Comparative Effects of Dihydroergotamine and Noradrenaline on Resistance, Exchange and Capacitance Functions in the Peripheral Circulation

Mellander, Stefan; Nordenfelt, I.

doi:10.1042/cs0390183

Cited by 296 publications

(268 citation statements)

References 13 publications

(9 reference statements)

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“…That concurrent activation of the two receptor types occurs simultaneously is demonstrated in this vessel by the increased magnitude of relaxation to NE that occurs after a-adrenergic receptor block and the contraction seen to similar doses of NE after ^-adrenergic receptor block. In the rabbit aorta and pulmonary artery, the ^-receptor-mediated relaxation is small in proportion to the contraction mediated through the a-receptors (Furchgott, 1955;Somlyo and Somlyo, 1970;Mellander and Johansson, 1968). The relaxation can be observed only after administration of an a-receptorblocking agent and the pharmacological initiation of muscle tone.…”

Section: Relative Magnitude Of the A-and ^-Receptormediated Responsesmentioning

confidence: 99%

“…Under various circumstances, slow, rhythmic, coordinated activity has been observed in just about all large and medium-sized blood vessels studied (Furchgott, 1955;Somlyo and Somlyo, 1968a;Mellander and Johansson, 1968;Bevan et al, unpublished observations). The existence of the capacity for synchronous activity implies that vascular smooth muscle cells can be functionally coupled.…”

Section: The Muscle Responsementioning

confidence: 99%

“…If the contraction of a vascular smooth muscle cell is mainly a function of the local concentration of transmitter, the concentration of NE that can be achieved in the vessel wall, and thus the overall response to nerve activity, would be limited by VASCULAR SYMPATHETIC RESPONSE/Bwon 165 transmitter diffusion (Ljung, 1976). Presumably, for this reason, the maximum neurogenic response of vessels with a small myogenic component, no matter how dense their innervation, is never more than half of their maximum response to exogenous transmitter (Ljung, 1976;Mellander and Johansson, 1968). This contrasts with the longitudinal muscle in the adventitia of the rat portal vein, a lightly innervated vessel in which the response is dominated by myogenic propagation and all vascular smooth muscle cells can be maximally influenced by neurogenic transmitter (Ljung et al, 1975).…”

Section: The Muscle Responsementioning

confidence: 99%

“…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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confidence: 99%

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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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Section: Relative Magnitude Of the A-and ^-Receptormediated Responsesmentioning

confidence: 99%

Section: The Muscle Responsementioning

confidence: 99%

Section: The Muscle Responsementioning

confidence: 99%

mentioning

confidence: 99%

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Some bases of differences in vascular response to sympathetic activity.

Bevan¹

1979

Circulation Research

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“…These latter factors were embodied in measurements of capillary permeabilitysurface area product by Renkin (1959) and capillary filtration coefficient by Mellander (1960). Factors which influence or control these variables have been reviewed by Mellander & Johansson (1968). Close arterial infusions of isoprenaline cause vasodilatation and increase capillary filtration coefficient in skeletal muscle and intestine in cats (Johnsson & Oberg, 1968; Diana, 1970;Folkow, Lundgren & Wallentin, 1963).…”

Section: Introductionmentioning

confidence: 99%

Effects of adrenaline, isoprenaline and histamine on transsinusoidal fluid filtration in the cat liver

Greenway

Lautt

1972

British J Pharmacology

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Summary1. Hepatic volume was recorded by a plethysmographic technique in cats anaesthetized with pentobarbitone. It has been shown previously that during an increase of hepatic venous pressure in this preparation, there is a maintained filtration of fluid from the sinusoids into the plethysmograph. The rate of this filtration is directly proportional to the increase in hepatic venous pressure.Infusions of drugs during this period of steady filtration provide a sensitive measure of the effects of the drugs on transsinusoidal fluid transfer. 2. Infusions of adrenaline, isoprenaline and histamine had no effect on the steady transsinusoidal filtration produced by an increased hepatic venous pressure. It is concluded that these agents do not change sinusoidal hydrostatic pressure by more than 15 mmHg (1 mmHg=-1-333 mbar) even though they alter hepatic arterial and portal flows. They do not change sinusoidal surface area by more than 20% and histamine does not change sinusoidal permeability. 3. The data are discussed in the light of current theories on the application of Starling's hypothesis to the liver sinusoids and to muscle capillaries. The postsinusoidal resistance appears to be very low in the liver and it does not increase during contraction of the capacitance vessels. The liver does not have presinusoidal sphincters, and closed sinusoids analogous to closed capillaries in skeletal muscle do not occur. The major factor controlling hepatic transsinusoidal fluid movements in the anaesthetized cat is hepatic venous pressure.

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