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At least 19 recordsLinked to original sources
PubMed1975

Vibration-induced inhibition of vascular smooth muscle contraction.

Vascular smooth muscle is known to be exposed to an oscillating strain under physiological and patho-physiological conditions as well as in different occupational and environmental situations. The effect of vibrations of smooth muscle seems to be largly unknown. In the present experiments on isolated preparations of the rat portal vein and the rabbit thoracic aorta, imposed sinusoidal changes in length were found to cause prompt reduction in active force, the extent of which was dependent on amplitude (1-10% of tissue length, peak to peak, i.e. approximately plus or minus 50-500 mum) and frequency of vibration (1-400 Hz) as well as on the prevailing level of active and passive forces. Vibration caused only small and inconsistant reductions of passive force of vascular smooth muscle. The results are in accordance with the hypothesis that vibrations exert a direct action on the contractile process by causing an increased rate of detachment of actin-myosin cross-links. It is suggested that, in vivo, vibrations may affect the diameter of conduit arteries locally in the case of turbulent blood flow as seen in post-stenotic dilation and arterio-venous anastomosis. Possibly, even the normal pulse pressure oscillations may sometimes tend to inhibit the smooth muscle activity in such arteries and thereby influence their diameters.

Animals↗
PubMed1975

Interaction of prostaglandin A2 and prostaglandin B2 on vascular smooth muscle tone, vascular reactivity and electrolyte transport.

The effects of prostaglandin A2 (PGA2) and prostaglandin B2 (PGB2) on vascular smooth muscle tone, electrolyte movements and responses to vasoactive stimuli were evaluated with superfused canine tibial arteries. PGA2 and PGB2 constricted superfused tibial arteries. PGB2 was 10.7 (8.3-14.1) times more potent as a constrictor than PGA2. PGA2 and PGB2-induced vasoconstriction was associated with a decrease in 22Na efflux and a tendency toward an increase in cellular sodium (expressed as micromoles per gram of wet weight). These prostaglandins also decreased the total potassium content of tibial arteries. 45Ca exchange was enhanced by PGA2 and PGB2. The time course of PG-induced increases in 45Ca efflux was similar to the temporal increase in force produced by PGA2 and PGB2. The duration of the contractile response to barium chloride was greatly prolonged during superfusion with both PGA2 and PGB2. These effects were probably not mediated by PG-induced alterations in the resting membrane potential of tibial arteries since presumed depolarization by both high potassium and zero-potassium physiologic saline solutions did not mimic the effects of these prostaglandins on vascular smooth muscle tone or responses to barium chloride. These data suggest that PGA2 and PGB2 may increase tone of vascular smooth muscle by inhibition of those processes involved in sequestration of calcium ion, i.e., the relaxation process, rather than acting on the contractile process.

Animals↗
PubMed1992

Prolonged activation of alpha 1 adrenoceptors induces down-regulation of protein kinase C in vascular smooth muscle.

Sustained exposure of vascular smooth muscle to catecholamines results in desensitization of alpha 1-adrenoreceptor-mediated vascular smooth muscle contraction. The present study was designed to determine the effects of prolonged exposure of blood vessels to catecholamines on protein kinase C (PKC) activity. Incubation of rat aortic smooth muscle with 10 microM norepinephrine (NE) for 4 h resulted in a threefold decrease in sensitivity of the contractile response of rat aortic smooth muscle to the phorbol ester 4 beta-phorbol 12,13-dibutyrate (PDBu); this loss in sensitivity was dependent on the presence of endothelium. NE induced a 45% decrease in enzymatic activity of the soluble and particulate forms of PKC. With [3H]PDBu used to label phorbol ester receptor binding sites in the aorta, there was a 34% decrease in [3H]PDBu binding sites in NE-treated blood vessels without change in binding affinity for the ligand. To determine whether this loss in enzymatic activity and [3H]PDBu binding resulted from a decrease in the quantity of the enzyme, Western blot analyses were performed using a monoclonal antibody (MoAb) against PKC. This approach confirmed the presence of an 80-Kd immunoreactive PKC in the soluble fraction of rat aortic smooth muscle and demonstrated a 44% decrease in the amount of PKC in blood vessels after sustained exposure to catecholamines. Our results demonstrate that prolonged activation of alpha-adrenoceptors in blood vessels leads to down-regulation of PKC which may contribute to desensitization of contraction mediated by vasoconstrictors.

