Biomedical subjects

M Tuncer

Publications and source records attributed to M Tuncer.

At least 109 records · Page 6Linked to original sources

PubMed1991

Role of prostanoids in the increased vascular responsiveness and delayed tachyphylaxis to serotonin in the kidney of spontaneously hypertensive rats.

The isolated and perfused kidney of the spontaneously hypertensive rat (SHR) exhibits an increased vascular reactivity and a delayed tachyphylaxis to serotonin (5-hydroxytryptamine) when compared with normotensive Wistar-Kyoto (WKY) rats. Experiments were designed to determine the involvement of products of cyclooxygenase in the augmented response and delayed tachyphylaxis to serotonin in the SHR kidney. Kidneys taken from male, 4-month-old SHR and WKY rats were studied in parallel and perfused with Tyrode's solution at constant, optimal flow rates. Vasoconstrictor responses were recorded as increases in perfusion pressure. The vasoconstrictor responses to serotonin, norepinephrine and angiotensin II were exaggerated in the SHR kidney compared with that of the WKY rat. Indomethacin did not affect the responsiveness to serotonin in the kidney of the SHR but increased the responses to the higher doses of the monoamine in the kidney of the WKY rats. Indomethacin accelerated the tachyphylaxis to serotonin in the SHR but delayed it in the WKY rats. Dazoxiben did not alter the responses to serotonin in the SHR. Responses to norepinephrine in the kidneys from both strains were not affected by indomethacin. The inhibitor of cyclooxygenase reduced the responses to angiotensin II in the kidneys from both hypertensive and normotensive animals. The basal and stimulated (serotonin, norepinephrine and angiotensin II) release of prostaglandins were measured by radioimmunoassay. The basal release of prostacyclin was lower, but that of thromboxane A2 higher, in the kidneys of SHR compared with those of WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed1990

N-acetylation phenotyping with sulphadimidine in a Turkish population.

The distribution of acetylator phenotypes was studied in 244 unrelated Turkish subjects. Sulphadimidine and its acetylated metabolite were measured in 6 h plasma and 0-6 h urine samples after an oral dose of 10 mg/kg. Subjects with 37.5% or less acetylsulphadimidine in plasma were regarded as slow acetylators and the others as rapid acetylators. The mean plasma concentration of acetylsulphadimidine was about 2.5-times lower in slow acetylators. Urinary excretion of total sulphadimidine (free + acetylated) was also significantly lower in slow acetylators compared to rapid acetylators. The frequency of slow acetylators was 60.7% in the population (95% confidence interval 54.3% to 66.8%). Sulphadimidine acetylation showed no variation due to sex, age, body weight or pre-existing disease.

Acetylation↗

PubMed1990

Dopamine receptor agonists, N,N-dipropyl-2-aminotetralin (TL-68) and 2-di-n-propylamino-4,7-dimethoxyindane (RDS-127) antagonize oxotremorine-induced tremors by antimuscarinic action in mice.

Central antimuscarinic actions of dopamine receptor agonists: N,N-dipropylaminotetrain (TL-68) and 2-di-n-propylamino-4,7-dimethoxyindane (RDS-127), were evaluated against oxotremorine-induced tremors in mice. Both TL-68 and RDS-127 inhibited the tremor intensity but were less potent than atropine.

Animals↗

PubMed1990

Sulphamethoxazole acetylation in fast and slow acetylators.

Acetylation of sulphamethoxazole was studied in 22 subjects previously phenotyped with sulphadimidine. Sulphamethoxazole and its acetylated metabolite were measured in 6 h plasma and 0-6 h urine samples. Percentage of plasma acetylated-sulphamethoxazole did not correlate with the percentage of urinary acetylated-sulphamethoxazole. There was also no correlation between the percentage of acetylated-sulphadimidine and percentage of acetylated-sulphamethoxazole in plasma. The finding suggest that the acetylation of sulphamethoxazole has no predictive value in determining acetylator status.

Acetylation↗

PubMed1988

Beta-adrenoceptor stimulating effects of phenylephrine and noradrenaline in the rat pulmonary vascular bed.

The effects of phenylephrine and noradrenaline have been investigated on the perfusion pressure of the rat isolated lung. Both drugs (0.3-30 micrograms) produced a dose-dependent decrease in perfusion pressure elevated by 20 mM KCl, which was reversed to a dose-dependent increase after addition of propranolol (1 x 10(-7) M) to the perfusion fluid. Increments due to both agonists in the presence of propranolol were antagonized by prazosin (1 x 10(-6) M). Propranolol, but not prazosin, elevated the basal perfusion pressure. The results indicate that phenylephrine and noradrenaline are more effective in stimulating beta-adrenoceptors than alpha-adrenoceptors in the rat pulmonary vascular bed and that beta-adrenoceptors may regulate the vascular tone of the rat pulmonary circulation.

