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Biomedical subjects

A B Ebeigbe

Publications and source records attributed to A B Ebeigbe.

At least 37 records · Page 2Linked to original sources
PubMed1987

Mechanism of contractile action of barium ion on rat aortic smooth muscle.

The mechanism of Ba2+-induced contraction has been examined in helical strips of Ca2+-depleted, 60 mM K+-depolarized rat aortae. The concentration-response curves to Ca2+ or Ba2+ were significantly potentiated by exposure to 3 X 10(-8) M Bay K 8644 (a Ca2+ channel agonist) in the order Ca2+ greater than Ba2+, suggesting an action of Ba2+ ions through potential-sensitive membrane Ca2+ channels. Exposure of strips to background concentration of Ca2+ (0.05 mM) enhanced the contractile responses to Ba2+, whereas background exposure to Ba2+ (0.1 mM) attenuated Ca2+ responses. Repeated stimulation with Ba2+ resulted in tachyphylaxis, contrary to the result when Ca2+ was used. The results suggest that Ba2+ ions enter rat aortic smooth muscle cells through Ca2+ channels and mobilize a noradrenaline-insensitive intracellular Ca2+ pool. Ba2+ may also cause a desensitization of some intracellular process.

Animals↗
PubMed1986

Inhibitory effect of dichlorvos on arterial smooth muscle contraction.

The effect of the organophosphate pesticide, dichlorvos, on the contractile responses of isolated rat tail arteries has been studied. Dichlorvos (10(-8)-10(-4) M) had no effect on baseline tension, but relaxed 10(-7) M norepinephrine (NE), 10(-7) M 5-HT or 100 mM KCl contractions dose-dependently. Dichlorvos also inhibited CaCl2 dose-response curves in K+-depolarized strips, as well as depressing both phasic and tonic components of NE-induced contractions. The results suggest a direct relaxant effect of dichlorvos on arterial smooth muscle by a mechanism probably related to interference with Ca2+ supply.

Animals↗
PubMed1986

Extracellular magnesium and contractile responses to noradrenaline in the rat tail artery.

The effects of variations in extracellular magnesium concentration (Mg2+)0 on contractile responses to noradrenaline (NA) were studied in isolated rat tail arteries. Mg2+-free or high Mg2+ exposures caused (respectively) enhancement or inhibition of NA dose-response curves. Increases in (Mg2+)0 significantly increased NA-induced phasic contractions due to Ca release from a "membrane-bound" pool. Increases in (Mg2+)0 diminished the magnitude of Ca2+-induced relaxations due to a "membrane-stabilizing" effect. It is hypothesized that high (Mg2+)0 enhances NA-induced mobilization of stored calcium, as well as preventing the membrane-stabilizing effect of calcium ions through competition with Ca2+ at intracellular and membrane sequestrating sites, thus interfering with Ca2+ sequestration.

Animals↗
PubMed1986

Species variations in the relaxation of tail arteries to electrical stimulation.

Relaxation in response to electrical stimulation has been studied in isolated tail arteries from rats, cats and pigs. Electrical stimulation elicited contractile responses in unstimulated strips, but caused frequency-dependent relaxations in tail arteries from all species studied, following contractile responses by various agents. The order of susceptibility to the relaxant effect of electrical stimulation in arteries from all three species was pig greater than cat greater than rat. Relaxations to electrical stimulation were unaffected by prior treatment of arteries with atropine, propranolol, tetrodotoxin, indomethacin, ouabain, pyrilamine and chemical denervation with 6-hydroxy-dopamine, but were prevented, dose-dependently, by cimetidine and aminophylline (antagonists of histamine H2-receptor and adenosine P1-receptor, respectively). The results suggest that relaxation of tail arteries from the rat, cat and pig in response to electrical stimulation is modulated by histamine and adenosine.

Animals↗
PubMed1986

Mechanism of chloroquine-induced inhibition of smooth muscle contraction.

The study was designed to characterize the mechanism of chloroquine-induced depression of contractility in isolated rat ileal smooth muscle. Chloroquine (10(-7)-10(-4) M) depressed both spontaneous as well as 10(-7) M acetylcholine-induced contractions dose-dependently. The decline in contractile responses to maximal dose of Ach (10(-6) M) in Ca-free medium was significantly increased by treatment with chloroquine. Restoration of Ca++ to Ach-stimulated "Ca-depleted" tissues produced contractions due to Ca++ influx; these contractions were prevented by chloroquine, dose-dependently. Using "Ca-loading" and "Ca-washing" procedures 10(-6) M Ach was observed to mobilize Ca++ from a "membrane-bound" pool, perhaps containing residual Ca++ of extracellular origin. Chloroquine significantly inhibited the rate of filling of such "membrane-bound" pool. The results show that chloroquine-induced depression of mechanical activity of the rat ileal smooth muscle is associated with diminished Ca++ influx, as well as impaired mobilization of Ca++ from an Ach-sensitive "membrane-bound" pool.

