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Biomedical subjects

M Endoh

Publications and source records attributed to M Endoh.

At least 469 records · Page 26Linked to original sources
PubMed1980

Scleritis and IgA nephropathy.

Follow-up studies on 113 patients with various types of primary glomerular diseases were performed for one to 33 months to determine the clinical spectrum of primary glomerulonephritis. Of those studied, six patients exhibited scleritis. All of these six patients with scleritis were identified as having "IgA nephropathy." None of the patients other than those with IgA nephropathy showed scleritis during the study period. It is suggested that some autoimmune mechanisms similar to the manifestation of IgA nephropathy may be involved in the development of scleritis.

Adult↗
PubMed1979

Failure of dibutyryl and 8-bromo-cyclic GMP to mimic the antagonistic action of carbachol on the positive inotropic effects of sympathomimetic amines in the canine isolated ventricular myocardium.

Effects of carbachol, dbcGMP and 8-bromo-cyclic GMP on the positive inotropic actions of sympathomimetic amines and dbcAMP were studied on the canine isolated right ventricular myocardium. Carbachol alone did not substantially change the developed tension of the muscle, but did markedly shift the dose response curve for isoprenaline on the developed tension to the right and depressed the maximal response to the drug in a concentration dependent manner. The positive inotropic action of phenylephrine was affected by carbachol in the same manner as that of isoprenaline. DbcGMP in concentrations of 10(-3) M and higher produced a significant increase in the developed tension. The positive inotropic action of dbcGMP was partly inhibited by a beta-adrenoceptor blocking agent, pindolol. In the presence of dbcGMP, isoprenaline produced an action similar to that seen in the control experiment, but this action was not maintained on such a steady state level as in the control. This rapid decline of the effect of isoprenaline in the presence of dbcGMP was prevented by adding ascorbic acid to the organ bath. The positive inotropic actions of phenylephrine and of dbcAMP were not substantially affected by dbcGMP. 8-Bromo-cyclic GMP in a concentration of 10(-4) M did not change either the basal developed tension or the positive inotropic actions of noradrenaline and of isoprenaline. The present results indicate that these cyclic GMP derivatives are not able to mimic the antagonistic action of cholinergic stimulation on the positive inotropic action of adrenergic stimulation on the positive inotropic action of adrenergic stimulation on the canine ventricular myocardium.

Animals↗
PubMed1979

Correlation of cyclic AMP and cyclic GMP levels with changes in contractile force of dog ventricular myocardium during cholinergic antagonism of positive inotropic actions of histamine, glucagon, theophylline and papaverine.

On the dog isolated right ventricular muscle, experiments were carried out in order to elucidate the characteristics of the cholinergic antagonism against the positive inotropic action (PIA) induced via different subcellular mechanisms. The relationship between cyclic AMP and cyclic GMP levels, and contractile force during cholinergic antagonism was assessed. Carbachol (10 microM) by itself decreased only slightly the tension developed, but inhibited prominently the PIAs of isoprenaline, histamine, glucagon, theophylline and papaverine. The action of dibutyryl cyclic AMP was inhibited less than PIAs of other agents mentioned above. In contrast, carbachol did not affect the PIAs of calcium and g-strophanthin. The antagonism by carbachol of PIAs of isoprenaline, histamine, glucagon, theophylline and papaverine was accompanied by a reduction of the intracellular cyclic AMP level elevated previously by these agents, and by an elevation of the intracellular cyclic GMP level. A good correlation was found between changes in the tension developed, and cyclic AMP and cyclic GMP levels during the cholinergic antagonism of PIAs induced by these agents in the dog ventricular myocardium.

Animals↗
PubMed1978

Effects of calcium-antagonistic coronary vasodilators, nifedipine and verapamil, on ventricular automaticity of the dog.

In isolated, blood-perfused canine papillary muscles intra-arterial injection of calcium-antagonistic coronary vasodilators, nifedipine and verapamil, produced a dose-related decrease in force of contraction. The ventricular rate of about 40 beats/min was not significantly changed by nifedipine even in doses which profoundly decreased the force of contraction. Verapamil changed the ventricular rate in a biphasic manner, but the changes remained as small as about 10% of the basal rate in doses which markedly suppressed the force of contraction. Calcium chloride elicited an increase in force of contraction but depressed automaticity. The present results show that in response to nifedipine, verapamil and calcium ions, ventricular automaticity has characteristics different from those of the sinus node.

