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Biomedical subjects

M Tuncer

Publications and source records attributed to M Tuncer.

At least 91 records · Page 5Linked to original sources
PubMed1996

5-HT1-like receptor-mediated contraction in the human internal mammary artery.

We wished to characterize the 5-hydroxytryptamine (5-HT) receptors mediating vasoconstriction in the human internal mammary artery (IMA). Segments of the IMA obtained from patients undergoing coronary by-pass surgery were suspended in an organ bath and exposed to 5-HT and sumatriptan (SUM), a 5-HT1-like receptor agonist, in the presence and absence of potassium chloride (KCl) and angiotensin II. 5-HT induced concentration-dependent contractions in all quiescent and pre-contracted preparations. SUM induced small contractions in 70% of quiescent IMA rings, whereas it elicited marked and concentration-dependent contractions in all of the preparations given a moderate tone by a threshold concentration of KCl and angiotensin II. The efficacy of SUM was higher in precontracted arteries. Concentration-effect curves (CEC) of 5-HT and SUM were not affected by the 5-HT3-receptor antagonist tropisetron (1 microM). The nonselective antagonist, methiothepin (30 nM), shifted the CEC of SUM to the right. 5-HT2A-receptor antagonist, ketanserin (1 microM) inhibited responses to 5-HT, whereas it affected only the responses to the smaller concentrations of SUM. When methiothepin (30 nM) was applied in the presence of ketanserin (1 microM), a further inhibition in the responses to 5-HT was observed. These results suggest that 5-HT1-like receptors mediate the contractile action of SUM and contribute to that of 5-HT in IMA.

Adult↗
PubMed1995

5-HT1-like and 5-HT2A receptors mediate 5-hydroxytryptamine-induced contraction of rabbit isolated mesenteric artery.

The contractions induced by 5-hydroxytryptamine (5-HT) and the 5-HT1-like receptor agonist, sumatriptan, were investigated in the open ring preparations of rabbit mesenteric artery in order to characterize the 5-HT receptors. 5-HT induced concentration-dependent contractions. Sumatriptan did not induce any contraction of unstimulated rings, whereas it elicited concentration-dependent contractions in preparations given a moderate tone by a threshold concentration of prostaglandin F2 alpha (PGF2 alpha). Pargyline, cocaine or normetanephrine were without significant effect on the contractions induced by 5-HT and sumatripan. The 5-HT concentration-effect curve was clearly biphasic. Methiothepin (0.01 microM) shifted the both phases of the concentration-effect curve to the right. Ketanserin (0.1 microM) shifted the second, low affinity, phase and prazosin did not alter concentration-effect curve to 5-HT. The sumatriptan concentration-effect curve was shifted by methiothepin (0.01 microM) to the right (pKB = 9.19) but not by ketanserin (1 microM). Concentration-effect curves to 5-HT and sumatriptan were not affected by the 5-HT3 receptor antagonist tropisetron (1 microM). These results suggest that 5-HT1-like type receptors are responsible for the first phase of 5-HT-induced contraction and 5-HT2A receptor for the second phase, in rabbit mesenteric artery. Sumatriptan-induced contractions appear to be mediated by 5-HT1-like type receptors in this artery. These results also suggest that this kind of amplification may be a common feature of vascular 5-HT1-like type receptor as has been shown in other vascular segments such as rabbit femoral, iliac and renal arteries, and guinea-pig iliac artery.

Adrenergic alpha-Agonists↗
PubMed1995

The effect of indomethacin on cyclosporin A- and its solvent-induced inhibition of endothelium-dependent relaxation and the drug-induced contraction of rabbit isolated arteries.

1. In the isolated rabbit arteries, the effects of intravenous cyclosporin A preparation (Sandimmun) and its solvent (Cremophor-EL) on acetylcholine-induced endothelium-dependent relaxation were investigated in the absence and presence of indomethacin (10(-5) M), a cyclooxygenase inhibitor. 2. The effect of indomethacin on the drug- and solvent-induced contraction of superior mesenteric artery was also evaluated. 3. The inhibitory effects of cyclosporin and the solvent on endothelium-dependent relaxations were decreased by indomethacin. The direct contractions produced by the drug and the solvent in rabbit mesenteric artery were inhibited by indomethacin.

Acetylcholine↗
PubMed1995

The effects of PGE2 and PGF2 alpha on rhythmic contractions of sphincter of Oddi.

