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Biomedical subjects

V Bauer

Publications and source records attributed to V Bauer.

At least 73 records · Page 4Linked to original sources

Extrarenal angiomyolipoma.

A case of angiomyolipoma arising in the anterior abdominal wall is reported and compared with other reported cases of extrarenal angiomyolipoma. None of the patients had tuberous sclerosis and no recurrence was noted following simple excision.

Female↗

Non-cholinergic, non-adrenergic responses to nerve stimulation of different regions of the guinea-pig small intestine.

Non-cholinergic, non-adrenergic responses to nerve stimulation recorded from smooth muscles of the guinea-pig duodenum, jejunum, proximal and terminal ileum were investigated in an attempt to characterize these responses. In the presence of atropine (1-2 mumol X l-1) and guanethidine (10 mumol X l-1) coaxial stimulation induced in all regions of the guinea-pig small intestine an initial relaxation (primary relaxation) upon which contraction (primary contraction) appeared, followed by rebound contraction. Noradrenaline decreased the cholinergic smooth muscle twitches, predominantly at low stimulation frequencies, and had a similar effect on the non-cholinergic, non-adrenergic primary relaxation, primary and rebound contractions. ATP decreased the smooth muscle twitches; however, this agent had only a transient influence on the non-cholinergic, non-adrenergic responses of muscle (tension and membrane potential) to single stimuli. With higher stimulus frequencies ATP increased the primary relaxation and decreased the contraction phases. ATP also inhibited the post-tetanic inhibition induced by non-cholinergic, non-adrenergic nerve stimulation. In most of the muscle cells of the guinea-pig proximal and terminal ileum the non-cholinergic, non-adrenergic nerve stimulation generated i.j.p.s., while about 15-20% of the cells responded with e.j.p.s. During long-lasting stimulation (10s) the i.j.p.s were sometimes "interrupted" by action potentials or by a gradual depolarization of the membrane. The i.j.p.s were followed by a marked rebound depolarization accompanying the action potentials. Those cells which generated i.j.p.s in response to field stimulation, were depolarized by ATP, while those cells, which generated e.j.p.s, were hyperpolarized by ATP. A reduction in the concentration of extracellular sodium chloride decreased both the primary and rebound contractions; the primary contraction was, however, more sensitive than was the rebound contraction. Theophylline increased the primary and rebound contractions with no marked influence on the primary relaxation, lowered the action potential threshold, increased the rebound depolarization and did not markedly influence the i.j.p.s. Quinidine enhanced the primary relaxation and inhibited the primary contraction in a concentration-dependent manner. Inhibition of the rebound contraction by quinidine was slight (less than 50%). The present results demonstrate that primary relaxation, primary and rebound contractions are associated with i.j.p.s and e.j.p.s, and rebound depolarization with action potentials, respectively; they are typical responses of various regions of the guinea-pig small intestine to activation of inhibitory and excitatory non-cholinergic, non-adrenergic nerves. The P1 and P2 receptors, proposed by Burnstock (1975), probably do not mediate the non-cholinergic, nonadrenergic postsynaptic responses of the guinea-pig small intestine...

Adenosine Triphosphate↗

Role of Ca2+ in non-cholinergic, non-adrenergic responses to nerve stimulation of the guinea-pig small intestine.

The effects of calcium channel blockers (D-600, verapamil), sodium nitroprusside, papaverine, indomethacin, local anaesthetics and blockade of sodium pump activity on the non-cholinergic, non-adrenergic transmission in the guinea-pig duodenum, jejunum, proximal and terminal ileum were analysed in the presence of atropine and guanethidine. A decrease of the extracellular Ca2+ concentration inhibited the primary and rebound contractions but only in Ca2+ -free solution was the primary relaxation diminished. D-600, verapamil, sodium nitroprusside and papaverine inhibited both the primary and rebound contractions to the same degree and their effects on the primary relaxation were less pronounced than on the contractions. Indomethacin dissolved in alkaline solution did not depress the non-cholinergic, non-adrenergic responses in any region of the small intestine, whereas indomethacin dissolved in ethanol antagonized both the primary and rebound contractions in the muscles. Local anaesthetics (procaine, trimecaine) in low concentrations inhibited only the primary contraction. Higher concentrations also inhibited both the rebound contraction and primary relaxation. Procaine in low concentrations did not markedly affect the non-cholinergic, non-adrenergic i.j.p.s and e.j.p.s, but did block the action potentials induced by e.j.p.s. Our findings indicate that the primary relaxation, and primary and rebound contractions are probably induced by different mechanisms and are not mediated by ATP. We confirmed that prostaglandins did not participate in the generation of the rebound contraction.

