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Biomedical subjects

A B Ebeigbe

Publications and source records attributed to A B Ebeigbe.

At least 19 recordsLinked to original sources
PubMed2002

Haematological influences of potassium adaptation in normotensive and renally-hypertensive Wistar rats.

Dietary potassium is known to cause reduction in blood pressure in several models of hypertension in human and animal studies but its haematological effects are not known. Here, experiments are designed to study the haematological effects of potassium adaptation (achieved by administering 0.75% KCl solution in drinking water for five weeks) in Wistar rats. The animals are divided into four groups comprising controls, potassium-adapted, renal hypertensive, and renal hypertensive with later adaptation to potassium. Packed cell volume (PCV) and platelet count (PC), whole blood and plasma viscosities, and platelet aggregation in the presence of sodium nitroprusside, levcromakalim, and glibenclamide, are studied. Results showed comparable PCV and PC in all groups. While relative whole blood viscosity was significantly higher (P<0.05) in the hypertensive group, relative plasma viscosity was similar in all groups. Adaptation significantly reduced (P<0.05) the tendency of platelets to aggregate to collagen. Sodium nitroprusside significantly reduced (P<0.05) the pro-aggregatory effects of collagen only in the control group. Neither of the potassium-channel modulators (levcromakalim, glibenclamide) caused any significant alteration in platelet response to collagen at the concentrations studied. Although these results suggest that potassium adaptation may not affect haemorheology, the reduced ability of platelets to aggregate--by mechanisms not clearly understood--has implications for reduced thromboembolism and the attendant cardiovascular sequelae.

Adaptation, Physiological↗
PubMed1998

Vasorelaxant effect of thiopentone in isolated human epigastric arteries.

The experiments were designed to elucidate the mechanism of thiopentone-induced inhibition of contractile responses in isolated human epigastric arteries. Segments of human epigastric arteries were obtained from patients who underwent elective or emergency caesarean section, placed in standard physiological salt solution (PSS), cut into rings at 3 mm intervals and suspended in organ baths for recording of isometric contractions at 37 degrees C, and pH 7.4. Three protocols were employed to examine the inhibitory effect of thiopentone: (a) concentration-dependent effect on 10(-7) M noradrenaline (NA)- or high-K+ (40 mM)-induced contractions: (b) effect on NA-induced extra-and intracellular Ca(2+)-dependent contractions and (c) effect on the dose-response curve when Ca2+ is restored to Ca(2+)-depleted rings in Ca(2+)-free 40 mM K(+)-depolarizing medium. Thiopentone (1 x 10(-6) -4 x 10(-3) M) caused concentration-dependent relaxation of both NA- and high-K(+)-induced contractions. The magnitudes of both precontractions were not significantly different but the IC50 values for thiopentone relaxation of high-K+ contractions were significantly lower than for NA contractions. Thiopentone (10(-4) M) significantly attenuated the phasic (intracellular Ca2+ dependent) contractile responses to 10(-5) M NA in Ca(2+)-free PSS as well as the tonic (extracellular Ca2+ dependent) contractions upon restoration of Ca2+. In contrast, nifedipine (1 microM) did not modify the phasic response but significantly attenuated the tonic response. Thiopentone (10(-4) M) also almost completely abolished concentration-dependent Ca(2+)-induced contractions in K(+)-depolarized Ca(2+)-depleted rings. The results suggest that in the smooth muscle of human epigastric arteries, thiopentone-induced relaxation is non-specific and is associated with impairment of Ca2+ supply from both extracellular and intracellular pools.

Calcium↗
PubMed1996

Depressed endothelium-dependent relaxation responses to acetylcholine and histamine in isolated human epigastric arteries from pre-eclamptic women.

The vasorelaxant effects of acetylcholine (Ach) and histamine have been examined on 10(-7) M-noradrenaline (NA)-precontracted ring preparations of epigastric arteries from normotensive and pregnancy-induced hypertensive women. Contractile responses to 10(-7) M-NA were significantly (p < 0.05) enhanced following removal of the endothelium. Both Ach and histamine (in the presence of H1-receptor blockers) elicited methylene blue-sensitive concentration-dependent relaxations only in endothelium-intact rings. The relaxation responses to both agents were significantly attenuated in arterial rings from pre-eclamptic women. Endothelium-independent relaxation responses induced by sodium nitroprusside were comparable in arterial rings from both patient groups. The results suggest an impairment of endothelial function in pre-eclampsia.