Adrenergic beta-Agonists↗

PubMed1987

The subtype of serotonin (5-HT) receptors in the rat pulmonary artery.

Serotonin (5-HT) and some alpha-agonists induced a marked contraction of ring segments of the rat pulmonary artery. Phenylephrine and 5-HT caused maximum contractions in the artery amounting to 91% and 66%, respectively, of the maximum effect of noradrenaline. Clonidine failed to induce contractions in the artery. The alpha 1-adrenoceptor blocker prazosin (1 X 10(-6)M) and alpha 2-adrenoceptor blocker yohimbine (5 X 10(-7)M) did not antagonize 5-HT-induced contractions. However 5-HT2 receptor antagonists ketanserin (3 X 10(-9)-1 X 10(-7)M), mianserin (3 X 10(-9)-1 X 10(-7)M) and pizotifen (3 X 10(-9)-1 X 10(-7)M) competitively antagonized 5-HT-induced contractions in the tissue studied, whereas the antagonist methysergide (5 X 10(-10)-1 X 10(-7)M) caused a noncompetitive antagonism. The pA2 values for ketanserin (8.98), mianserin (9.1) and pizotifen (9.14) against 5-HT were not different from the values obtained in other tissues which were shown to contain 5-HT2 receptors. The results suggest that 5-HT receptors in rat main pulmonary artery are of the 5-HT2 subtype.

Animals↗

PubMed1986

Are there any presynaptic 5-HT receptors in frog atria?

The effect of 5-hydroxytryptamine (5-HT) on the stimulation-induced inotropic responses was investigated in the isolated frog atria and ventricles. 5-HT (1 X 10(-5)-2 X 10(-4) M) inhibited the contractile responses elicited by intramural nerve stimulation (INS) in atria. The inhibitory action of 5-HT was antagonized by raising the external Ca++ concentration. Pizotifen and methysergide (1 X 10(-6) M) antagonized the inhibitory action of 5-HT on high frequency INS responses. Higher concentrations of methysergide by itself depressed the responses to low frequency INS. Ketanserin, metoclopramide and phentolamine (1 X 10(-6) M) failed to antagonize the inhibitory action of 5-HT. The results suggest that the inhibitory effect of 5-HT in frog atria is mediated through a subtype of 5-HT receptors which is neither of 5-HT2 nor of "M" type but may correspond to the 5-HT1 subtype of serotoninergic receptors. In contrast with atria, 5-HT-induced inhibition of INS responses was not observed in frog ventricles.

Animals↗

PubMed1985

Acute leukemia in two patients with hemophilia.

A 10-year-old classic hemophiliac and 1.5-year-old child with hemophilia B who developed acute lymphocytic and acute myelomonocytic leukemia respectively are presented. No changes in coagulation status of the patients were observed. It is suggested that hemophiliacs should be regarded as "population at risk" for the development of leukemia.

Blood Coagulation Tests↗

PubMed1985

Receptor mechanisms for 5-hydroxytryptamine in isolated human umbilical artery and vein.

In order to characterize the 5-hydroxytryptamine (5-HT) receptors, the contractile effects of both 5-HT and alpha-adrenoceptor agonists were studied in helically-cut human umbilical artery and vein in the presence of different antagonists. Noradrenaline, phenylephrine and clonidine caused maximum contractions in vein amounting to only 9%, 14% and 11% of the maximum effect of 5-HT, respectively. The maximum effects of noradrenaline and phenylephrine in artery were only 18% and 29% of that of 5-HT. Clonidine failed to induce contractions in the artery. The alpha 1-adrenoceptor blocker, prazosin (1 X 10(-6) and 1 X 10(-5)M) did not antagonize 5-HT-induced contractions in the tissues studied. However, yohimbine, an alpha 2-adrenoceptor blocker, shifted the concentration-effect curves of the 5-HT to the right without any reduction in the maximum responses in both tissues. The pA2 values for yohimbine against 5-HT (6.46 and 6.72 in artery and vein, respectively) were different from the values for yohimbine against alpha 2-adrenoceptor agonists (8.2 and 8.6 against clonidine and M-7, respectively) in dog saphenous vein which contains postsynaptic alpha 2-adrenoceptors. 5-HT2 receptor antagonists, ketanserin (1 X 10(-7)-1 X 10(-6)M) and mianserin (1 X 10(-7)-1 X 10(-6)M) competitively antagonized 5-HT-induced contractions in both tissues. The pA2 values for ketanserin (7.89 and 7.86 in artery and vein, respectively) and mianserin (8.06 and 7.73 in artery and vein, respectively) were significantly lower than those obtained in other tissues which were shown to contain 5-HT2 receptors by the other authors. The results suggest that alpha-adrenoceptors play a minor role in 5-HT-induced contractions in both tissues. Yohimbine antagonized 5-HT action competitively, by blocking probably 5-HT receptors. The results also indicate that 5-HT receptors in human umbilical vessels are less sensitive to certain 5-HT2 antagonists than those of other tissues. A third subtype of 5-HT receptors different from the 5-HT1 and 5-HT2 receptors may be present in the human umbilical artery and vein.