Adenosine Triphosphate↗

Distribution and types of adrenoceptors in the guinea-pig ileum: the action of alpha- and beta-adrenoceptor blocking agents.

1 Transmurally stimulated segments of the guinea-pig ileum have been used to analyse the different adrenoceptors in the terminal (0 to 3 cm) and the proximal (> 50 cm from the ileocaecal valve) ileum.2 The prejunctional adrenoceptors (located on the final, cholinergic, motor nerve terminals) and postjunctional adrenoceptors (located on the smooth muscle membrane) have been characterized according to their sensitivity to alpha- and beta-agonists and antagonists.3 Phentolamine, phenoxybenzamine and yohimbine, in concentrations of 0.1 muM, transiently enhanced (up to 10%) the twitch response. At higher concentrations all the alpha- and beta-antagonists studied depressed the neurogenic twitches and relaxed the smooth muscle.4 The twitch-inhibitory effects of adrenoceptor agonists (noradrenaline, adrenaline and ephedrine) were not antagonized by phenoxybenzamine (0.1, 0.5 and 1 muM), carbidine (0.5, 1 and 5 muM) and propranolol (0.5, 1 and 5 muM); however, they were depressed by phentolamine (0.1, 0.5, 1.25 and 5 muM) and yohimbine (0.25, 0.5 and 5 muM).5 The smooth muscle contractions induced by noradrenaline and adrenaline in the terminal ileum and by phenylephrine in both the terminal and proximal ileum were antagonized by phenoxybenzamine, carbidine and phentolamine but were not influenced by yohimbine and propranolol.6 The smooth muscle relaxations of the proximal ileum induced by noradrenaline, adrenaline and ephedrine were inhibited by yohimbine, phentolamine, carbidine and phenoxybenzamine, and the isoprenaline-induced relaxation was antagonized by propranolol.7 All the agonists studied, except phenylephrine, elicited relaxations of the acetylcholine-induced sustained contraction of both proximal and terminal ileum. The relaxation induced by isoprenaline was antagonized by propranolol, and the effects of noradrenaline and ephedrine by yohimbine.8 It is concluded that in the guinea-pig ileum there are postsynaptic beta-adrenoceptors and at least two types of alpha-adrenoceptors: alpha(1)-excitatory postjunctional adrenoceptors activated by phenylephrine, noradrenaline and adrenaline and antagonized by phenoxybenzamine, carbidine and phentolamine; alpha(2)-inhibitory prejunctional adrenoceptors activated by ephedrine, noradrenaline and adrenaline and inhibited by yohimbine and phentolamine. The inhibitory postjunctional alpha-adrenoceptors are more close to the alpha(2)-adrenoceptors, since they were stimulated predominantly by ephedrine and noradrenaline and inhibited by yohimbine.9 It has been shown that all alpha-adrenoceptor subtypes are to be found at every distance (0 to 70 cm) from the ileocaecal valve and that they can be activated in the resting or in the acetylcholine-contracted states.

Adrenergic alpha-Agonists↗

Homogeneous and non-homogeneous distribution of inhibitory and excitatory adrenoceptors in the longitudinal muscle of the guinea-pig ileum.

