Ethanol reduces Ca2+ concentrations in arterial and venous smooth muscle.

The present results, using isolated rat aortic strips and portal vein segments, demonstrate that ethanol (170--430 mM) significantly inhibits calcium uptake in these 2 different types of vascular smooth muscle.     

Ca2+ uptake and distribution in alloxan-diabetic rat arterial and venous smooth muscle

Summary This report demonstrates that in experimental diabetes mellitus (DM) calcium uptake and its distribution is altered in rat aortic but not in portal venous smooth muscle. Results are interpreted as consequences of increased calcium binding by aortic smooth muscle in experimental DM, which could account for the hyporeactivity of alloxan diabetic rat aorta reported previously.Supported by NIH grant No.HL-18015 and NIDA grant No. DA-02339.     

The Ca2+-transport ATPases in smooth muscle

Summary A calmodulin stimulated Ca²⁺-transport ATPase which has many of the characteristics of the erythrocyte type Ca²⁺-transport ATPase has been purified from smooth muscle. In particular, the effect of calmodulin on these transport enzymes is mimiced by partial proteolysis and antibodies against erythrocyte Ca²⁺-transport ATPase also bind to the smooth muscle (Ca²⁺+Mg²⁺)ATPase. A correlation between the distribution of the calmodulin stimulated (Ca²⁺+Mg²⁺)ATPase and (Na⁺+K⁺)ATPase activities in smooth muscle membranes separated by density gradient centrifugation suggests a plasmalemmal distribution of this (Ca²⁺+Mg²⁺)ATPase. A phosphoprotein intermediate in smooth muscle which strongly resembles the corresponding phosphoprotein in sarcoplasmic reticulum of skeletal muscle may indicate the presence in smooth muscle of a similar type of Ca²⁺-transport ATPase.     

Response of briefly glycerinated smooth muscle to Ca2+ and Mg2+

Summary Smooth muscle, treated with 50% glycerol solution at 27°C for 20 min, contracted on the application of Ca²⁺ or Mg²⁺. The briefly glycerinated smooth muscle can be used as a model system of smooth muscle contraction.     

Differential effects of ethanol on prostaglandin responses of arterial and venous smooth muscle

Summary The present results, using isolated rat aortic strips and portal vein segments, demonstrate that ethanol, depending upon concentration, can either enhance or attenuate the contractile actions of PGF₂ on at least 2 different types of vascular smooth muscle. At the very least, the present findings question the use of ethanol as a solvent when investigating the contractile actions of PG molecules on smooth muscles.Supported by NIH grant No. HL-18015 and NIMH grant No. MH-26236. The authors are indebted to Dr.John E. Pike and Dr.John Babcock of the Upjohn Company for generously providing us with the PGF₂ used in this study.     

A Ca2+-sensitive myosin light chain kinase, regulating pig carotid smooth muscle actomyosin ATPase

In this paper the correlation between phosphate incorporation into the regulatory light chain of myosin by a Ca2+-dependent myosin light chain kinase, and the Ca2+-sensitive ATPase activity and superprecipitation behaviour of arterial actomyosin, is described.     

Types of cell contacts in arterial smooth muscle

Zusammenfassung Nachweis, dass in Arteriolen sowie in präkapillaren Arteriolen des Hunde-Duodenums nur eine einfache Aneinanderlagerung der Muskelzellen erfolgt und keine gap junctions, wie sie in den Muskelschichten der Hohlwandorgane vorhanden sind.     

A Ca2+-sensitive myosin light chain kinase,regulating pig carotid smooth muscle actomyosin ATPase1

Summary In this paper the correlation between phosphate incorporation into the regulatory light chain of myosin by a Ca²⁺-dependent myosin light chain kinase, and the Ca²⁺-sensitive ATPase activity and superprecipitation behaviour of arterial actomyosin, is described.Acknowledgment. The financial support of the Deutsche Forschungsgemeinschaft (SFB 90) is gratefully acknowledged.     

Mechanisms of sympathetic regulation of arterial smooth muscle

Zusammenfassung Der Wirkungsbereich der Querschnittsregulation der A. dorsalis pedis durch den Sympathikus bei Hunden wurde erfasst und die Relation Reizerfolg-Reizfrequenz durch eine Hyperbel charakterisiert. Mittels Fluoreszenzmethode gewonnene Befunde weisen darauf hin, dass die durch Sympathikusreizung freigesetzen Monoamine zu den nervenfreien Mediaschichten diffundieren.

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For the supply of Nialamide we are indebted to Pfizer Corporation, Eastern Europe Division.     

Colchicine-induced appearance (proliferation) of smooth sarcoplasmic reticulum in arterial smooth muscle cells

Colchicine treatment resulted in the appearance and proliferation of smooth sarcoplasmic reticulum in some smooth muscle cells of the aortic and pulmonary trunk walls in the rabbit. The significance of cytoplasmic microtubules and/or membrane-bound tubulin for the morphogenesis, functioning and control of smooth endoplasmic reticulum in different kinds of cells is discussed.     