Animals↗
PubMed1978

Characterization of adrenoceptors mediating positive inotropic responses in the ventricular myocardium of the dog.

1 The pharmacological characteristics of adrenoceptors mediating the positive inotropic action in the dog heart were assessed by the use of blood-perfused papillary muscles and isolated strips of ventricular myocardium.2 On the blood-perfused papillary muscle driven at 2 Hz and in sinus node preparations, phenylephrine induced positive inotropic and chronotropic responses in the same dose range and was much less potent than isoprenaline. The dose-response curve for the chronotropic action of phenylephrine was parallel to that of isoprenaline, whilst the dose-response curve for the inotropic action of phenylephrine was less steep than that of isoprenaline.3 The infusion of pindolol, a beta-adrenoceptor blocking agent, at a rate of 1 mug/min, shifted the isoprenaline dose-response curves to the right, and to the same extent, in both papillary muscle and sinus node preparations. In contrast to isoprenaline, the antagonism of phenylephrine by pindolol was noncompetitive. Phentolamine did not affect the positive inotropic and chronotropic actions of phenylephrine.4 On isolated ventricular strips alpha-adrenoceptor blockade by 10(-6) M phentolamine did not affect dose-response curves to phenylephrine or dopamine. Pindolol shifted the dopamine dose-response curves to the right in a competitive manner and those of phenylephrine in a noncompetitive manner.5 On ventricular strips from reserpine-pretreated dogs phenylephrine and tyramine dose-response curves were shifted markedly to the right and downwards. Desipramine (10(-5) M) which enhanced the action of noradrenaline considerably reduced the myocardial responses of phenylephrine.6 Papaverine (10(-5) M) decreased the threshold concentration of phenylephrine required to stimulate the myocardium and shifted phenylephrine dose-response curves to the left.7 Raising the temperature from 32 degrees C to 37 degrees C shifted phenylephrine dose-response curves to the right; when the temperature was raised from 37 degrees C to 42 degrees C the affinity of the drug was not changed.8 Other alpha-adrenoceptor stimulants, methoxamine and clonidine, decreased the active tension of ventricular strips. The responses to noradrenaline and adrenaline (in the presence of pindolol; 3 x 10(-8) M) were not affected by phentolamine (10(-6) M).9 The results indicate that adrenoceptors mediating positive inotropic responses in the dog ventricle are of the beta-type and that post-synaptic alpha-adrenoceptors are not involved. Phenylephrine acts mainly by releasing noradrenaline from adrenergic nerve endings and partly by a weak direct action on beta-adrenoceptors.

Adrenergic beta-Antagonists↗
PubMed1977

Influence of temperature and frequency on the positive inotropic action of phenylephrine in the isolated rabbit papillary muscle.

On the isolated papillary muscle of the rabbit the maximal developed tension induced by phenylephrine bia alpha-adrenoceptors was not affected by changing the temperature, while the basal developed tension of the muscle was significantly increased or decreased by lowering the temperature from 37 degrees C to 32 degrees C or by raising it to 42 degrees C, respectively. When the temperature was lowered from 37 degrees C to 32 degrees C in the muscle stimulated at a frequency of 0.5 Hz, the dose-response curve for phenylephrine via alpha-adrenoceptors was shifted to the left (delta pD2-0.47), while that for phenylephrine via beta-adrenoceptors was also shifted to the left to a similar extent (delta pD2=0.43). When the temperature was raised from 37 degrees C to 42 degrees C, the dose-response curve for phenylephrine via alpha-adrenoceptors was markedly shifted to the right (delta pD2=1.58), whereas that via beta-adrenoceptors was not affected at all by this elevation of the temperature (delta pD2=0.04). The change of the stimulation frequency affected chiefly the intrinsic activity of phenylephrine but not the affinity of the drug for alpha-adrenoceptors expressed as the pD2-value.

Animals↗
PubMed1976

Relationship between the level of cAMP and the contractile force under stimulation of alpha- and beta-adrenoceptors by phenylephrine in the isolated rabbit papillary muscle.