1. Spontaneous rhythmic activity observed in some of the guinea-pig sphincter of Oddi preparations was completely abolished by PGE2 (10(-8) M) but not altered by PGF2 alpha (10(-6) M). 2. Indomethacin (10(-5) M), a cyclooxygenase inhibitor, elicited long-lasting rhythmic contractions in 50% of the preparations tested, which did not show any spontaneous activity. PGE2 (10(-8) M) completely inhibited, however PGF2 alpha (10(-8)-10(-6) M) did not change the rhythmic contractions induced by indomethacin. 3. Both initial phasic contraction and the frequency and amplitude of peristaltic waves induced by ACh (10(-3) M) were increased by indomethacin (10(-5) M), decreased by PGE2 (10(-7) M) and not altered by PGF2 alpha (10(-7) M).

Acetylcholine↗
PubMed1995

Amplification of responses to sumatriptan by various agonists in rabbit isolated iliac artery.

Rabbit iliac arteries (IA) were almost unresponsive to the serotonin (5-HT1-like) receptor agonist sumatriptan under control conditions, whereas this agent elicited concentration-dependent contractions in IA rings given a moderate tone by threshold concentrations (EC10-EC20) of prostaglandin F2 alpha (PGF2 alpha), angiotensin II (AII), histamine, norepinephrine (NE), phenylephrine (PE), or potassium chloride. These results suggest that 5-HT1-like receptors are uncovered not only by histamine or thromboxane/prostaglandin receptor agonists, as shown in rabbit renal and femoral arteries, but also by various agonists in rabbit IA as shown in this study.

Angiotensin II↗
PubMed1995

Effect of nitrovasodilators on the rhythmic contractions of guinea-pig isolated sphincter of Oddi.

The effects of amyl nitrite (CAS 8017-89-8) isosorbide dinitrate (CAS 87-33-2) and sodium nitroprusside (CAS 14402-89-2), on the acetylcholine-induced tachyrhythmia (greater than 9 waves/min) were investigated in the isolated guinea-pig sphincter of Oddi. Acetylcholine (10(-3) mol/l) produced an initial rapid rise in tension, the peak being followed by a gradual decrease associated with the initiation of the peristaltic waves. Nitrovasodilators significantly decreased the initial response to acetylcholine. Methylene blue (5 x 10(-5) mol/l), a soluble guanylate cyclase inhibitor, increased the tonic response to acetylcholine and reversed the inhibition caused by nitrovasodilators. The frequency and amplitude of peristaltic waves were decreased by nitrovasodilators. Methylene blue significantly increased both the frequency and amplitude of peristaltic waves, however, it did not reverse the inhibition caused by nitrovasodilators tested. Results suggest that nitrates decrease the acetylcholine-induced contraction and peristaltism of isolated guinea-pig sphincter of Oddi and NO released by acetylcholine may partially suppress its own tonic contractile response.

Acetylcholine↗
PubMed1994

The action of amyl nitrite and isosorbide dinitrate on the contractility of sphincter of Oddi of guinea-pigs.

1. This study was designed to investigate whether relaxation of isolated guinea-pig sphincter of Oddi preparation by nitrates is mediated by guanylate cyclase activation indirectly by nitric oxide (NO), as in vascular tissues. 2. Sodium nitroprusside, isosorbide dinitrate and amyl nitrite induced dose-dependent relaxations of Oddi's sphincter precontracted by potassium chloride (150 mM). Methylene blue (5 x 10(-5) M), an inhibitor of guanylate cyclase, did not significantly inhibit the relaxations caused by nitrovasodilators. 3. Unlike potassium chloride, acetylcholine (10(-7) - 10(-3) M) induced unsustained contractions which were significantly increased by methylene blue. NG-monomethyl-L-arginine (L-NMMA; 4 x 10(-4) M), an inhibitor of NO biosynthesis, also increased the contractile response to acetylcholine. 4. These results suggest that another mechanism rather than inhibition of guanylate cyclase is involved in the nitrovasodilators-induced relaxations and that acetylcholine releases a relaxing factor, possibly NO, that may modulate its own contraction in this preparation.

Acetylcholine↗
PubMed1993

Serotonin releases a vasoconstrictor prostanoid in the kidney of the aging spontaneously hypertensive rat.