Acetylcholine↗
PubMed1994

Differential effects of prostanoid synthesis inhibitors on cicletanine-induced relaxation of isolated human epigastric arteries.

We have examined the influence of prostanoid synthesis inhibitors on the relaxation responses induced by cicletanine in ring preparations of isolated human epigastric arteries following precontraction induced by 10(-7) M noradrenaline. Cicletanine caused concentration-dependent relaxations, uninfluenced by the cyclooxygenase inhibitors, meclofenamate (1, 10 microM) and indomethacin (1, 10 microM) but significantly (p < 0.05) attenuated by the specific prostacyclin synthesis inhibitor, tranylcypromine (0.1-10 microM) (n > 6 in each). In contrast, cromakalim-induced relaxations were significantly attenuated by indomethacin, meclofenamate and tranylcypromine. The tranylcypromine-sensitive cicletanine-induced relaxation suggests, at least in part, the involvement of prostacyclin in the vasodilator action of cicletanine.

Abdominal Muscles↗
PubMed1994

Evidence for preservation of epithelial function in cryopreserved porcine and human bronchi.

Porcine and human bronchi have been investigated in vitro without or after storage at -196 degrees C in Krebs-Henseleit solution containing 2.0 M dimethyl sulphoxide and 0.1 M sucrose as cryoprotectants. In bronchi from both species maximal post-thaw contractile responses to acetylcholine (ACh) were reduced by about 25-30% compared to unfrozen bronchi. To assess the viability of bronchi and endothelium-denuded rat aortic strips, was employed. The release of an epithelium-derived inhibitory factor (EpDIF) was induced by ACh and assessed in terms of concentration-dependent relaxation of the endothelium-denuded rat aortae. Following removal of bronchial epithelium, ACh failed to elicit any relaxation of rat aorta. With cryopreserved bronchi from both pig and human about 5 and 30 times higher concentrations of ACh, respectively, were required to elicit the same relaxant response as with unfrozen bronchi. The results suggest that after the freezing-thawing process both smooth muscle and epithelial function is largely preserved and provide support for the use of cryopreservation for storage of airway preparations for pharmacological studies.

Acetylcholine↗
PubMed1992

Responses of isolated human epigastric arteries to histamine.

Responses to histamine have been studied on ring preparations of epigastric artery obtained from normal and from pregnancy-induced hypertensive (PIH) women to characterize the mode of action of histamine in this vascular preparation. In non-contracted arterial rings, histamine elicited concentration-dependent H1 receptor-mediated contractions, competitively antagonised by mepyramine and cicletanine with pA2 values of 9.1 and 7.5, respectively. Arterial rings from pregnancy-induced hypertensive patients displayed greater sensitivity to histamine, but no change in maximal contractions, and were (at the EC30 histamine response) more susceptible to antagonism by mepyramine and cicletanine. Following precontraction by noradrenaline, histamine elicited relaxation responses only in the presence of H1 receptor antagonists. Endothelium removal or exposure to methylene blue significantly attenuated histamine-induced relaxation; the residual relaxations under these conditions appear to be due to a direct effect on H2 receptor on smooth muscle cells. The results show that, in human epigastric artery, histamine elicits H1 receptor-mediated contractions and that, following NA precontraction and in the presence of H1 receptor blockade, relaxations occur. Arterial rings from pregnancy-induced hypertensive patients showed modest but somewhat greater sensitivity to histamine, as well as being more susceptible to cicletanine and mepyramine.

Abdominal Muscles↗
PubMed1991

Mechanism of dichlorovos-induced inhibition of calcium-dependent contractions in the rat tail artery.

The inhibitory effect of dichlorovos (an organophosphate pesticide) on Ca(2+)-dependent contractions has been studied in isolated helical strips of rat tail arteries. Isometric contractions were evaluated under standard organ bath conditions. Dichlorovos caused concentration-dependent relaxation of 10(-7) M NE-induced contractions as well as inhibition of both phasic and tonic components of NE contractions. Extracellular calcium-dependent contractions in K(+)-depolarized medium as well as NE-induced contractions due to mobilization of membrane-bound calcium pool and intracellular calcium-dependent caffeine contractions were significantly attenuated by dichlorovos. The results strongly support our previous observation that dichlorovos interferes with calcium metabolism in the rat tail artery.

Animals↗
PubMed1991

Altered responses of aortic smooth muscle from Sprague-Dawley rats with salt-induced hypertension.