1 The effects of adrenoceptor agonists and antagonists on spontaneous and evoked membrane activities of longitudinal muscle cells from different parts of the guinea-pig ileum were observed, using microelectrode methods.2 Isoprenaline inhibited the generation of spikes in cells in the terminal (0-3 cm from the ileocaecal valve) and proximal (more than 50 cm from the ileocaecal valve) regions of the ileum, with no change on the membrane potential and ionic conductance of the membrane. These actions of isoprenaline were abolished by propranolol.3 Noradrenaline and phenylephrine depolarized the membrane and increased both the spike frequency and ionic conductance of cell membranes of the terminal ileum, whereas noradrenaline and clonidine hyperpolarized the membrane, increased the ionic conductance of the membrane and inhibited the spontaneously generated spikes from cells of the proximal ileum. The excitatory effect of phenylephrine in the cells of the proximal ileum and the inhibitory effect of clonidine on cells of the terminal ileum were less pronounced.4 The excitatory actions of noradrenaline or phenylephrine were antagonized by prazosin and phentolamine, but not by yohimbine, whereas the inhibitory actions of noradrenaline or clonidine were antagonized by yohimbine and phentolamine but not by prazosin.5 The cholinergic e.j.ps evoked by field stimulation to the tissue were not affected by isoprenaline or phenyleprine but were inhibited by noradrenaline and clonidine, in both the terminal and proximal regions of the ileum. These actions of noradrenaline and clonidine were antagonized by yohimbine but not by prazosin.6 The results indicate that in the myenteric plexus and longitudinal muscle tissues of the guinea-pig ileum there are prejunctional inhibitory (alpha(2)), postjunctional inhibitory (alpha(2) and beta) and postjunctional excitatory (alpha(1)) adrenoceptors. The homogeneous distributions of prejunctional alpha(2)- and postjunctional beta-adrenoceptors in the ileum are responsible for inhibitions of cholinergic excitatory junction potentials (e.j.ps) and spontaneous spike activities, respectively. The density of distribution of the postjunctional alpha(1)-adrenoceptors is higher in the terminal than in the proximal regions, and these distributions are reversed in the case of the postjunctional alpha(2)-adrenoceptors. The postjunctional alpha(1)-adrenoceptors are probably responsible for the membrane depolarization and alpha(2)-adrenoceptors for the hyperpolarization induced by catecholamines.

Animals↗

Evidence for non-cholinergic, non-adrenergic transmission in the guinea-pig ileum.

To elucidate further the innervation of the longitudinal and circular muscle cells of the guinea-pig ileum, junction potentials elicited by field stimulation were recorded from both muscle layers in the presence and absence of atropine (1-2 muM) with guanethidine (10 muM) at 36 degrees C.1. In longitudinal muscle cells, a single stimulus elicited an atropine-sensitive transient depolarization (cholinergic e.j.p.), whereas in circular muscle cells, a transient hyperpolarization (non-cholinergic non-adrenergic i.j.p.) was elicited. With stimulation of nerves in the presence of atropine and guanethidine, responses of circular muscle cells to nerve stimulation were preserved while the longitudinal muscle cells generated depolarization (non-ch., non-adr. e.j.p.), hyperpolarization (non-ch., non-adr. i.j.p.) or both depolarization and subsequent hyperpolarization. These potential changes ceased with application of TTX or excess Mg(2+).2. The latency for junction potentials recorded from longitudinal muscles after field stimulation was in the following order; non-ch., non-adr. e.j.p. < cholinergic e.j.p. < non-ch., non-adr. i.j.p. The cholinergic e.j.p.s had a lower, and non-ch., non-adr. i.j.p.s a higher threshold.3. At low frequencies of stimulation (below 1 Hz) amplitudes of successively generated cholinergic e.j.p.s and non-ch., non-adr. i.j.p.s were gradually reduced, but at higher frequencies (2-20 Hz) of stimulation they were summated. The amplitudes of non-ch., non-adr. e.j.p.s were, however, not affected at low frequencies of stimulation (up to 0.5 Hz) and were summated at higher frequencies (over 1 Hz) of stimulation.4. Reversal potentials for non-ch., non-adr. e.j.p.s and i.j.p.s estimated from the amplitude of junction potentials and membrane potential were -27 and -80 mV, respectively. The reversal potential for non-ch., non-adr. e.j.p.s was higher (more negative) than that for cholinergic e.j.p.s5. Generation of i.j.p.s in longitudinal muscle cells elicited by repetitive stimulation was followed by a rebound depolarization on which was superimposed a burst of spikes. During repetitive stimulation, the amplitude of hyperpolarization was gradually reduced but the rebound depolarization and spike discharge were enhanced. Thus, while the rebound depolarization was related to the amplitude of the preceding hyperpolarization it was more related to the duration of the stimulation.6. Therefore longitudinal muscles of the guinea-pig ileum show evidence of having in addition to cholinergic and adrenergic innervation, both excitatory and inhibitory non-ch., non-adr. innervation. In the longitudinal muscle layer of the ileum, the non-ch., non-adr. excitatory fibres are more densely distributed in the terminal rather than in the proximal region, while in the case of non-ch., non-adr. inhibitory fibres, the distribution is reversed. Circular muscle cells are, however, homogenously innervated by non-ch., non-adr. inhibitory nerves.

