Adrenergic Stimulation of Depolarized Arterial Muscle

Waugh, William H.

doi:10.1161/01.res.11.2.264

Cited by 39 publications

(15 citation statements)

References 12 publications

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“…Activation of the contractile mechanism has previously been demonstrated in different types of depolarized muscle (9)(10)(11). In the previous article, dissociation of electrical and mechanical activity was shown for polarized portal vein in K + -free and Ca 2 + -free solutions (4).…”

Section: Discussionmentioning

confidence: 89%

Electrical and Mechanical Characteristics of Vascular Smooth Muscle Response to Norepinephrine and Isoproterenol

Johansson

Johsson²,

Axelsson

et al. 1967

Circulation Research

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Effects of norepinephrine (NE) and isoproterenol on simultaneously recorded electrical and contractile activity in rat portal vein were studied using a sucrose-gap technique. This vascular smooth muscle shows spontaneous phasic contractions correlated with bursts of action potentials. Norepinephrine (10" 9 to 10" 7 w/v) increases the duration of the bursts and shortens the interval between bursts after an initial period of continuous spike discharge. The tension response is greater than can be accounted for by the increase in electrical activity. High NE concentrations (10~3) produce depolarization, decrease of spike amplitude, or even abolition of spikes and maintained contractions. Norepinephrine increases contracture tension of K + -depolarized portal vein without changing membrane potential. Electrical and mechanical activity is reinitiated in preparations inactivated by elimination of Ca 2 + ; this may be due to release of bound calcium. Phenoxybenzamine abolishes the above NE responses. The typical response to isoproterenol (10" 9 to 10~7) in a normal ionic environment consists of moderate depolarization, decreased burst duration, but increased frequency of bursts and inhibition of tension development which is not simply correlated with the change in electrical activity. This pattern resembles that produced by lowering [Ca agent used and on the vascular bed studied. The cellular mechanisms responsible for these opposite reactions of vascular smooth muscle to adrenergic agents are insufficiently understood. A better understanding of these excitatory and inhibitory actions would require, among o:her things, a more complete knowledge of the electrophysiological events associated with the mechanical changes.In the previous article in this issue (4), we have described the technique used here for simultaneous recording of electrical and mechanical activity of the isolated rat portal vein and the responses of this preparation to changes in ionic composition of extracellular fluid. The present paper describes the electrical and mechanical responses to norepineph-

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Section: Discussionmentioning

confidence: 89%

Electrical and Mechanical Characteristics of Vascular Smooth Muscle Response to Norepinephrine and Isoproterenol

Johansson

Johsson²,

Axelsson

et al. 1967

Circulation Research

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“…external diameter were excised, stripped of adventitia, and perfused by a constant-flow technique, as previously described. 20 The constant-flow rate used in various experiments was 0.75 to 0.90 ml./ min. Test doses of chemicals in volumes of 0.10 to 0.25 ml.…”

Section: Methodsmentioning

confidence: 99%

“…The results extend a recent study of arterial smooth muscle in which adrenergic neurohormone appeared to activate contraction by some mechanism other than primarily through membrane depolarization or sodium or chloride influx. 20 …”

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confidence: 99%

Role of Calcium in Contractile Excitation of Vascular Smooth Muscle by Epinephrine and Potassium

Waugh

1962

Circulation Research

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A technique of constant-flow perfusion of isolated segments of dog intestinal arteries was used to investigate the role of calcium in contractile excitation of vascular smooth muscle by epinephrine and potassium. Contractile responses of the arterial muscle to epinephrine, perfused at constant concentration, and to potassium, perfused at high concentration, were both promptly prevented by calcium deionizing accomplished by simultaneous perfusion with solutions containing ethylenediaminetetraacetate (EDTA) for the chelation of available calcium ions. Potassium-induced muscular contracture was removed in a few minutes and epinephrine-induced contractions of potassium-depolarized muscle were soon prevented by perfusion with solutions containing ionic species of EDTA which chelated calcium ions. In muscle depolarized by potassium and calcium deionized by perfusion with solution containing MgK 2 EDTA, the contractile responses to epinephrine were immediately restored by combined perfusate injection of calcium ion and epinephrine. Injections of isosmotic calcium chloride solution of subthreshold or threshold contractile strength, when the artery had been perfused with sodium chloride-rich solution and the muscle had been relaxed, produced much greater contractions during both potassium and epinephrine excitation. The contractions from injected calcium chloride solution were increased by epinephrine excitation of muscle already depolarized by the external application of potassium sulfate, as they were in the previously polarized or resting muscle excited by epinephrine. The thesis is advanced that the relative muscular contractions induced by standard injected volumes of isosmotic calcium chloride solution were a relative index of the calcium influx and calcium permeability of the arterial smooth muscle cells in the various experimental conditions prevailing. Equimolar injections of isosmotic calcium iodide solution produced greater muscular contractions than did injections of isosmotic calcium chloride solution. The possibility is discussed that transmembranous passage of calcium into vascular muscle cells occurs significantly in the form of associated ion pairs. A dual effect of potassium on vascular smooth muscle behavior was observed in that a previously contractile-inducing amount of injected potassium exerted a relaxing effect on the arterial segment perfused with low-potassium solution when the muscle was contracted by epinephrine. It is concluded that: (a) calcium is essentially involved in excitation-contraction coupling of vascular smooth muscle; (b) the calcium permeability and calcium influx of vascular smooth muscle is greatly increased during both epinephrine and potassium excitation of the muscle cells, and epinephrine accomplishes these calcium changes even in muscle already depolarized by potassium; (c) adrenergic neurohormones exert their vasoexcitatory contractile effect by a membrane reaction which is basically nonelectrical and which primarily triggers an increased permeability and influx of calcium into the vascular myoplasm; and (d) the migrated calcium activates intracellularly the myoplasmic events of vascular smooth muscle contraction.