Adrenergic alpha-Agonists↗

PubMed1985

Serotonin-induced contraction of canine saphenous vein: mediation by 5-HT1 receptors.

The action of serotonin (5-HT) on alpha 1- and alpha 2-adrenoceptors was investigated on the isolated dog saphenous vein strip. Prazosin (1 X 10(-6) and 1 X 10(-5) M), an alpha 1-adrenoceptor blocker, did not alter 5-HT-induced contractions. However, yohimbine (1 X 10(-6) and 1 X 10(-5) M), an alpha 2-adrenoceptor blocker, shifted the concentration-response curve of 5-HT to the right without any reduction in the maximum response. The pA2 value for yohimbine against 5-HT (7.61 +/- 0.28, mean +/- S.E.M.) is different from the value for yohimbine against clonidine (8.35 +/- 0.08) or M-7 (8.58 +/- 0.07), a substance which stimulates postsynaptic alpha 2-adrenoceptors. Mianserin (1 X 10(-8)-1 X 10(-6) M) and ketanserin (1 X 10(-7)-1 X 10(-5) M) antagonized 5-HT-induced contractions noncompetitively. The results suggest that yohimbine competitively antagonizes 5-HT action by blocking probably 5-HT1 receptors, independently from its alpha 2-adrenoceptor blocking effect.

Animals↗

PubMed1984

The interaction between metoclopramide and dopaminergic agonists at the level of sympathetic ganglion.

The interaction of metoclopramide and two dopaminergic agonists, dopamine and apomorphine, was investigated on ganglionic transmission at the superior cervical ganglion of the anaesthetized cat. Dopamine (100 micrograms, i.a.) and apomorphine (100 micrograms, i.a.) decreased the height of action potential induced by supramaximal preganglionic stimulation. Metoclopramide (3 mg/kg, i.v.) antagonized the inhibition caused by dopamine and apomorphine. But it did not alter the transmission block caused by hexamethonium (100 micrograms, i.a.) or noradrenaline (100 micrograms, i.a.). The results suggest that dopamine-induced inhibition of the ganglionic transmission is related to the activation of dopaminergic receptors of the ganglion cells.

Action Potentials↗

PubMed1984

Effects of pyridine and some of its derivatives on prostaglandin synthesis.

Effects of pyridine and some of its derivatives namely, nicotinic acid, nicotinyl alcohol, pyridinol carbamate, pyridoxine hydrochloride and pyridostigmine bromide were investigated on the release of a prostaglandin E2-like substance (PGE2-LS) from the isolated perfused rat heart. Furthermore, the effect of neostigmine bromide was also studied as a non-pyridine control compound. At 2 X 10(-5) M concentration, only pyridoxine hydrochloride stimulated the release of PGE2-LS significantly. At 2 X 10(-4) M concentration, pyridine, nicotinic acid and pyridinol carbamate were also found to be active in addition to pyridoxine hydrochloride. At 1 X 10(-3) M concentration, pyridine and all of its derivatives studied increased the release of PGE2-LS significantly. However, neostigmine bromide (1 X 10(-3) M) failed to exert any effect. Indomethacin, a prostaglandin synthetase inhibitor, reduced both the basal release (28%) and the release stimulated by pyridine and its derivatives at 1 X 10(-3) M concentration (more than 50%). These findings suggest that the active substance released is a prostaglandin. It is concluded that the PGE2-LS releasing effect of pyridine and its derivatives from isolated rat heart may be due to the action of the pyridine moiety of the molecules of the compounds studied.

Animals↗

PubMed1974