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At least 19 recordsLinked to original sources
PubMed1979

Estrogen receptors and effects of estrogen on membrane electrical properties of coronary vascular smooth muscle.

The effect of estrogen stimulation in vitro on the electrical properties of vascular smooth muscle (VSM), and the concentration of estrogen receptors in VSM were measured in isolated coronary arteries. Microelectrode measurements of the dog coronary artery membrane potential (Em) showed quiescent values of -51 millivolts (mV) and an input resistance (rin) of 10 megohms. Addition by diethylstilbestrol (DES) at 10(-6) M hyperpolarized the membrane to -64 mV and reduced input resistance (rin) to 5 megohms within 15 minutes. Extrapolation of the Em vs. log [K]o curve to zero potential gave similar values of [K]i of around 170 mM in both normal and DES treated muscles suggesting that the DES induced hyperpolarization is not due to increased Na-K pump activity. The 0.5% ethanol vehicle alone had no effect on the membrane potentials. Tetraethylammonium ion (TEA) induced action potentials in the previously quiescent tissue. When DES was applied in the presence of TEA, the membrane potential increased and the action potentials were abolished. Scatchard analysis of the estrogen receptor binding demonstrated both a high and a low affinity receptor for estrogen in the VSM. These data indicate that DES hyperpolarizes the VSM cells by a mechanism other than an increased Na-K pump activity. The mechanism of this increased Em may be due to factors which increase K+ conductance either mediated directly through estrogen interaction with its cytosolic receptors or through some unidentified second mechanism.

Action Potentials↗
PubMed1979

Urethane and contraction of vascular smooth muscle.

1 In vitro studies were undertaken on rat aortic strips and portal vein segments in order to determine whether or not the anaesthetic, urethane, can exert direct actions on vascular smooth muscle. 2 Urethane was found to inhibit development of spontaneous mechanical activity. This action took place with a urethane concentration as little as one tenth of that found in anaesthetic plasma concentratios, i.e., 10(-3) M. 3 Urethane (10(-3 to 10(-1) M) dose-dependently attenuated contractions induced by adrenaline, angiotensin and KCl. These inhibitory actions were observed with urethane added either before or after the induced contractions. 4 Ca2+-induced contractions of K+-depolarized aortae and portal veins were also attenuated, dose-dependently, by urethane. 5 All of these inhibitory effects were completely, and almost immediately, reversed upon washing out the anaesthetic from the organ baths. 6 A variety of pharmacological antagonists failed to mimic or affect the inhibitory effects induced by urethane. 7 These data suggest that plasma concentrations of urethane commonly associated with induction of surgical anaesthesia can induce, directly, relaxation of vascular muscle.

Angiotensin II↗
PubMed1979

Na,K-ATPase in excitation-contraction coupling of vascular smooth muscle from cattle.

Lowering the extracellular K+ content from 6 to 0.6 mM causes a rise, and elevation from 6 to 8.5 mM a fall of 45Ca++ efflux from the vascular smooth muscle cells of the arteria carotis communis of cattle. In contrast, a level of 17 mM K+ has no influence. Removal of extracellular calcium does not block these effects. 10(-4) M ouabain also induces a rise in Ca++ efflux, additional potassium reduction then being without effect; 10(-9) M ouabain is of no influence. The 45Ca++ efflux kinetics correlates with the activity of the isolated Na,K-ATPase. Tonus increases of the vascular strips by 10(-4) M ouabain and potassium deficiency cannot be blocked by 4 mM lanthanum or removal of extracellular calcium. Unlike sodium, potassium stimulates the active Ca++ binding and the activity of the Ca-ATPase of the microsomal fraction. The ative Ca++ binding of the mitochondria is stimulated by both ions. It is postulated that the activity of the plasma membrane Na,K-pump is able to regulate the tonus of big arteries through alteration of Ca++ storage processes.

Animals↗
PubMed1979

Effect of vasopressin on vascular smooth muscle from cold- and warm-acclimated rabbits.

Contractile properties of helical auricular arterial strips from warm- and cold-acclimated (WA and CA) rabbits were studied to determine whether vascular smooth muscle shows a cold-induced alteration in response to vasopressen (Vp), similar to the effect seen with catecholamines. The CA response was decreased at all Vp concentrations tested and the decreases were significant at doses between 0.4--100.0 mUnits Vp/ml. Results are discussed in relation to the altered renal tubular response to Vp which has previously been reported to occur in cold-acclimated animals.