Animals↗
PubMed1992

Tetrahydrobiopterin synthesis. An absolute requirement for cytokine-induced nitric oxide generation by vascular smooth muscle.

Nitric oxide (NO) synthesis is induced in vascular smooth muscle cells by lipopolysaccharide (LPS) where it appears to mediate a variety of vascular dysfunctions. In some cell types tetrahydrobiopterin (BH4) synthesis has also been found to be induced by cytokines. Because BH4 is a cofactor for NO synthase, we investigated whether BH4 synthesis is required for LPS-induced NO production in rat aortic smooth muscle cells (RASMC). The total biopterin content (BH4 and more oxidized states) of untreated RASMC was below our limit of detection. However, treatment with LPS caused a significant rise in biopterin levels and an induction of NO synthesis; both effects of LPS were markedly potentiated by interferon-gamma. 2,4-Diamino-6-hydroxypyrimidine (DAHP), a selective inhibitor of GTP cyclohydrolase I, the rate-limiting enzyme for de novo BH4 synthesis, completely abolished the elevated biopterin levels induced by LPS. DAHP also caused a concentration-dependent inhibition of LPS-induced NO synthesis. Inhibition of NO synthesis by DAHP was reversed by sepiapterin, an agent which circumvents the inhibition of biopterin synthesis by DAHP by serving as a substrate for BH4 synthesis via the pterin salvage pathway. The reversal by sepiapterin was overcome by methotrexate, an inhibitor of the pterin salvage pathway. Sepiapterin, and to a lesser extent BH4, dose-dependently enhanced LPS-induced NO synthesis, indicating that BH4 concentration limits the rate of NO production by LPS-activated RASMC. Sepiapterin also caused LPS-induced NO synthesis to appear with an abbreviated lag period phase, suggesting that BH4 availability also limits the onset of NO synthesis. In contrast to the stimulation of LPS-induced NO synthesis, observed when sepiapterin was given alone, sepiapterin became a potent inhibitor of NO synthesis in the presence of methotrexate. This is attributable to a direct inhibitory action of sepiapterin on GTP cyclohydrolase I, an activity which is only revealed after blocking the metabolism of sepiapterin to BH4. Further studies with sepiapterin, methotrexate, and N-acetylserotonin (an inhibitor of the BH4 synthetic enzyme, sepiapterin reductase) indicated that the BH4 is synthesized in RASMC predominantly from GTP; however, a lesser amount may derive from pterin salvage. We demonstrate that BH4 synthesis is an absolute requirement for induction of NO synthesis by LPS in vascular smooth muscle. Our findings also suggest that pterin synthesis inhibitors may be useful for the therapy of endotoxin- and cytokine-induced shock.

Amino Acid Oxidoreductases↗
PubMed1992

Vascular smooth muscle proliferation in hypertensive transgenic rats.

In vascular smooth muscle cell (VSMC) cultures from Sprague-Dawley (SD) and hypertensive transgenic rats for the mouse renin gene Ren-2 (TGR), the DNA synthesis, which was analyzed by the uptake of [3H]thymidine, was higher in TGR than SD VSMCs (2.5- to 8-fold, mean of 5.6-fold) under basal conditions. DNA synthesis was increased by fetal calf serum (10%) in SD cells more than in TGR VSMCs, and was decreased by heparin (400 micrograms/ml) and by phorbol-12,13-dibutyrate (10(-7) M) in TGR VSMCs to a higher degree than in SD cells. Neither endothelin (10(-7) M), angiotensinogen (10(-8) M), the renin inhibitor CGP 29,287 (10(-4) M), angiotensin I (10(-7) M), captopril (10(-5) M), angiotensin II (10(-7) M), nor saralasin (10(-6) M) modified DNA synthesis in either type of VSMCs. Sodium nitroprusside (10(-4) and 10(-3) M) increased DNA synthesis in both kinds of VSMCs but in TGR cultures it became toxic at 10(-3) M. 8-Bromocyclic GMP (10(-7) to 10(-5) M) reduced DNA synthesis in SD cells more than in TGR VSMCs. These results suggest that (a) cellular mechanisms of proliferation appear to be more activated in TGR VSMCs, likely involving a protein kinase C-dependent pathway but not the renin-angiotensin system, and (b) in both type of cells, sodium nitroprusside possesses proliferative properties whereas 8-bromocyclic GMP has antiproliferative properties.

