Sympathetic Mechanisms in Blood Vessels: Nerve and Muscle Relationships

Bevan, John A.; Su, Che

doi:10.1146/annurev.pa.13.040173.001413

Cited by 92 publications

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“…The suggestions have been advanced that Uptake2 might be involved in allowing access of transmitter to intracellular receptor sites (Bevan & Su, 1973) and that it may serve to prolong tissue responses to transmitter by providing a labile extraneuronal store from which noradrenaline could be released again into the vicinity of the receptor (Gillespie, 1973). Recently Gershon, Hagopian & Nunez (1974) observed that tritiated noradrenaline taken up by Uptake2 into the muscle cells of the rat heart was concentrated in the vicinity of the contractile elements, and they suggested that Uptake2 may be implicated in mediation of the inotropic response to catecholamines.…”

Section: Effect Of Blood Oestrogen On Uptake2mentioning

confidence: 99%

Involvement of uptake2 in the termination of activity of neurogenic noradrenaline in the rat isolated atrium.

Bell¹,

Grabsch²

1976

The Journal of Physiology

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SUMMARY1. An examination has been made of the relative effect of drugs which affect Uptake, and Uptake2 on the mechanical responses to adrenergic nervous stimulation (0.5-5 Hz for 5 see) in rat isolated atrium.2. Inhibition of Uptake1 with desmethylimipramine (2 ,UM) prolonged by 50-90% the time taken for recovery of normal heart rate after a five see train of nervous stimulation. Inhibition of Uptake2 with metanephrine (4#M) prolonged by 20-40% the time taken for recovery of normal heart rate.3. Neither desmethylimipramine nor metanephrine had any consistent effect on the time course of the inotropic response to stimulation or on the amplitudes of either inotropic or chronotropic responses.4. After administration of desmethylimipramine, metanephrine had a somewhat greater effect on chronotropic responses than when given alone. After administration of metanephrine, desmethylimipramine still further prolonged chronotropic responses to low frequency stimulation (0.5, 1 Hz) but had no effect at 5 Hz. These results agree with the known affinities of each uptake process for different concentrations of noradrenaline in the rat heart. 5. It is concluded that both Uptake1 and Uptake2 participate in the termination of physiological activity of neurogenic noradrenaline in rat isolated atrium even at low frequencies of nervous activation.6. No evidence was obtained to indicate that manipulation of circulating oestrogen levels by o6phorectomy and oestrogen-priming of female rats had any effect on the efficiency of the cardiac Uptake2 process.

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Section: Effect Of Blood Oestrogen On Uptake2mentioning

confidence: 99%

Involvement of uptake2 in the termination of activity of neurogenic noradrenaline in the rat isolated atrium.

Bell¹,

Grabsch²

1976

The Journal of Physiology

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“…These adrenergic nerves contain noradrenaline which is released from the nerve as the transmitter (Bevan & Su, 1973).…”

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

Suzuki

1981

The Journal of Physiology

101

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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.

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“…Finally, some considerations that help in understanding the underlying basis of variation or distinctiveness in blood vessels will be outlined. For further details on this subject-the sympathetic control of the vasculature-the reader should refer to a number of reviews (Furchgott, 1955;Somlyo and Somlyo, 1968a;Somlyo and Somlyo, 1970;Mellander and Johansson, 1968;Spector et al, 1972;Bevan and Su, 1973a;Fleisch, 1974;de la Lande, 1975; Vanhoutte and Leusen, 1978;Bevan et al in press). …”

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Some bases of differences in vascular response to sympathetic activity.

Bevan¹

1979

Circulation Research

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IN 1858 Claude Bemarde summarized much of his research into the physiology of the control of the circulation by the statement that the sympathetic nervous system acted as a "vasoconstrictor nerve." Subsequent study has shown that this division of the autonomic nervous system, although not always constrictor, exerts a control over the tone of both arteries and veins, which is of profound physiological significance. The influence on a particular vascular segment, however, varies widely, both qualitatively and quantitatively, according to its location within the vascular tree.In this brief review, three general patterns of sympathetic control of vascular tone are described (Fig. 1). These are patterns of neuromuscular organization and are distinguished on the basis of both anatomical and functional criteria derived from in vitro studies. They are specific types of relationships between the contractile system of the blood vessel wall, particularly the individual vascular smooth muscle cells, and the postganglionic adrenergic neural terminations. Their adequate description includes a detailed consideration of the transmitter mechanism that links the two types of cells. In general, these patterns vary with vessel diameter and function. In each instance the different neuromuscular organization reflects a different functional role of the blood vessel. Although for convenience, three basic patterns of neuroeffector organization are presented, these are disparate examples selected from the two extremes and probably the middle of a wide-ranging continuum. They have been recognized by parallel structural and functional investigation, the results of which complement each other.

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Sympathetic Mechanisms in Blood Vessels: Nerve and Muscle Relationships

Cited by 92 publications

References 0 publications

Involvement of uptake2 in the termination of activity of neurogenic noradrenaline in the rat isolated atrium.

Involvement of uptake2 in the termination of activity of neurogenic noradrenaline in the rat isolated atrium.

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

Some bases of differences in vascular response to sympathetic activity.

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