Acetylcholine↗
PubMed1985

Barium and strontium as calcium substitutes for contractile responses in the rat tail artery.

The ability of Ba2+ and Sr2+ to substitute for Ca2+ in contractile responses of the rat tail artery has been examined. Both Ba2+ and Sr2+ caused comparable contractions in Ca-depleted NA-stimulated, or K+-depolarized strips. Ba2+ and Sr2+ substitute poorly for Ca2+ at noradrenaline-sensitive membrane sites. At high concentrations, the three divalent cations stabilize the membrane in the order: Ca2+ greater than Sr2+ greater than Ba2+. The relaxation rates following high-K+ contractions were similar for all three divalent cations, suggesting a common mechanism for sequestration/extrusion.

Animals↗
PubMed1985

Mechanism of hydralazine-induced relaxation of arterial smooth muscle.

The effect of hydralazine on contractile responses by various agents has been studied in isolated rat tail artery strips. Hydralazine caused dose-dependent relaxation of contractions produced by 10(-7) mol.litre-1 noradrenaline (N); 10(-7) mol.litre-1 5-HT or 100 mmol.litre-1 KCl, suggesting that the relaxation response is non-specific. CaCl2 dose-response (in the presence of 10(-5) mol.litre-1 N; 10(-5) mol.litre-1 5-HT or 100 mmol.litre-1 KC1) was significantly inhibited by 5 X 10(-4) mol.litre-1 hydralazine in the order: KCl greater than 5-HT greater than N. Hydralazine also inhibited BaCl2 dose-response curve (in K+-depolarised strips); maximal contraction to BaCl2 was depressed by 87%. In other experiments, hydralazine significantly depressed (by 20%) the phasic contractile response to N due to mobilisation of calcium from a membrane-bound pool. D 600, a calcium entry blocker, also caused dose-dependent relaxation of contractile responses to all three agents studied; and inhibited CaCl2 and BaCl2 dose-response curves in K+-depolarised media, as well as depressed the phasic contractile response to N in Ca-free media by 17%. These results suggest that in the rat tail artery, hydralazine interferes with Ca2+ influx, as well as release from a membrane-bound pool.

Animals↗
PubMed1984

Vascular membrane permeability during hypoxia.

Extracellular space measurements using radioisotope markers (35S-sulphate and 14C-sorbitol) and ultrastructural examination of lanthanum distribution have been carried out on two vascular tissues (aorta, portal vein) exposed to normoxic and hypoxic media to see if hypoxia is associated with membrane damage. Extracellular space values did not change significantly with hypoxia of up to 60 min duration. Lanthanum remained distributed in the extracellular space in both normoxic and hypoxic specimens. These findings suggest that hypoxia may not be associated with increased vascular membrane permeability to lanthanum, as has been reported by some workers to occur with more severe metabolic deprivation.

Animals↗
PubMed1984

Differential effects of calcium removal on acetylcholine- and potassium-induced contractions of rat ileal smooth muscle.

The contractile responses to 10(-6)M acetylcholine (Ach) and 100 mM K+ solution have been studied in the rat ileal smooth muscle exposed to calcium-free media (with or without 1.0 mM EGTA) to further examine the calcium pools mobilized by these agents for activation of contraction. Both stimulants produced contractions in Ca-free media, only in the absence of EGTA. The phasic component of the contractile responses to Ach as well as the tonic component of K+-induced contractions were relatively resistant to short periods of Ca-free exposure; this suggests that Ach mobilizes Ca from some tightly-bound or intracellular pool, whereas high-K+ contraction involves mobilization of Ca from some superficial or loosely-bound pool. Both Ach and high-K+ still caused phasic contractions following D600 treatment, with high-K+ stimulation also maintaining a tonic component, suggesting that in this tissue, high-K+ contractions are relatively resistant to calcium deficiency compared to Ach.

Acetylcholine↗
PubMed1983

Relaxation of rat tail artery to electrical stimulation.

Rat tail artery strips relax in response to electrical stimulation (0.1-8Hz, 9V, 1.0msec) following contraction induced by norepinephrine (5.9 X 10(-7)M). The relaxation is not altered by treatment of the strips with atropine, propranolol, tetrodotoxin or indomethacin nor by chemical denervation with 6-hydroxydopamine. Incubation of strips in calcium-free solution reduced the contractile response to norepinephrine and blocked relaxation in response to 4Hz electrical stimulation. Histamine antagonists (H2 receptor subclass: cimetidine, metiamide) inhibited the relaxation to electrical stimulation in a dose-dependent manner. These results suggest that relaxation to electrical stimulation in rat tail artery is modulated by calcium and by the H2 subclass of histamine receptors.