Animals↗
PubMed1992

Substrate-bound fibrinogen, fibrin and other cell attachment-promoting proteins as a scaffold for cultured vascular smooth muscle cells.

We have previously reported that fibrinogen/fibrin can induce the migration of vascular smooth muscle cells in vitro. In this study, we examined the effect of substrate-bound fibrinogen/fibrin and other cell attachment-promoting proteins on the adhesion of vascular smooth muscle cells. The amount of fibrinogen/fibrin adsorbed to plastic wells and the adhesion of smooth muscle cells to the wells were found to depend on the concentration of fibrinogen used for coating the wells. The effect of fibrinogen/fibrin was comparable to that of so-called cell attachment-promoting proteins (fibronectin, vitronectin, and type I collagen). Adhesion of smooth muscle cells to fibrinogen/fibrin-coated wells was inhibited by the synthetic peptide GRGDS, but not by a control peptide, GRGES. Vitronectin, fibronectin, type I collagen, denatured type I collagen and commercial gelatin also induced smooth muscle cell adhesion. The adhesion induced by vitronectin, denatured type I collagen, and commercial gelatin was inhibited by GRGDS. However, the adhesion induced by type I collagen was not influenced and that induced by fibronectin was only slightly inhibited. These observations suggest that fibrinogen/fibrin deposited extracellularly in the arterial intima may act as a scaffold in the process of smooth muscle cell migration.

Animals↗
PubMed1976

Hypersensitivity of scleroderma cutaneous vascular smooth muscle to 5-hydroxytryptamine.

Vascular smooth muscle strips from subcutaneous wrist vessels of patients with scleroderma (systemic sclerosis) were studied in an isolated system. No difference between catecholamine response of scleroderma or control vessel strips was observed. Three of four patients demonstrated significant hypersensitivity to 5-hydroxytryptamine as compared to control values. Serotonin hypersensitivity may play a role in the evolution of Raynaud's phenomenon and vascular scleroderma.

Adenosine Triphosphate↗
PubMed1992

Platelet-derived growth factor AA homodimer stimulates protein synthesis rather than DNA synthesis in vascular smooth muscle cells from spontaneously hypertensive rats but not from normotensive rats.

Platelet-derived growth factor (PDGF) AB and BB isoforms were potent mitogens for cultured vascular smooth muscle cells from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). PDGF-AA promotes protein synthesis in a dose-dependent manner in SHR cells, whereas DNA synthesis was stimulated only slightly. However, this isoform did not activate either DNA or protein synthesis in WKY cells. PDGF-AA stimulated tyrosine phosphorylation of its receptor protein and phospholipase C-gamma 1 in SHR cell but not in WKY cells. These results indicate that vascular smooth muscle cell of SHR is uniquely responsive to PDGF-AA, presumably due to abnormality in receptor expression, in its hypertrophic response.

Animals↗
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↗
PubMed1992

Decreased insulin-sensitive Ca2+ transport in cultured vascular smooth muscle cells from spontaneously hypertensive rats.

To investigate the role of insulin on Ca2+ regulation of vascular smooth muscle cells (VSMC) in hypertension, the effect of insulin on Ca2+ transport and intracellular free calcium concentration ([Ca2+]i) was measured in cultured VSMC from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Insulin produced a substantial increase in 45Ca uptake as well as [Ca2+]i in quiescent cultured VSMC. The stimulatory effects of insulin were completely inhibited by diltiazem, and partially by H-7, TMB-8, and 5-N,N(hexamethylene)amiloride (HMA), but not by W-7 or trifluoroperazine. Insulin-sensitive 45Ca uptake of SHR VSMC was significantly smaller than that of WKY VSMC. Insulin-sensitive increase in [Ca2+]i of SHR VSMC was also smaller than that of WKY VSMC. It is concluded that insulin increases 45Ca uptake, leading to an increase in [Ca2+]i, presumably through the voltage-dependent Ca2+ channel, intracellular Ca2+ release, or protein kinase C mediated mechanisms in cultured VSMC. A blunted response of insulin-sensitive Ca2+ uptake and [Ca2+]i in SHR VSMC suggests the differential regulation of Ca2+ transport in response to insulin in primary hypertension.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1975

Ajamline-induced changes in mechanical and electrical activity of vascular smooth muscle.

