Biphasic Vasoconstriction of the Rabbit Ear Artery

Steinsland, Odd S.; Furchgott, Robert F.; Kirpekar, S. M.

doi:10.1161/01.res.32.1.49

Cited by 135 publications

(51 citation statements)

References 10 publications

(9 reference statements)

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“…17,18) In response to vasoconstrictor agonists, a slowly developing monophasic contraction is induced in splanchnic arteries such as aorta and iliac arteries, whereas biphasic contraction is induced in cutaneous arteries such as plantar, tail, and ear arteries. 9,[19][20][21] The present study also showed that the pattern of depolarization-induced contraction depends on the type of artery: High K + -induced contraction was monophasic in the aorta and iliac artery and biphasic in the tail artery. It should be noted, however, that our results suggest the contribution of nerve-derived noradrenaline to high K + -induced contraction in the tail artery.…”

Section: Discussionsupporting

confidence: 71%

Differential Contribution of Nerve-Derived Noradrenaline to High K<sup>+</sup>-Induced Contraction Depending on Type of Artery

Ishida

Hishinuma

Ishikawa

2017

Biological & Pharmaceutical Bulletin

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High K -induced contraction of arterial smooth muscle is thought to be mediated by membrane depolarization and subsequent activation of voltage-dependent Ca 2 channels (VDCCs). In line with this, this study found that contraction induced by 80 mM K was almost abolished by nifedipine (1 µM), a VDCC inhibitor, in isolated rat aorta, and was markedly suppressed in the iliac artery. However, nifedipine (1 µM) only partially suppressed high K -induced contraction in the tail artery. The contractions remaining in the arteries were further reduced by non-selective cation channel (NSCC) inhibitors, including 2-aminoethoxydiphenyl borate (2-APB) (100 µM), SK&F96365 (10 µM), and 3,4-dihydro-6,7-dimethoxy-α-phenyl-N,N-bis[2-(2,3,4-trimethoxyphenyl)ethyl]-1-isoquinolineacetamide hydrochloride (LOE908) (10 µM). In particular, sustained tonic contraction was nearly abolished. Prazosin (0.3 µM), an α 1 -adrenoceptor antagonist, partially inhibited high K -induced contraction in the tail and iliac arteries, but had no effect in the aorta. Consistently, tyramine potently induced contraction in the tail and iliac arteries, but not in the aorta. Furthermore, the inhibition by prazosin and NSCC inhibitors of the high K -induced contraction in the presence of nifedipine was comparable. These results suggest that depending on the type of artery, high K -induced contraction is mediated by Ca 2 influx not only through VDCCs but also through NSCCs, the activation of which is due to the activation of α 1 -adrenoceptors by the released noradrenaline from sympathetic nerve terminals resulting from high K stimulation. Key words high K +; tail artery; non-selective cation channel; voltage dependent calcium channel; noradrenaline Ca 2+ elevation in cytosol causes contraction in smooth muscle. In arterial smooth muscle, the primary pathways of Ca 2+ influx from extracellular space are through L-type voltagedependent Ca 2+ channels (VDCCs) and non-selective cation channels (NSCCs). 1) Elevating extracellular K + concentration decreases the K + gradient between the inside and outside of the cell membrane, which in turn causes cell membrane depolarization. VDCCs are activated by this depolarization, which leads to Ca 2+ influx, thereby causing smooth muscle contraction. Therefore, high K + stimulation is frequently used as an estimation of VDCC-mediated contraction.2) It is interesting to note, however, that our preliminary study showed insufficient inhibition of high K + -induced contraction by the VDCC inhibitor nifedipine in isolated rat tail artery. We thus further investigated the mechanism underlying high K + -induced contraction in different types of arteries, i.e., the aorta, and the iliac and tail arteries. The present data show that, depending on the type of artery, high K + -induced contraction is mediated not only through VDCCs but also through NSCCs activated by noradrenaline released from sympathetic nerve terminals. MATERIALS AND METHODS Measurement of ContractionProtocols for animal use were reviewed and approved by the Institutio...

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Section: Discussionsupporting

confidence: 71%

Differential Contribution of Nerve-Derived Noradrenaline to High K<sup>+</sup>-Induced Contraction Depending on Type of Artery

Ishida

Hishinuma

Ishikawa

2017

Biological & Pharmaceutical Bulletin

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“…Differences in the magnitude of contractile responses after external and internal perfusion have been observed by other investigators, mainly in vascular preparations, and were also mostly attributed to the presence of an active neuronal uptake (De la Lande et al, 1967;Steinsland et al, 1973). However, a complete understanding of the role played by neuronal uptake in the present case will only be obtained after the use of uptake blockers or of denervated preparations.…”

Section: Differences In Position Ofthe Dose-response Curvessupporting

confidence: 66%

Simultaneous measurement of contractile effects in the circular and longitudinal smooth muscle of the rat vas deferens by drugs perfused externally or via the lumen

Busatto

Jurkiewicz

1985

British J Pharmacology

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1 The effects of noradrenaline and barium chloride were studied in the rat isolated vas deferens by perfusion of drugs either externally or through the lumen of the organ. Two effects were recorded simultaneously in the same preparation: (a) isometric contractions, due to the tension elicited by drugs on the external (longitudinal) smooth muscle layer and (b) pressure of internal perfusion, due to contractions of the internal (circular) smooth muscle layer. 2 It was found with the longitudinal muscle that: (a) the potency, expressed as pD2 values, and the maximum response to noradrenaline were lower if the drug was perfused internally rather than externally; (b) the differences in maximum effects were pronounced on the prostatic half but were not observed on the epididymal half; (c) the maximum response obtained by internal perfusion could be increased by simultaneously adding the same dose of drug externally; (d) when barium chloride was used instead of noradrenaline no significant differences were observed on pD2 values, but differences on maximal responses were similar to that observed for noradrenaline; (e) it was possible to block completely the effect of internal or external noradrenaline on the longitudinal muscle, by perfusing external phenoxybenzamine. In these conditions the responses of the circular muscle to the agonist were only partly blocked. 3 With the circular muscle, the differences related to internal and external perfusion were less marked than in the longitudinal muscle. However, unlike the latter, the circular layer was slightly more sensitive to drugs applied internally, in relation to pD2 values. 4 It is suggested that the difference in pD2 values may be due to the removal of noradrenaline by the neuronal uptake process, whereas the difference in maximal effect is due to the inaccessibility of part of the receptor population when drugs are added through the lumen.

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“…The first phase is dependent on Ca 2+ sequestered in the cell, and the second is dependent on Ca 2+ entering via the extracellular space. These two phases of contraction may be preferentially altered by pharmacological procedures Steinsland et al 1973). However, not all phasic contractions reflect propagative activity.…”

Section: The Muscle Responsementioning

confidence: 99%

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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Biphasic Vasoconstriction of the Rabbit Ear Artery

Cited by 135 publications

References 10 publications

Differential Contribution of Nerve-Derived Noradrenaline to High K<sup>+</sup>-Induced Contraction Depending on Type of Artery

Differential Contribution of Nerve-Derived Noradrenaline to High K<sup>+</sup>-Induced Contraction Depending on Type of Artery

Simultaneous measurement of contractile effects in the circular and longitudinal smooth muscle of the rat vas deferens by drugs perfused externally or via the lumen

Some bases of differences in vascular response to sympathetic activity.

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