Adrenergic Fibers↗

The nature of non-cholinergic, non-adrenergic transmission in longitudinal and circular muscles of the guinea-pig ileum.

1. The nature of the non-cholinergic, non-adrenergic (non-ch., non-adr.) excitatory and inhibitory transmission in the longitudinal and circular muscle layers of the guinea-pig ileum was investigated, and the effects of various agents on the junction potentials were observed using the micro-electrode method.2. In longitudinal muscle cells, ATP (3 x 10(-5)-10(-4) M) and adenosine (10(-5)-10(-4) M) depolarized the membrane, decreased the input resistance, increased the spike activity and abolished the generation of cholinergic excitatory junction potentials (e.j.p.s).3. In the presence of atropine (10(-6) M) with guanethidine (10(-5) M), field stimulation evoked three different types of the response (non-ch., non-adr. e.j.p.s, i.j.p.s (inhibitory junction potentials) or both) from cells of the longitudinal muscle layers, and only one type of the response (non-ch., non-adr. i.j.p.s) from cells of the circular muscle layer. In the following experiments atropine and guanethidine were present in the bathing fluid for at least 20 min.4. In some longitudinal muscle cells (non-ch., non-adr. i.j.p. type), ATP (5 x 10(-6)-10(-3) M) and adenosine (10(-5)-3 x 10(-5) M) depolarized the membrane, while in other cells (non-ch., non-adr. e.j.p. type), ATP (10(-5)-10(-4) M) and adenosine (10(-5)-3 x 10(-5) M) hyperpolarized the membrane and further increases in the concentration of ATP (10(-3) M) resulted in a depolarization of the membrane.5. Apamin (10(-7)-3 x 10(-6) M) inhibited the generation of non-ch., non-adr. i.j.p.s in both longitudinal and circular muscle cells, while this agent had no effect on the non-ch., non-adr. e.j.p.s. As a consequence, in some cells of the longitudinal muscle layer (non-ch., non-adr. e.j.p. and i.j.p. type) the amplitude of e.j.p.s was enhanced in the presence of apamin. TEA (5 x 10(-3)-1.5 x 10(-2) M) suppressed the after-hyperpolarization of the spike and i.j.p.s recorded from both muscle layers, whereas the duration and amplitudes of cholinergic and non-ch., non-adr. e.j.p.s were enhanced.6. Vasoactive intestinal polypeptide (VIP; 10(-8)-10(-7) M) had no effect on the membrane potential and junction potentials of longitudinal and circular muscle layers.7. Substance P (SP; 10(-8)-10(-7) M) depolarized the membrane of cells of the longitudinal layer (non-ch., non-adr. e.j.p. type), while this agent had no effect on cells of longitudinal (non-ch., non-adr. i.j.p. type) and circular muscle layers. SP suppressed the generation of non-ch., non-adr. e.j.p.s but had no effect on i.j.p.s. Generation of non-ch., non-adr. e.j.p.s was not restored under conditions of repolarization of the membrane to the resting level by application of inward current.8. Bradykinin (BK; 10(-8)-10(-5) M) hyperpolarized the membrane and suppressed the generation of i.j.p.s in the cells of longitudinal (non-ch., non-adr. i.j.p. type) and circular muscle layers. However, when the membrane potential was displaced to the control level by outward current in the presence of BK, field stimulation evoked the i.j.p. In cells of non-ch., non-adr. e.j.p. type of the longitudinal muscle layer, BK depolarized the membrane, increased the spike activity, generated slow waves and blocked the generation of non-ch., non-adr. e.j.p.s. Displacement of the membrane potential to the control level by inward current did not restore the non-ch., non-adr. e.j.p.s.9. These results suggest that in the guinea-pig ileum ATP and adenosine probably do not contribute to the generation of non-ch., non-adr. e.j.p.s and i.j.p.s, as transmitter substances. The actions of other possible candidates such as SP and BK, are discussed.