Acclimatization↗
PubMed1976

Subcellular fractions of vascular smooth muscle exhibiting calcium transport properties.

Vascular smooth muscle relies on two general sources of activator calcium, one the extracellular fluid and the other intracellular sites in the coupling between stimulation at the external membrane and tension development. Electron microscopic studies have demonstrated at least two subcellular elements, mitochondria and sarcoplasmic reticulum, that may participate in the release and/or sequestration of this activator calcium. In order to obtain quantitative answers to questions concerning the rates of calcium transport by these subcellular elements attempts to use differential centrifugation to obtain subcellular fractions from whole muscle homogenate have been reported. Mitochondrial enriched preparations have received little quantitative study as yet, although they possess active calcium uptake mechanisms. Nonmitochondrial preparations having active calcium uptake mechanisms have been found in a variety of smooth muscles. The method of preparation and properties of these nonmitochondrial preparations show a great deal of variation, indicating they are probably a heterogeneous mixture of sarcoplasmic reticulum and plasma membrane. Some preliminary experiments on the effects of vasoactive agents and cyclic AMP on the calcium transport by these nonmitochondrial preparations have yielded conflicting results. Resolution of these problems awaits clear identification of the calcium transport mechanisms with their appropriate subcellular structure.

Animals↗
PubMed1977

Vascular smooth muscle and neurohypophyseal hormones.

Experimental studies relating to the direct peripheral vascular actions of neurohypophyseal hormones and their synthetic variants are reviewed. In addition, the available data on the comparative pharmacologic actions of these peptides on mammalian vascular smooth muscle are reviewed. Experiments relating to mechanisms by which neurohypophyseal peptides induce contraction of blood vessels are discussed. Neurohypophyseal peptide hormones appear to be able to contract and relax vascular smooth muscle, the exact type of response being dependent on species, vascular bed, and region within a vascular bed. Receptors that subserve both contraction and relaxation may exist on different blood vessels within a species, with a preponderance of receptors that subserve contraction being present in most blood vessels. Concentrations of vasopressin that can be considered physiologic (i.e., 10(-13) to 10(-11) M) are capable of evoking responses on a variety of microscopic as well as large blood vessels. Arginine-vasopressin appears to be, relatively, the most potent contractile substance on rat blood vessels investigated to date; angiotensin is not. Preservative-free oxytocin is a contractile agent on all mammalian arterial and arteriolar vessels so far investigated. A great deal of the controversy surrounding the exact vascular actions elicited by these peptide hormones can be attributed to many factors that were not controlled in older experiments. Moreover, rat pressor assays cannot be utilized to determine structure-activity relationship for neurohypophyseal peptides on vascular smooth muscles. Nuerohypophyseal peptide-induced contractions of vascular smooth muscles can be markedly affected by sex, sex hormones, alcohols, [Ca2+]0, [mg2+]0, oxygen deficit, and glucose-deprivation. Extracellular sodium and potassium ions appear to play relatively little role in vasopressin-induced contractions of rat arterial smooth muscle. The terminal amino group, phenolic hydroxyl, aromatic ring and basicity in positions 1, 2, 3, and 8, respectively, of the neurohypophyseal hormones are important for optimizing hormone-receptor affinity and intrinsic contractile activity on vascular smooth muscle. Basicity in position 8 of these peptide hormones is not an absolute requirement for contractile activation of these smooth muscles. Alterations in molecular structure can result in neurohypophyseal peptides with unique, and selective, microcirculatory effects that may be beneficial in the treatment of low-flow states.

Angiotensin II↗
PubMed1979

Action of indapamide on excitation-contraction coupling in vascular smooth muscle.

The effects of indapamide on electrophysiological and mechanical parameters of longitudinal smooth muscle strips isolated from mammalian portal vein were studied by means of a double sucrose gap method associated with a photoelectric device for recording contraction. Indapamide (10(-4) M) reduced both the amplitude of the action potential and the contraction. The calcium inward current decreased and consequently the phasic contraction was also reduced. The potassium outward current was diminished while the tonic contraction was not modified significantly. The depressant nature of the indapamide response could counterbalance the stimulating action of angiotensin II but not that of noradrenaline. The results suggest that indapamide acts primarily on the plasma membrane of vascular smooth muscle by reducing the transmembrane calcium current, although a secondary decrease in the intracellular bound calcium could not be completely excluded.