Animals↗
PubMed1983

Ca2+, histamine antagonists and relaxation to electrical impulses in dog coronary artery.

Isolated dog coronary arteries relax in response to electrical stimulation (0.1-8.0 Hz, 9 V, 1.0 ms) following contraction induced by serotonin. Cimetidine, metiamide and ranitidine inhibited this relaxation. The relaxation was not blocked by pyrilamine. Reducing the concentration of Ca+ (0.1 mM) decreased the rate of relaxation whereas relaxation was more rapid when the Ca2+ concentration was increased (3.2 mM). These results suggest that relaxation to electrical stimulation is modulated by Ca2+ and by the H2-subclass of histamine receptors.

Animals↗
PubMed1982

Calcium pools for noradrenaline and potassium-induced contractions of rat portal vein.

The contractile responses of isolated normal and Ca-depleted rat portal veins to varying concentrations of noradrenaline (NA) and K+ have been studied with a view to further clarifying the sources of Ca for contraction using both agents. The comparably rapid times-to-peak of NA and K+ contractions of normal (Ca-containing) strips suggest mobilization of a common Ca pool, perhaps superficial: whereas, following Ca-depletion. NA appears to mobilize a superficial pool more readily than K+. Following K+ depolarization in Ca-free medium, NA produced a contraction sensitive to ryanodine, suggesting Ca release from an intracellular pool.

Animals↗
PubMed1980

Responses of systemic vascular smooth muscle to hypoxia.

The rapidity and extent of hypoxic relaxation of vascular smooth muscle (VSM) from different systemic vessels is relevant to the study of mechanisms of vasodilation in different vascular beds. Variations between sites may also assist understanding of the link between oxygen tension and mechanical activity, which has been shown not to be a simple deprivation of aerobic processes. Strips of rat portal vein (RPV), rabbit ear artery (REA) and rabbit common carotid artery (RCC) were studied under isotonic conditions, contracted by 10(-6) noradrenaline (NA). Reduction of Po2 to less than 3KPa during NA constraction led to relaxation which was rapid and 90% complete in RPV, rapid and 60% in REA: the relaxation began when tissue Po2 was decreasing and was not lower than 5.5 K Pa. RCC responded slowly and only some strips relaxed. The rapidity and magnitude of relaxation for each type of vessel was comparable to that produced by removal of external calcium. Also for any one type of VSM the response to NA was abolished or diminished to a similar extent by preliminary exposure to hypoxia, or by preliminary removal of calcium. Preliminary hypoxia diminished 50 mmol.1(-1) K+ contractions as much as it diminished NA contractions. Preliminary 1-2 hour exposure to hyperoxia diminished the subsequent relaxant effect of hypoxia. Inhibition of glycolysis (iodoacetic acid) had no effect on normoxic NA contraction or on hypoxic relaxation, but prevented or diminished the subsequent recovery on reoxygenation. Low oxygen tension appears to act in VSM as though it interferes with net influx or utilisation of external calcium.

Animals↗
PubMedDate not supplied

Effects of potassium adaptation on blood pressure and pressor responses in normotensive and renal hypertensive Wistar rats.

Potassium adaptation reduces blood pressure (BP) in hypertensive humans and animals but its effects on normotensive BP and the nature of pressor responses to vasoactive drugs are not known. We measured directly, the mean arterial pressure (MAP) of normotensive control, normotensive potassium-adapted (given 0.75% potassium chloride solution for 5 weeks), renal hypertensive (RHP), and renal hypertensive Wistar rats later adapted to potassium. The maximum percentage change, the ED25, and recovery times after bolus injections of noradrenaline (NA), angiotensin II (Ang. II), sodium nitroprusside (SNP), and acetylcholine (ACh) were compared. The MAP of normotensive potassium-adapted rats was significantly lower than that of the normotensive controls (95.6+/-5.0 vs. 110.8+/-2.8 mmHg, p<0.05). The potassium-adapted hypertensive rats (RHP-A) also had significantly lower MAP values than the non-adapted hypertensive ones (116.0+/-4.4 vs. 138.2+/-4.1 mmHg, p<0.01). Potassium adaptation significantly blunted responses to NA and augmented responses to SNP but while the duration of action of Ang. II was significantly shortened, that of SNP was significantly increased. We conclude that potassium adaptation reduces BP in the normotensive and hypertensive rats and may influence both the degree and duration of action of vasoactive drugs given as bolus injections.

Adaptation, Physiological↗