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“…However, the ability of the peripheral vasculature to respond to changes in sympathetic activity has received less attention. Indeed, for sympathetic nerve impulses to influence vascular tone, there must be successful release of neurotransmitter(s) into the synaptic cleft (2), abundant receptor binding (35), and widespread signal transduction within vascular smooth muscle (34) to result in a vasomotor response (29). Although this paradigm is widely accepted (3,12,26), limited data are available in humans.…”

mentioning

confidence: 99%

Spontaneous bursts of muscle sympathetic nerve activity decrease leg vascular conductance in resting humans

Fairfax

Padilla

Vianna

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

109

123

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Fairfax ST, Padilla J, Vianna LC, Davis MJ, Fadel PJ. Spontaneous bursts of muscle sympathetic nerve activity decrease leg vascular conductance in resting humans. Am J Physiol Heart Circ Physiol 304: H759 -H766, 2013. First published January 4, 2013 doi:10.1152/ajpheart.00842.2012.-Previous studies in humans attempting to assess sympathetic vascular transduction have related large reflex-mediated increases in muscle sympathetic nerve activity (MSNA) to associated changes in limb vascular resistance. However, such procedures do not provide insight into the ability of MSNA to dynamically control vascular tone on a beat-by-beat basis. Thus we examined the influence of spontaneous MSNA bursts on leg vascular conductance (LVC) and how variations in MSNA burst pattern (single vs. multiple bursts) and burst size may affect the magnitude of the LVC response. In 11 young men, arterial blood pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 min of supine rest. Signal averaging was used to characterize percent changes in LVC for 15 cardiac cycles following heartbeats associated with and without MSNA bursts. LVC significantly decreased following MSNA bursts, reaching a nadir during the 6th cardiac cycle (single bursts, Ϫ2.9 Ϯ 1.1%; and multiple bursts, Ϫ11.0 Ϯ 1.4%; both, P Ͻ 0.001). Individual MSNA burst amplitudes and the total amplitude of consecutive bursts were related to the magnitude of peak decreases in LVC. In contrast, cardiac cycles without MSNA bursts were associated with a significant increase in LVC (ϩ3.1 Ϯ 0.5%; P Ͻ 0.001). Total vascular conductance decreased in parallel with LVC also reaching a nadir around the peak rise in arterial blood pressure following an MSNA burst. Collectively, these data are the first to assess beat-by-beat sympathetic vascular transduction in resting humans, demonstrating robust and dynamic decreases in LVC following MSNA bursts, an effect that was absent for cardiac cycles without MSNA bursts.MSNA; sympathetic vascular transduction; vascular responsiveness; blood pressure; femoral blood flow THE GENERATION AND REGULATION of central sympathetic outflow has been a primary focus of autonomic cardiovascular research for decades (5, 10). However, the ability of the peripheral vasculature to respond to changes in sympathetic activity has received less attention. Indeed, for sympathetic nerve impulses to influence vascular tone, there must be successful release of neurotransmitter(s) into the synaptic cleft (2), abundant receptor binding (35), and widespread signal transduction within vascular smooth muscle (34) to result in a vasomotor response (29). Although this paradigm is widely accepted (3,12,26), limited data are available in humans. Furthermore, previous studies attempting to demonstrate sympathetic vascular transduction in humans have related large reflex-mediated increases in muscle sympathetic nerve activity (MSNA) to associated changes in vascular resistance (6,17,23). While such procedures reveal that elevated MSNA increases vascular...

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Adrenergic Stimulation of Depolarized Arterial Muscle

Cited by 39 publications

References 12 publications

Electrical and Mechanical Characteristics of Vascular Smooth Muscle Response to Norepinephrine and Isoproterenol

Electrical and Mechanical Characteristics of Vascular Smooth Muscle Response to Norepinephrine and Isoproterenol

Role of Calcium in Contractile Excitation of Vascular Smooth Muscle by Epinephrine and Potassium

Spontaneous bursts of muscle sympathetic nerve activity decrease leg vascular conductance in resting humans

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