Action Potentials↗
PubMed1977

A review of recent advances in vascular smooth muscle pharmacology.

An understanding of the physiology of vascular smooth muscle and knowledge of the reaction of such muscle to certain drugs are essential for the development of a means of treating cerebral arterial spasm. The role of cyclic nucleotides in vascular smooth muscle activity is reviewed and possible therapeutic approaches are listed. Probably the safest and most effective treatment would be 1) stimulation of the adenyl cyclase-cyclic adenosine monophosphate system by a beta(2)-adrenergic drug combined with 2) inhibition of the phosphodiesterase system.

Adenylyl Cyclases↗
PubMed1978

How vascular smooth muscle works.

Electrical recordings made from vascular smooth muscle during the last 15 years make it clear that the role of electrical activity in controlling contraction is often important but varies greatly both between different vessels and for different responses of a given vessel. Only a few mammalian vessels have widely conducted electrical activity, but others can develop this activity, with consequent rhythmical contraction, when made anoxic and stimulated. Action potentials play a part in smooth non-rhythmical responses of arteries to nerves and hormones, while passive conduction of depolarization round the vessel wall is responsible for ring contractions of arteries after local injury. Ca and K cause vasodilatation largely by hyperpolarizing the smooth muscle cells. Electrical activity plays no part in some responses. In particular noradrenaline can contract arteries by directly promoting entry of extracellular Ca, and also by releasing Ca stores by non-electrical means. These processes are particularly important in the inner muscle of arteries, which is not directly innervated.

Action Potentials↗
PubMed1976

A simple method for differentiating vascular smooth muscle cells and fibroblasts in tissue culture.

The morphologic differentiation of vascular smooth muscle cells and fibroblasts in tissue culture is difficult if not impossible. By direct immunofluorescence, it is possible to distinguish between vascular smooth muscle cells and fibroblasts after 6 to 10 days in tissue culture. Microfilaments appear from the 6th to the 10th day. After an incubation period of 30 minutes with antibody against smooth muscle actomyosin at room temperature, microfilaments are demonstrable in smooth muscle cells. In contrast, fibroblasts, if incubated for the same period, show strong nuclear fluorescence and a primary fluorescence of the cytoplasm, but filaments are not visible. If fibroblasts are incubated with antiactomyosin for one hour at 37 degrees C, however microfilaments are easily detectable. With this method it is possible to differentiate in a simple manner vascular smooth muscle cells from fibroblasts in a heterologous tissue culture.

Actomyosin↗
PubMed1977

Mobilization of cellular calcium and contraction-relaxation of vascular smooth muscle.

In order to clarify the Ca2+ mediated regulatory mechanism of vascular smooth muscle, the correlation between Ca2+ movements in the cell and mechanical response was investigated using isolated rat aorta and bovine basilar artery. K+ induced contraction of vascular smooth muscle required Ca2+ in the medium, and the contraction was always associated with a large increase in Ca2+ influx. In the absence of external Ca2+, norepinephrine (NE) or serotonin (5HT) induced rapid contraction of the aorta and basilar artery, respectively. Caffeine (20 mM) also induced tension in the absence of Ca2+. The results obtained in these experiments suggest that at least four kinds of calcium exist in bound from in the cell, i. e., (1) loosely and (2) tightly bound calcium on the external surface of the cell membrane, (3) calcium localized in the internal surface of the cell membrane and (4) calcium stored in the intracellular store site, such as the sarcoplasmic reticulum. The intracellulary stored calcium, both (3) and (4), which can be mobilized by the action of certain drugs (NE, 5HT or caffeine), probably plays an important role for the regulation of the mechanical activity of vascular smooth muscle.

Animals↗
PubMed1976

Ultrastructural aspects of activation and contraction of vascular smooth muscle.