Colchicine-induced appearance (proliferation) of smooth sarcoplasmic reticulum in arterial smooth muscle cells

Summary Colchicine treatment resulted in the appearance and proliferation of smooth sarcoplasmic reticulum in some smooth muscle cells of the aortic and pulmonary trunk walls in the rabbit. The significance of cytoplasmic microtubules and/or membrane-bound tubulin for the morphogenesis, functioning and control of smooth endoplasmic reticulum in different kinds of cells is discussed.     

Effects of bunaphtine on 45Ca movements in rat aortic smooth muscle

The effect of bunaphtine (BNA, 5 X 10(-5)M) on La3+ -resistant 45Ca content and 45Ca efflux was studied on rat aortic smooth muscle. BNA decreased both control and norepinephrine-stimulated La3+-resistant 45Ca content and increased the 45Ca efflux. These effects could explain the inhibition of the contractile responses induced by BNA.     

Effects of bunaphtine on45Ca movements in rat aortic smooth muscle

Summary The effect of bunaphtine (BNA, 5×10^–5 M) on La³⁺-resistant⁴⁵Ca content and⁴⁵Ca efflux was studied on rat aortic smooth muscle. BNA decreased both control and norepinephrine-stimulated, La³⁺-resistant⁴⁵Ca content and increased the⁴⁵Ca efflux. These effects could explain the inhibition of the contractile responses induced by BNA.     

Differential effects of ethanol on prostaglandin responses of arterial and venous smooth muscles.

The present results, using isolated rat aortic strips and portal vein segments, demonstrate that ethanol, depending upon concentration, can either enhance or attenuate the contractile actions of PGF2alpha on at least 2 different types of vascular smooth muscle. At the very least, the present findings question that the use of ethanol as a solvent when investigating the contractile actions of PG molecules on smooth muscles.     

Velocity and myosin phosphorylation transients in arterial smooth muscle: effects of agonist diffusion

Summary Transients in myoplasmic [Ca²⁺] and in phosphorylation of the 20,000 dalton light chain of myosin have been reported following stimulation of vascular smooth muscle by various agonists. Since these transients are rapid compared with the time required to attain a steady-state stress, agonist diffusion rates may be a significant limitation in activation. The purpose of this study was to estimate the effect of agonist diffusion rates on the time course of activation as assessed by mechanical measurements of stress development and isotonic shortening velocities and by determinations of the time course of myosin phosphorylation. The approach was to measure these parameters in K⁺-stimulated preparations of the swine carotid media of varying thicknesses and to estimate the theoretical contributions imposed by diffusion rates and the presence of a diffusion boundary layer surrounding the tissue. The results show that the time course of parameters which are tissue averages such as stiffness, active stress, and myosin phosphorylation is dominated by agonist diffusion rates. The sequence of events involved in excitation-contraction coupling including agonist actions on the cell membrane, Ca²⁺ release, activation of myosin light chain kinase, and cross-bridge phosphorylation appear to be very rapid events compared with stress development. Estimates of unloaded or lightly loaded shortening velocities which are not simple tissue averages appear to provide an imporoved estimate of activation rates.Supported by a grant from the National Institutes of Health 5-PO1-HL19242. K. E. Kamm was supported by a National Heart, Lung, and Blood Institute Research Service Award HL-05957.     

Velocity and myosin phosphorylation transients in arterial smooth muscle: effects of agonist diffusion

Transients in myoplasmic [Ca2+] and in phosphorylation of the 20,000 dalton light chain of myosin have been reported following stimulation of vascular smooth muscle by various agonists. Since these transients are rapid compared with the time required to attain a steady-state stress, agonist diffusion rates may be a significant limitation in activation. The purpose of this study was to estimate the effect of agonist diffusion rates on the time course of activation as assessed by mechanical measurements of stress development and isotonic shortening velocities and by determinations of the time course of myosin phosphorylation. The approach was to measure these parameters in K+ -stimulated preparations of the swine carotid media of varying thicknesses and to estimate the theoretical contributions imposed by diffusion rates and the presence of a diffusion boundary layer surrounding the tissue. The results show that the time course of parameters which are tissue averages such as stiffness, active stress, and myosin phosphorylation is dominated by agonist diffusion rates. The sequence of events involved in excitation-contraction coupling including agonist actions on the cell membrane, Ca2+ release, activation of myosin light chain kinase, and cross-bridge phosphorylation appear to be very rapid events compared with stress development. Estimates of unloaded or lightly loaded shortening velocities which are not simple tissue averages appear to provide an improved estimate of activation rates.     

Ca2+ release-activated Ca2+ (CRAC) current, structure, and function

Store-operated Ca²⁺ entry describes the phenomenon that connects a depletion of internal Ca²⁺ stores to an activation of plasma membrane-located Ca²⁺ selective ion channels. Tremendous progress towards the underlying molecular mechanism came with the discovery of the two respective limiting components, STIM and Orai. STIM1 represents the ER-located Ca²⁺ sensor and transmits the signal of store depletion to the plasma membrane. Here it couples to and activates Orai, the highly Ca²⁺-selective pore-forming subunit of Ca²⁺ release-activated Ca²⁺ channels. In this review, we focus on the molecular steps that these two proteins undergo from store-depletion to their coupling, the activation, and regulation of Ca²⁺ currents.