1. The contractile responses of aortic ring preparations from Sprague-Dawley rats made hypertensive by 6-week dietary salt loading were studied. The test and control diet contained 8.0 and 0.3% NaCl, respectively. Aortic rings from salt-loaded rats showed enhanced sensitivity to noradrenaline (NA) but not to serotonin. Contractile responses to CaCl2 in Ca-free NA-containing medium was significantly enhanced in salt-loaded rats, but was unchanged in K(+)-depolarised medium. K(+)-induced relaxation (a functional indicator of Na-K adenosine triphosphatase activity) was sensitive to 10 mumol/L ouabain and was significantly attenuated in aortic rings from salt-loaded rats. The results suggest that hypertension induced by salt-loading is associated with enhanced sensitivity to NA, increased Ca2+ entry through receptor-operated channels, and impairment of Na-K ATPase enzyme activity.

Animals↗
PubMed1991

In vitro vascular effects of cicletanine in pregnancy-induced hypertension.

1. The vascular effects of cicletanine have been studied in vitro on ring preparations of inferior epigastric arteries from normotensive human females and human females with pregnancy-induced hypertension (preeclampsia). 2. Cicletanine (10(-7)-10(-3) M) elicited concentration-dependent relaxation of vessels precontracted with 10(-7) M noradrenaline (NA) or 60 mM K+ but was more potent in the former. Relaxation was significantly greater in rings from preeclamptic patients and was uninfluenced by endothelium removal. 3. The intracellular Ca-dependent contractile responses to 10(-5) M NA in Ca-free medium as well as the subsequent extracellular Ca-dependent contractions (on restoration of external Ca) were significantly attenuated dose-dependently by cicletanine (10(-5) M, 3 x 10(-4) M) in arterial rings from both normotensive and preeclamptic patients. Cicletanine also relaxed rings precontracted by 25 mM K+ but was ineffective against 80 mM K(+)-induced contractions. 4. The inhibition of intracellular Ca-dependent contractions was significantly greater in rings from preeclamptic than from normotensive patients whereas extracellular Ca-dependent contractions were comparably inhibited in both groups. Nifedipine, on the other hand, had little effect on the intracellular Ca-dependent contractions but significantly depressed extracellular Ca-dependent contractions. 5. Cicletanine-induced relaxation was uninfluenced by pretreatment with propranolol, ouabain, tetraethylammonium, procaine, indomethacin, cimetidine or tetrodotoxin but was antagonized by glibenclamide. 6. The results show that cicletanine inhibits contractile responses of human isolated inferior epigastric arteries by a mechanism unrelated to endothelial factors but associated with inhibition of calcium metabolism. An action of cicletanine on glibenclamide-sensitive K+ channels is also suggested. Cicletanine-induced inhibition was significantly greater in arteries from preclamptic patients.

Calcium↗
PubMed1991

Dietary salt-loading attenuates endothelium-dependent relaxation in response to histamine but not to acetylcholine in rat aortic rings.

Endothelium-dependent relaxation in response to histamine and ACh has been studied on precontracted aortic rings from control and salt-loaded Sprague-Dawley rats. Both ACh and histamine caused relaxation of the noradrenaline-induced precontraction only in the presence of the endothelium. The relaxation response to ACh in rings from control and salt-loaded rats did not differ significantly whereas histamine-induced relaxation was significantly attenuated in aortae from salt-loaded rats. The results suggest that salt-induced hypertension is associated with impairment of endothelium-dependent relaxation to histamine but not to ACh.

Acetylcholine↗
PubMed1990

Influence of NG-monomethyl-L-arginine on endothelium-dependent relaxations in the perfused mesenteric vascular bed of the rat.

Endothelium-dependent relaxation mediated by the formation of nitric oxide (NO) from L-arginine, is prevented by the arginine analog NG-monomethyl L-arginine (L-NMMA) (Palmer et al., Biochem. Biophys. Res. Comm. 153:1251-1256 (1988)). In the rat mesenteric arterial bed, incubation with L-NMMA did not prevent acetylcholine-induced relaxation, which, however, was reversed when L-NMMA was added during its maximum effect. A similar profile of action was observed with methylene blue, an inhibitor of guanylate cyclase. Methylene blue, but not L-NMMA, increased basal perfusion pressure. These data indicate that in the mesenteric arterial bed, NO formation via the L-NMMA-sensitive pathway occurs during stimulation with acetylcholine, but not under basal conditions.

Acetylcholine↗
PubMed1989

Effects of cicletanine on histamine-induced contractions of isolated rabbit mesenteric arteries.