Ultrastructural studies of potential intracellular calcium storage sites and of the organization of contractile proteins in vascular smooth muscle are reviewed. The sarcoplasmic reticulum (SR) is a system of closed tubules present in every smooth muscle examined. The volume of the SR varies in different smooth muscles (from approximately 2.0 to 7.5% of cytoplasmic volume) and correlates with the ability of a given smooth muscle to contract in calcium-free media. The SR accumulates the divalent cation strontium and forms couplings with the surface membrane. Mitochondria are other potential sites of calcium accumulation in vascular smooth muscle, as indicated by the respiration supported accumulation of calcium (with a Km of approximately 17 muM) by isolated mitochondria and by the energy dependent accumulation of barium by mitochondria in situ. The presence of barium in mitochondrial granules in tissues contracted with barium and the presence of strontium and calcium in appropriately incubated preparations have been verified with electron probe microanalysis. Calcium has also been demonstrated in mitochondrial granules in frozen dried cardiac muscle sections and in cultured vascular smooth muscle cells. This technique appears suitable for eventual quantitation of mitochondrial calcium content in vascular and other smooth muscles. Thin (actin, 50-80 A), thick (myosin, approximately 155 A), and intermediate (approximately 100 A) filaments are present in suitably fixed vascular smooth muscle. In rabbit portal anterior mesenteric vein intermediate high voltage stereo electron microscopy shows the myosin filaments to be tapered and approximately 2.2 mum long: significantly longer than the myosin filaments in vertebrate striated muscle. Actin filaments insert on dense bodies. The ultrastructural findings are compatible with physiological evidence suggesting the contributions of intracellular organelles to the regulation of cytoplasmic free calcium levels and the operation of a sliding filament mechanism of contraction in vertebrate smooth muscle.

Animals↗
PubMed1978

The differential effect of cooling on the responses of splenic capsular and vascular smooth muscle to nerve stimulation and noradrenaline.

The responses of the capsular and vascular smooth muscle of the dog's spleen to splenic nerve stimulation and to infused noradrenaline have been studied in the isolated, blood-perfused preparation at 37 degrees C, at 27 degrees C and again after rewarming to 37 degrees C. It was found that cooling per se had no effect on perfusion pressure but reduced splenic arterial blood flow, and caused no appreciable alteration in spleen volume. The increase in splenic flow resistance in response to nerve stimulation and noradrenaline was significantly greater at 27 degrees C than at 37 degrees C, but the concomitant reduction in spleen volume was significantly reduced. The enhanced effect of splenic nerve stimulation and noradrenaline on splenic flow resistance is discussed in terms of the relative contributions of an increased smooth muscle response and increased blood viscosity. The different effects of cooling on the responses of splenic vascular and capsular smooth muscle to nerve stimulation and noradrenaline are discussed in the context of the effect of cooling on other vascular and non-vascular smooth muscle.

Animals↗
PubMed1979

Digoxin-norepinephrine response and calcium blocker effects in vascular smooth muscle.

The mechanism of potentiation by digoxin of the response of vascular smooth muscle to norepinephrine was investigated in 5-cm intact segments of rabbit carotid artery. Segments were mounted in a chamber and perfused at constant pressure while flow and upstream and downstream pressures were recorded and resistance was calculated. Each vessel was perfused with a submaximal vasoconstricting concentration of norepinephrine (6 x 10(-6)M) alone, in the presence of digoxin (6 x 10(-5)M), and during exposure to both digoxin and one of the following calcium antagonists: lanthanum chloride (5 x 10(-4)M procaine hydrochloride (5 x 10(-3)M), or verapamil (5 x 10(-5)M). Digoxin potentiated the response to norepinephrine alone by 20% (P less than 0.01), to norepinephrine plus lanthanum chloride by 10% (P less than 0.001), and to norepinephrine plus procaine hydrochloride by 17% (P less than 0.001). Digoxin did not potentiate the norepinephrine response in the presence of verapamil. These data suggest that the mechanism of digoxin potentiation of the norepinephrine response in vascular smooth muscle may involve an alteration in a cellular calcium sequestration or release process. The potential cellular sites that may contribute to this phenomenon are discussed.

Animals↗
PubMed1976

Cell potential and the sodium-potassium pump in vascular smooth muscle.

An electrogenic sodium-potassium pump appears to contribute materially to the steady-state potential and to certain of the transient potential responses of vascular smooth muscle. Since changes in cell potential in turn can lead to changes in contractile state, the pump is implicated in some of the constriction-dilation responses of blood vessels. The vasodilator action of potassium is explainable, for instance, through an effect on cell potential if (and only if) an electrogenic pump is assumed to be extruding sodium at a faster rate than it takes up potassium. This is supported by the observation that ouabain, an inhibitor of Na,K-ATPase activity, will eliminate or reverse the vascular effect of potassium. Furthermore, when the in vivo and in vitro effects on vascular smooth muscle of altered extracellular potassium concentration are compared to calculated cell potentials based on a model that includes an electrogenic pump, the experimental findings are shown to be logical and predictable.

