Abstract.The following result is shown. If T is a lipschitzian pseudo-contractive map of a compact convex subset E of a Hubert space into itself and x^ is any point in E, then a certain mean value sequence defined by xn+1 = anT[ßnTxn+ (1 -ßn)xn] + (1 -a")x" converges strongly to a fixed point of T, where {a"} and {/?"} are sequences of positive numbers that satisfy some conditions.It was recently shown in [1] that a mean value iteration method is available to find a fixed point of a strictly pseudo-contractive map. In this paper we shall prove that a certain sequence of points which is iteratively defined converges always to a fixed point of a lipschitzian pseudo-contractive map. For the definitions of a strictly pseudo-contractive map and a pseudo-contractive map in a Hubert space, see, for example, [3]. Theorem.If E is a convex compact subset of a Hubert space H, T is a lipschitzian pseudo-contractive map from E into itself and x, is any point in E, then the sequence {x"},?=1 converges strongly to a fixed point ofT, where xn is defined iteratively for each positive integer n by 71=1As a particular case, we may choose for instance an=ßn=n~'1/2.

Abstract.The following result is shown. If T is a lipschitzian pseudo-contractive map of a compact convex subset E of a Hubert space into itself and x^ is any point in E, then a certain mean value sequence defined by xn+1 = anT[ßnTxn+ (1 -ßn)xn] + (1 -a")x" converges strongly to a fixed point of T, where {a"} and {/?"} are sequences of positive numbers that satisfy some conditions.It was recently shown in [1] that a mean value iteration method is available to find a fixed point of a strictly pseudo-contractive map. In this paper we shall prove that a certain sequence of points which is iteratively defined converges always to a fixed point of a lipschitzian pseudo-contractive map. For the definitions of a strictly pseudo-contractive map and a pseudo-contractive map in a Hubert space, see, for example, [3]. Theorem.If E is a convex compact subset of a Hubert space H, T is a lipschitzian pseudo-contractive map from E into itself and x, is any point in E, then the sequence {x"},?=1 converges strongly to a fixed point ofT, where xn is defined iteratively for each positive integer n by 71=1As a particular case, we may choose for instance an=ßn=n~'1/2.

Greater beta adrenergic receptor density and/or increased myocardial responsiveness to adenylate stimulation in apical myocardium compensates, at least in part, for its sparse sympathetic innervation.

Peripheral monocytosis is associated with LV dysfunction and LV aneurysm, suggesting a possible role of monocytes in the development of LV remodeling after reperfused AMI.

Abstract.The following result is shown. If T is a nonexpansive mapping from a closed convex subset D of a Banach space into a compact subset of D and x, is any point in D, then the sequence (xn) defined by xn+l = 2~](xn + Txn) converges to a fixed point of T. As a matter of fact, a theorem which includes this result is proved. Furthermore, a similar result is obtained under certain restrictions which do not imply the assumption on the compactness of T.

Two types of histamine receptor, the H1- and H2-receptors, are found not only on vascular smooth muscle cells but on the perivascular autonomic nerve terminals. Activation of the prejunctional histamine receptors modifies transmitter release from the nerve terminals. Recently, histamine was shown to inhibit its own release from depolarized slices of rat cerebral cortex. This phenomenon was found to be mediated by a novel class of histamine receptor, the H3-receptor, that was pharmacologically distinct from the H1- and H2-receptors. Up to now, there has been no indication whether this third class of histamine receptor is present in any tissue other than the brain. We report here that histamine depresses sympathetic neurotransmission in the guinea-pig mesenteric artery by interacting with histamine H3-receptors on the perivascular nerve terminals. The pharmacological properties of these receptors are similar to those reported for the H3-receptors in the brain. Our data provide evidence for the existence of H3-receptors in the autonomic nervous system.

SUMMARY1. Responses ofthe smooth muscle membrane ofthe rabbit bladder to intramuscular nerve stimulation were investigated by the micro-electrode and double sucrose-gap methods.2. The cell generated regular spontaneous action potentials. Acetylcholine produced a maintained increase in the frequency and ATP a transient increase. Noradrenaline only increased the frequency at very high concentrations.3. Application of short current pulses (50/isec) produced an initial excitatory junction potential (e.j.p.) with a superimposed spike, followed by a late depolarization. On some occasions, hyperpolarization of the membrane appeared between initial e.j.p. and the late depolarization. All these responses were abolished by tetrodotoxin.4. The late depolarization was enhanced by pre-treatment with neostigmine and abolished by atropine. This means that the delayed depolarization is due to activation ofthe muscarinic receptor. When the late depolarization was abolished, the amplitude of hyperpolarization was enhanced.5. The e.j.p. and contraction were unaffected by guanethidine, phentolamine, methysergide, mepyramine, quinidine or theophylline. This means that the e.j.p. is not mediated by activation of adrenergic, tryptaminergic, histaminergic or purinergic receptors.6. ATP reduced the amplitude of the e.j.p. due to depolarization of the membrane and reduction in the membrane resistance. The amplitude of the e.j.p. was gradually reduced by repetitive stimulation (0-5-2-0 Hz). However, the rate of depression was unchanged in the presence of ATP. Dipyridamole did not change the electrical and mechanical responses to field stimulation. These results do not support the proposal that ATP is the non-cholinergic excitatory transmitter.7. Apamine and tetraethylammonium (TEA) suppressed the hyperpolarization produced by field stimulation but guanethidine did not inhibit the hyperpolarization. Therefore, the hyperpolarization is due to increased K conductance of the membrane but it is not possible to conclude whether this component is due to the inhibitory action of a neurotransmitter or solely to after hyperpolarization of the spike.8. It was concluded that the rabbit bladder receives both cholinergic and noncholinergic excitatory neurones.

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