The antagonism by cicletanine of contractile responses to histamine has been examined in vitro on ring preparations of rabbit mesenteric arteries. Cicletanine (10(-8)-10(-6) M) caused a parallel rightward shift of histamine concentration response curve, with a pA2 value of 7.48 (slope = 0.89 +/- 0.19, not significantly different from unity). Histamine-induced contractions were nifedipine-sensitive and associated with cicletanine-sensitive increased 45Ca uptake. Endothelium removal resulted in enhanced contractile responses to histamine, but did not significantly modify cicletanine-induced antagonism: KB (dissociation constant) values for cicletanine antagonism in the presence or absence of endothelium were: 3.7 (+/- 0.1) X 10(-8) M and 3.6 (+/- 0.3) X 10(-8) M, respectively. Cicletanine (greater than 10(-4) M) also significantly attenuated 10 mM caffeine-induced contractions in rings exposed to Ca-free 100 mM K+ depolarizing medium. The results suggest that cicletanine-induced antagonisms of histamine H1 receptor-mediated contractions of rabbit mesenteric arteries is associated with interference with calcium entry as well as at high concentrations, release from intracellular stores.

Animals↗
PubMed1988

Effects of calcium channel blockade in canine saphenous veins after storage at -190 degrees C.

1. Canine saphenous veins were investigated in vitro either within 24 h after removal or after storage at -190 degrees C for 4-5 weeks of foetal calf serum containing 1.8 M dimethyl sulphoxide. 2. Contractions and 45Ca2+ uptake in response to both depolarization and guanfacine were studied in the absence and presence of the calcium channel antagonists diltiazem, verapamil, nifedipine and the two stereoisomers of a 1,4-dihydropyridine derivative, namely the (+)-(S) enantiomer and the (-)-(R) enantiomer of 202-791 (isopropyl 4-(2,1,3-benzoxadiazol-4-yl)-1,4-dihydro-2,6-dimethyl-5-nitro-3- pyridinecarboxylate). 3. Comparison of the data obtained on unfrozen and frozen/thawed veins revealed a good preservation of both contractile responsiveness and 45Ca2+ uptake mechanisms after storage at -190 degrees C. 4. It is suggested that cryopreservation is a useful technique for storing venous smooth muscle for pharmacological studies.

Adrenergic alpha-Agonists↗
PubMed1987

Responses of arterial smooth muscle from normotensive and pre-eclamptic subjects to the calcium channel agonist, Bay K 8644.

The effect of Bay K 8644, a dihydropyridine Ca2+ agonist, on in vitro contractile responses of inferior epigastric arteries from normotensive (N) and pre-eclamptic (P) subjects has been investigated, with a view to further defining the mechanism of the increased vascular sensitivity associated with pregnancy-induced hypertension. Bay K 8644 (10(-10)-10(-7) M) caused dose-dependent contractions of N as well as P arteries under resting conditions in the order: P greater than N and caused development of rhythmic contractions in both N and P arteries. Bay K 8644 effects were prevented by 3 X 10(-8) M Nifedipine (a Ca+2 antagonist). Bay K 8644 also significantly (P less than 0.05) enhanced the sensitivity as well as maximal contractile responses to CaCl2 in 40 mM K+-depolarized Ca-depleted N and P arteries in the order: P greater than N. The results suggest that the increased peripheral vascular sensitivity associated with pregnancy-induced hypertension may be due, at least in part, to enhanced activity of the potential-sensitive Ca2+ channels in arterial smooth muscle plasmalemma.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

Role of endothelium in magnesium-induced relaxation of rat aorta.

The role of endothelium in the relaxation of rat aortic smooth muscle to raised extracellular magnesium concentration (Mg2+)o has been examined. Following contractile responses to norepinephrine (NE) or high-K+ in Mg2+-free media, cumulative increases in (Mg2+)o caused concentration-dependent relaxations in intact (+E) as well as endothelium-denuded (-E) strips. In NE-stimulated strips, Mg2+-induced relaxation was significantly greater in +E strips, whereas the reverse was the case in K+-stimulated strips. Bay K8644, a Ca2+ channel agonist, did not modify Mg2+-induced relaxation in NE-stimulated strips, but significantly attenuated the relaxation in K+-stimulated strips in the order: -E greater than +E. The results suggest that Mg2+-induced relaxation of rat aorta is associated, at least in part, with the release of an endothelium-derived relaxant factor in receptor-mediated, but not in depolarisation-dependent contractions.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