Adenosine Triphosphatases↗
PubMed1978

Control of cerebral vascular smooth muscle during general anaesthesia.

The effects of some general anaesthetics, for example thiopentone, Althesin (alphaxalone + alphadolone) and ketamine, on cerebral vascular smooth muscle are those which would be expected from their metabolic actions. With other anaesthetics, mainly those administered by inhalation, and especially the volatile agents, cerebral blood flow increases in excess of the metabolic activity, which is usually depressed to varying degrees. During general anaesthesia with any of these agents, responses to changes in arterial Pco2 or blood pressure are maintained. Furthermore, when seizure activity occurs during enflurane administration, there is a flow response to the associated metabolic stimulation. The time course of the flow response to the metabolically depressant drug Althesin has been measured in baboons and shown to be very rapid. Wtih this drug cerebrovascular resistance begins to increase within 2 s of its arrival in the brain. This rapid flow change occurs also after sympathetic denervation. Extracellular fluid pH of the cortex does not alter until after the initiation of the vascular smooth muscle response.

Alfaxalone Alfadolone Mixture↗
PubMed1979

Evidence for two distinct types of postsynaptic alpha-adrenoceptor in vascular smooth muscle in vivo.

1 The effects of the highly selective alpha(1)-adrenoceptor antagonist, prazosin, and the relatively selective alpha(2)-adrenoceptor antagonist, yohimbine, on the pressor responses to intravenous injections of phenylephrine and noradrenaline have been examined in anaesthetized cats and pithed rats in an attempt to determine whether alpha(1)- and alpha(2)-adrenoceptors are located postsynaptically on vascular smooth muscle.2 In anaesthetized cats prazosin caused a much greater reduction in the pressor responses to phenylephrine than to noradrenaline or splanchnic nerve stimulation (after adrenalectomy). Yohimbine was of similar potency in reducing the pressor responses to each stimulus.3 A differential blocking activity of prazosin against intra-arterial injections of phenylephrine and noradrenaline was also demonstrated in the blood-perfused cat hind limb. As in the whole animal, prazosin was more potent against phenylephrine than noradrenaline. A similar, though less marked, effect was seen in the mesenteric circulation, but not in the renal circulation, where prazosin was almost equipotent in reducing responses to phenylephrine and noradrenaline.4 In pithed rats prazosin was a potent, competitive antagonist of phenylephrine, but had little effect against noradrenaline; only the responses to high doses of noradrenaline were reduced by prazosin. Yohimbine was approximately equipotent as an antagonist of phenylephrine and noradrenaline. In the anococcygeus muscle, prazosin was as potent an antagonist of noradrenaline as it was of phenylephrine on vascular smooth muscle.5 The results suggest that there are two types of alpha-adrenoceptor in the vasculature of cats and rats. Phenylephrine produces pressor responses by stimulating one type of postsynaptic alpha-adrenoceptor that is blocked by prazosin and yohimbine; these are alpha(1)-adrenoceptors. Noradrenaline exerts some of its effect via these receptors but most of its effect appears to be exerted through prazosin-insensitive receptors. The latter receptors appear to differ from alpha(2)-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1979

The undamped and damped series elastic components of a vascular smooth muscle.

Small arterial resistance vessels (internal diameter about 175 micrometer) have been mounted on a myograph that enabled their wall tension, T, and internal circumference, L, to be measured and controlled with a time resolution of about 4 ms. Maximally activated vessels were subjected to isometric releases (step changes in L) and isotonic releases (step changes in T) of varying extents and at two different temperatures (27 degree C and 37 degree C). The recovery from an isometric release was monotonic and did not include the two phases seen in skeletal muscles. The isotonic release response did, however, contain a velocity transient lasting about 150 ms: the velocity immediately after the release was about six times the steady shortening velocity. The form of both the isometric and isotonic release responses and their dependence on the extent of release can be explained in terms of a modified Hill model in which the "series elastic component" (SEC) is replaced by the series combination of an undamped-SED (that is, an undamped elastic element) and a damped-SEC (a Voigt element). Although the initial response to both types of release was independent of temperature, all stages of subsequent responses were temperature dependent, with Q10's in the range 1.5 - 2.0. The results suggest that the responses to isotonic and isometric releases may in part be due to active processes.

Animals↗