Action Potentials↗

Distribution and types of adrenoceptors in the guinea-pig ileum: the action of alpha- and beta-adrenoceptor agonists.

1 Segments of guinea-pig ileum and the myenteric plexus-longitudinal smooth muscle preparation were used for a study of the actions of adrenaline, noradrenaline, isoprenaline, ephedrine and phenylephrine on the responses of coaxially stimulated ileum at different distances from the ileocaecal valve.2 The responses of the ileum to electrical stimulation were suppressed by adrenaline, nonadrenaline and ephedrine, while phenylephrine and isoprenaline inhibited them only partially.3 The twitch inhibition elicited by these adrenoceptor agonists was the same at all distances from the ileocaecal valve. There was no significant difference between their cumulative and non-cumulative concentration-response curves.4 Smooth muscle relaxation was induced only by isoprenaline and contraction only by phenylephrine at all distances from the ileocaecal junction. Adrenaline and noradrenaline evoked smooth muscle contraction in the terminal (0 to 20 cm), a concentration-dependent, biphasic response in the intermediate part (21 to 50 cm) and a relaxation in the proximal ileum (> 50 cm from the ilecocaecal valve). Ephedrine did not change significantly the smooth muscle tension in the terminal and the intermediate segments and induced smooth muscle relaxation in the proximal ones.5 Ouabain and a potassium-free solution did not appear to influence the prejunctional action of noradrenaline nor the amplitude of smooth muscle relaxation in the proximal ileum, whereas the concentration-contractor response curves were significantly depressed and shifted to the right by ouabain and in a potassium-free solution.6 The brief initial (phasic) contraction induced by acetylcholine was not influenced during the sustained increase or decrease in tension induced by catecholamines. On the contrary, the stimulatory catecholamine actions disappeared or were changed to smooth muscle relaxation by acetylcholine pretreatment. Potassium chloride pretreatment did not change the character of the adrenoceptor agonist action of the agonists studied.7 Since there is a similar prejunctional action at all distances from the ileocaecal valve and a different postjunctional effect of the adrenoceptor agonists at different distances from the ileocaecal junction, it could be suggested that in the guinea-pig ileum there are at least two alpha-adrenoceptors (inhibitory prejunctional-alpha(2), stimulatory postjunctional-alpha(1)), an inhibitory postjunctional beta-adrenoceptor and an as yet uncharacterized inhibitory postjunctional receptor.8 Based on the specific postjunctional action of phenylephrine and the prejunctional action of ephedrine in the guinea-pig ileum, these drugs could be used with success as ;specific' alpha(1)- and alpha(2)-adrenoceptor stimulants.

Adrenergic alpha-Agonists↗

The effect of new local anaesthetics on tracheal and anococcygeal smooth muscle.

The effects of pentacaine and heptacaine were compared with that of procaine on the isolated tracheal smooth muscle of guinea-pigs and anococcygeal muscle of rats. Pentacaine increased the initial tone of the tracheal smooth muscle. In higher concentration however pentacaine and heptacaine induced smooth muscle relaxation. Pentacaine diminished the action of histamine on the tracheal smooth muscle and both pentacaine and heptacaine depressed the effects of noradrenaline and acetylcholine on anococcygeal muscle.

Anal Canal↗