. In the intact animal, application of acetylcholine causes splanchnic (20,21) and cutaneous (4,22,23) veins to contract.…”

Section: Introductionmentioning

confidence: 99%

Venous Relaxation Caused by Acetylcholine Acting on the Sympathetic Nerves

Vanhoutte

Shepherd

1973

Circulation Research

View full text Add to dashboard Cite

Experiments were performed to determine whether acetylcholine affects the sympathetic activation of the cutaneous veins of the dog. Changes in isometric tension of saphenous vein strips were recorded at 37°C in an organ bath. Addition of acetylcholine at 10 -11 to 10 -8 g/ml did not affect basal tension, but larger doses (5 x 10 -8 to 5 x 10 -7 g/ml) caused a contraction of the strips which varied from slight to marked. Acetylcholine at 10 -8 to 10 -7 g/ml caused a further increase in tension when it was added to strips already contracted by norepinephrine, tyramine, KCl, or BaCl 2 ; in contrast, similar doses of acetylcholine caused relaxation of strips contracted by liberation of norepinephrine from the nerve terminals by electrical stimulation (1-10 cps). This relaxation was not influenced by propranolol or hexamethonium but was abolished by atropine (10 -8 g/ml). In intact dogs, the lateral saphenous vein was perfused with autologous blood at constant flow. A sustained venoconstriction was induced either by electrical stimulation of the lumbar sympathetic chain or by a continuous infusion of norepinephrine. An infusion of acetylcholine (10 -7 to 10 -6 g/ml min -1 ) relaxed veins constricted by sympathetic stimulation but not those constricted by norepinephrine. Thus, acetylcholine, in doses smaller than those known to have a direct constrictor effect, causes relaxation of cutaneous veins, probably by inhibiting the release of norepinephrine from nerve terminals.

show abstract

“…There is evidence that in many vascular smooth muscles, exogenously applied noradrenaline depolarizes the membrane through the activation of alpha-adrenergic receptors (Keatinge, 1964;Cuthbert & Sutter, 1966;Holman et al 1968;Somlyo & Somlyo, 1968;von Loh, 1971;Golenhofen, Hermstein & Lammel, 1973;Kuriyama & Suzuki, 1978a, b;Takata, 1979). Theionicmechanismsunderlyingthenoradrenalineinduced depolarization are, however, not understood well.…”

mentioning

confidence: 99%

Effects of endogenous and exogenous noradrenaline on the smooth muscle of guinea‐pig mesenteric vein

Suzuki

1981

The Journal of Physiology

101

View full text Add to dashboard Cite

SUMMARYMembrane responses of smooth muscles of the guinea-pig mesenteric vein to noradrenaline released from perivascular nerves or applied exogenously were investigated.1. Exogenously applied noradrenaline depolarized the muscle membrane at concentrations ofover 10-6 M, and generated slow waves or action potentials. Application of phentolamine but not propranolol suppressed the depolarization.2. The depolarization induced by exogenous noradrenaline was associated with increase in the membrane resistance. The level of the membrane depolarization was3. Repetitive but not single stimulation ofthe nerves produced slow depolarization of the membrane. The amplitude of the slow depolarization was dependent on the frequency or number of stimuli within a certain range, but beyond this an increased frequency or an increased number of stimulating pulses produced no further increase in amplitude of the slow depolarization.4. The slow depolarization induced by nerve stimulation was analysed in relation to the diffusion of transmitter. The rising phase of the slow depolarization fitted well with the theoretically predicted one, while the falling phase did not.5. Stimulation of nerves with a high frequency and a large number of pulses produced slow waves or action potentials superimposed on the slow depolarization of the membrane.6. Membrane responses induced by nerve stimulation did not appear in the presence of TTX or phentolamine. TEA enhanced the nerve-induced responses.7. Myogenic electrical activities insensitive to TTX and phentolamine were recorded from the mesenteric vein. These activities were induced by nerve stimulation only in the fresh tissues, were usually irregular in shape, size and frequency, and lasted for 5-20 min.8. It was concluded that alpha-adrenergic receptors on the muscle membrane reacted in a similar manner to noradrenaline either released from the nerves or applied exogenously. Noradrenaline depolarized the muscle membrane by the decrease in potassium conductance of the membrane.

show abstract

Untersuchungen zur Acetylcholin-Wirkung auf die Vena portae des Meerschweinchens

Cited by 8 publications

References 16 publications

The Effects of Acetylcholine on the Membrane and Contractile Properties of Smooth Muscle Cells of the Rabbit Superior Mesenteric Artery

The Effects of Acetylcholine on the Membrane and Contractile Properties of Smooth Muscle Cells of the Rabbit Superior Mesenteric Artery

Venous Relaxation Caused by Acetylcholine Acting on the Sympathetic Nerves

Effects of endogenous and exogenous noradrenaline on the smooth muscle of guinea‐pig mesenteric vein

Contact Info

Product

Resources

About