The effects of ajmaline on vascular smooth muscle were studied using helical aortic strips and portal veins of male rats. This report is based on the results of 104 mechanical experiments. In 30 additional experiments electrical activity was recorded simultaneously at different points of the preparation using extracellular methods (liquid paraffine or pressure electrodes technique). Ajmaline induces relaxation of aortic helical strips (activated by 2.0 mug/l norepinephrine) to 75 percent of initial tension in a dose of 0.6 mg/l, to 50 percent by 2.0 mg/l, and to 25 percent by 4-5 mg/l. The relaxation slope is shifted to the right by increasing the [Ca++]o from 2.0 to 4.0 mM, by increasing the initial norepinephrine concentration to 4.0-10 mug/l, or by KCl depolarization, [K+]o ranging from 15 to 60 mM. The relaxing effect of ajmaline on aortic strips can partly be attributed to a change in electrical activity with a dose-dependent conduction impairment or block and, at high concentrations, also a decrease in the frequency of pacemaker excitations. Experiments on aortic strips in K+ contracture show relaxation independent of changes in phasic electrical events. Ajmaline ranging from 0.2 to 80-100 mg/l causes on the portal vein a marked increase in amplitude and a small decrease in frequency of rhythmical contractions. Integrated isometric force reaches 300 percent of initial values. The increasing amplitude of contractions is related to a prolongation of excitation trains, while the frequency and amplitude of the individual spike are reduced. Our results suggest that the effects of ajmaline on the mechanical and electrical activity of vascular smooth muscle may be partly related to a reduction in Ca++ and probably Na+ conductance.

Ajmaline↗
PubMed1992

OPC-13340, a new dihydropyridine calcium channel blocker attenuates rapid vascular smooth muscle cell growth in spontaneously hypertensive rats.

We investigated the mechanism of the antimitotic effects of calcium channel blockers in vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR). VSMC from SHR exhibited rapid proliferation through a quick transition from the G0/G1 to the DNA synthetic (S) phase and from the S to the G2/mitotic (M) phase, whereas the DNA synthetic rate itself was equal to that of Wistar-Kyoto rats (WKY). OPC-13340, a new dihydropyridine calcium channel blocker, dose-dependently decreased incorporation of [3H]thymidine into the DNA fragments in randomly cycling VSMC in SHR. Cell cycle analysis showed that the rapid transition from the S to the G2/M period was restored by OPC-13340 to the control level in WKY, whereas the quick transition from G0/G1 to S was unaffected. This antimitotic effect of OPC-13340 was reflected by attenuation of enhanced cellular protein synthesis during the G2/M period. Protein synthesis in the G0/G1 period was not influenced by OPC-13340. Thus, these data indicate that the calcium channel blocker OPC-13340 mitigates the enhanced proliferation observed in randomly cycling VSMC from SHR and that this effect is primarily due to normalization of the premature mitosis during the G2/M period.

Animals↗
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↗
PubMed1975

Effects of ethanol and its interaction with vasoactive agents in bovine vascular smooth muscle.

The vascular effects of ethanol were evaluated using isolated arteries from bovine brain, eye, and kidney. Ethanol induced contraction in all vessels, but only at concentrations in excess of lethal blood levels in man. At a concentration approximating that found in the blood during intoxication (43 mM), ethanol had no effect on renal vascular responses to norepinephrine, serotonin, or histamine. The response of ocular vessels to norepinephrine and histamine was significantly diminished by 43 mM ethanol, suggesting a possible mechanism underlying the "bloodshot" eyes found in acute intoxication. Cerebral vascular responses to vasoactive agents were generally unaffected by 43 mM ethanol, indicating that regional differences in brain perfusion are probably not a cause of the behavioral changes found during intoxication.

Animals↗
PubMed1992

Calcium channel blocker-like action of 1,9-dideoxyforskolin in vascular smooth muscle.

The inhibitory effect of 1,9-dideoxyforskolin (DFK) on the contraction of rat aorta was compared with that of forskolin. DFK inhibited the contraction induced by high K+ more strongly than that induced by norepinephrine, whereas forskolin more strongly inhibited the norepinephrine-induced contraction. The inhibitory effect of DFK on high K(+)-induced contraction was antagonized by an increase in extracellular Ca2+ concentration. DFK inhibited the increase in cytosolic Ca2+ level and contraction in parallel whereas forskolin inhibited the contraction more strongly than the cytosolic Ca2+ level. These results suggest that DFK, but not forskolin, inhibits vascular smooth muscle contraction by a Ca2+ channel blocker-like action.

Animals↗