The isolated and perfused kidney of the spontaneously hypertensive rat (SHR) exhibits an increased vascular reactivity to serotonin when compared to normotensive Wistar-Kyoto (WKY) rats. Experiments were designed to determine the involvement of a prostanoid constricting factor in the augmented response to serotonin in the SHR kidney. Kidneys taken from male (12 months) SHR and WKY rats were studied in parallel and perfused with Tyrode's solution at constant, optimal flow rates. Vasoconstrictor response were recorded as increases in perfusion pressure. The dose-response curves to serotonin obtained in the SHR were shifted to the left compared to the WKY. Indomethacin decreased the responses to the smaller doses of serotonin in the SHR, but increased those to the higher doses of the monoamine in the WKY. The responsiveness to the monoamine was no longer significantly different in the two strains in the presence of the inhibitor of cyclooxygenase. Dazoxiben, an inhibitor of thromboxane synthetase, did not alter the responses to serotonin in either the WKY and SHR kidneys. These experiments suggest that a prostanoid, but not thromboxane A2, may play a role in the augmented response to serotonin in the kidney of aged SHR.

Aging↗
PubMed1993

Response to the endothelium-dependent vasodilator acetylcholine in perfused kidneys of normotensive and spontaneously hypertensive rats.

The possible role of endothelium-derived relaxing factor (EDRF) was investigated in resistance vessels of the kidney obtained from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Kidneys were studied in parallel and perfused with Tyrode's solution at constant optimal flow rates. In the presence of indomethacin, during vasoconstriction (increase in perfusion pressure) produced by prostaglandin F2 alpha, acetylcholine caused a graded dilatation (pressure fall) that was greater in kidneys of WKY than of SHR. Methylene blue and hydroquinone, but not oxyhemoglobin, inhibited the decreases in perfusion pressure induced by acetylcholine, but not those by papaverine. The results suggest that part of the renal vasodilatation induced by acetylcholine is mediated by endothelium-derived relaxing factor, and that the response is impaired in the resistance vessels of the hypertensive rat kidney.

Acetylcholine↗
PubMed1992

Actions of cyclosporin A preparation and Cremophor-EL in rabbit mesenteric artery and thoracic aorta in vitro.

1. We studied the in vitro and direct effects of intravenous cyclosporin A preparation (Sandimmun) and its solvent (Cremophor-EL) on acetylcholine-induced endothelium-dependent relaxation, phenylephrine-induced contraction and drug-induced contraction of rabbit thoracic aorta and superior mesenteric artery segments. 2. At the lower concentration (5 micrograms/ml), cyclosporin A preparation inhibited endothelium-dependent relaxation of the superior mesenteric artery but not of the thoracic aorta. At this concentration cyclosporin A preparation augmented phenylephrine-induced contraction in both segments but by more in the superior mesenteric artery, and induced a slow increase in the tone of isolated superior mesenteric artery and thoracic aortic rings, which was greater in magnitude in the superior mesenteric artery than in the thoracic aorta. 3. Acetylcholine-induced endothelium-dependent relaxation was inhibited by cyclosporin A preparation (50 micrograms/ml) in both arteries but to a greater extent in the superior mesenteric artery. 4. The solvent of the intravenous cyclosporin A preparation (Cremophor-EL) in concentrations corresponding to those of the drug caused less inhibitory effects than cyclosporin A preparation on acetylcholine-induced endothelium-dependent relaxation, had comparable effects on phenylephrine-induced contraction, and produced similar contractions of both arteries. 5. The results indicate that Cremophor-EL may contribute to the inhibitory action of cyclosporin A preparation on acetylcholine-induced endothelium-dependent relaxation in the superior mesenteric artery, but is fully responsible for the smooth-muscle-contracting effect and the potentiation of phenylephrine-induced contraction in both arteries.

Acetylcholine↗
PubMed1991

Antiplatelet antibodies in childhood idiopathic thrombocytopenic purpura.

Antiplatelet antibodies were shown by the Handin and Stossel method in the sera of all 103 patients with acute idiopathic thrombocytopenic purpura (ITP) and in 100 cases following recovery from it. These antibodies were also shown in the sera of all 46 patients with chronic ITP and 32 cases after recovery. The decrease in level of antiplatelet antibodies was significant in all these children following recovery (P less than 0.001 for acute ITP, P less than 0.05 for chronic ITP). Antiplatelet antibodies could be determined in 67 acute and 21 chronic ITP cases in thrombocytopenic phase and following recovery, which showed very significant decreases in levels in each case in a later period. Antiplatelet antibody levels corresponding to the thrombocytopenic phase and recovery in acute and chronic ITP were significantly higher than normal and thrombocytopenic control values (P less than 0.001 for each).

Acute Disease↗