The time course of changes of the level of 3',5'-cyclic AMP (cAMP) and of the tension developed under stimulation of alpha- and beta-adrenoceptors by phenylephrine was investigated in the isolated rabbit papillary muscle. Furthermore the dose-response relationships for increases of cAMP and of developed tension elicited by phenylephrine were determined. 1. A submaximally effective concentration of phenylephrine (10(-5) M) increased significantly the level of cAMP of the papillary muscle at 15 and 30 s by 45 and 36% respectively; the level of cAMP returned to the control value at 60 s after the administration. The developed tension increased significantly not before 45 s and reached its maximal level at 180 s. 2. When alpha-adrenoceptors were blocked by phentolamine (10(-6) M), the positive inotropic effect of phenylephrine was decreased significantly but the increase of cAMP induced by phenylephrine was not reduced. In the presence of phentolamine the increase of cAMP induced by phenylephrine lasted longer than in the control experiments. 3. The effects of phenylephrine (10(-5) M) both on the level of cAMP and the developed tension mediated via stimulation of beta-adrenoceptors in the presence of phentolamine were enhanced by the phosphodiesterase inhibitor papaverine throughout the course of responses. 4. Phenylephrine produced an increase in developed tension as well as in cAMP. The corresponding dose-response curves run parallel to each other but differed by about 1.5 log units whereby the developed tension was evoked by lower concentrations. Phentolamine (10(-6) M) shifted the curve for the positive inotropic action by about 1.5 log units but did not affect that for increase in cAMP. Therefore, in the presence of the alpha-adrenolytic drug phentolamine the difference between both curves became smaller so that both curves were superimposed. Papaverine (10(-5) M) shifted the whole curve for cAMP upwards and enhanced the maximal contractile response to phenylephrine mediated by stimulation of beta-adrenoceptors. 5. The present results indicate that the positive inotropic action of phenylephrine in lower concentrations (less than 10(-5) M) induced by stimulation of alpha-adrenoceptors is independent of the level of cAMP. The positive inotropic action of the higher concentrations of phenylephrine induced via stimulation of beta-adrenoceptors was preceded by an accumulation of cAMP; the inhibition of the cAMP phosphodiesterase activity by papaverine enhanced the actions of phenylephrine both on the level of cAMP and on the contractile force.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1976

alpha-Adrenoceptors in the ventricular myocardium: clonidine, naphazoline and methoxamine as partial alpha-agonists exerting a competitive dualism in action to phenylephrine.

Tha alpha-sympathomimetic agonists, clonidine, naphazoline, methoxamine, oxymetazoline and phenylephrine were used to further characterize the alpha-adrenoceptors mediating the positive inotropic effect in the isolated papillary muscle of the rabbit heart. The maximal inotropic effects of these amines were compared with the effect of isoprenaline and it was examined whether or not these amines compete for alpha-adrenoceptors. On the papillary muscle stimulated at 0.5 Hz, phenylephrine showed a high affinity (pD2 value=6.13) and produced the most pronounced intrinsic activity of the alpha-sympathomimetic amines. Therefore, the intrinsic activity of phenylephrine, in the presence of prindolol (3 X 10(-8) M), was used for comparison with those of the other alpha-agonists. Clonidine caused a positive inotropic effect: the intrinsic activity amounted to 0.32 of that of phenylephrine; the affinity was the highest among the amines tested (pD2 value=6.46); its effect was inhibited by 10(-6) M phentolamine. The affinity and the intrinsic activity of naphazoline were slightly lower than those of clonidine. Methoxamine showed a relatively high intrinsic activity (0.56) but the lowest affinity (4.68). Oxymetazoline did not cause any positive inotropic effect. Clonidine, naphazoline and oxymetazoline antagonized the positive inotropic effect of phenylephrine, mediated via the alpha-adrenocaptors in the presence of 3 X 10(-8) M prindolol, in a competitive manner. This observation suggests that these alpha-sympathomimetic amines compete with phenylephrine for the same receptor site. Thus the present results provide additional evidence for alpha-adrenoceptors mediating the positive inotropic actions of sympathomimetic amines in the rabbit papillary muscle.

Adrenergic alpha-Antagonists↗