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At least 19 recordsLinked to original sources
PubMed1978

Actions of O-ethyl-S-(2-dimethylaminoethyl)-methylphosphonothioate and some pyridine aldoximes on isolated guinea-pigs heart atria.

1. The effects of acetylcholine and methylfurmetide on isolated guinea-pigs heart atria in the presence or absence of O-ethyl-S-(2-dimethylaminoethyl)-methylphosphonothioate (EDMM) were investigated. The influence of three cholinesterase reactivators on the heart atria pretreated with EDMM has been studied. 2. In the presence of EDMM, the negative inotropic effect of acetylcholine on the isolated heart atria was not significantly increased. This effect of methylfurmetide on heart atria was significantly decreased in the presence of EDMM. 3. EDMM alone caused negative inotropic and negative chronotropic effects depending on its concentration. These pharmacological effects were accompanied with inhibition of acetylcholinesterase activity in the heart muscle. 4. Addition of cholinesterase reactivators normalized the inotropic response of the isolated guinea-pig heart atria altered by EDMM and also increased the acetylcholinesterase activity in the heart.

Acetylcholine↗
PubMed1991

The subunit proportions and kinetic properties of 6-phosphofructo-1-kinase isozymes from rat heart atria and ventricle progressively change during aging.

Relative to 2-3 month rats, total 6-phosphofructo-1-kinase (PFK) activity in heart atria from 12 month rats declined 31%; but, by 24 months it was decreased by only 13%. PFK activities from 12 and 24 month ventricles relative to the 2-3 month rats were decreased by 40% and 30%, respectively. This change in PFK activity in each heart region was associated with alterations of subunit composition. In heart atria from 12 and 24 month rats when compared to 3 month rats, the levels of L-type subunit were not significantly different; but the levels of the M-type subunit were decreased by 43% and 38%, respectively. With respect to levels in 2-3 month atria, the C-type subunit in 12 month atria decreased by 27%; and at 24 months it increased by 31%. Making the same comparison for the heart ventricle at 12 and 24 months, L-type subunit decreased by 30% and 24% respectively; M-type subunit decreased by approximately 47%; and the C-type subunit increased 1.9 and 4.7 fold, respectively. These age-related changes of subunit composition in atrial and ventricular PFK isozyme pools led to changes in their kinetic and regulatory properties suggesting that the aged rat could exhibit a diminished capacity to produce ATP from glucose.

Aging↗
PubMed1976

The effects of some cholinesterase reactivators on contractility of the isolated guinea-pig heart atria.

The effect of eight monoquaternary and bisquaternary pyridine aldoxime cholinesterase reactivators was tested on isolated guinea-pig heart atria. 2. Acetylcholine and methylfurthretonium in concentrations ranging from 10(-7) M to 10(-5) M have negative inotropic effects in the electrically stimulated atria and negative chronotropic effects in the spontaneously beating atria. 3. In the presence of higher concentration of cholinesterase reactivators alone, the parameters of heart muscle contractility are significantly altered. 4. Cumulative dose-response curves of methylfurthretonium in the presence of reactivators in the range of concentrations from 10(-5) M to 10(-3) M are shifted parallelly to higher concentrations of the agonist.

Acetylcholine↗
PubMed1992

[The effect increased choline levels on the synthesis and release of acetylcholine in heart atria in white rats].

The paper addresses the problem of (1) the relationship of choline in extracellular fluid and acetylcholine (ACh) synthesis in chambers of the heart of white rats, and (2) the possibility of physiological involvement of this ACh in the control of cardiac activity. Within 60 min after s.c. administration of choline in the dose of 300 mg/kg body weight the ACh content rose to 136% of the control value in isolated heart chambers and after administration of 400 mg/kg body weight to 159% of the control value. Increased ACh synthesis failed to affect the heart rate, nor did it increase the tonic effect of vagus innervation of the heart. Excessive ACh could however be released by electric transmural stimulation of isolated heart chambers as well as by potassium depolarization. The release depended on the presence of calcium ions. The obtained results demonstrate that an increase in the level of choline in extracellular fluid results in increased ACh synthesis in nerve terminals. Enhanced release of this ACh is a precondition for high choline levels to induce an increase in parasympathetic control of cardiac function.

Acetylcholine↗
PubMedDate not supplied

[Action potentials of the heart atria and ventricles of Rana temporaria frogs and Cyprinus carpio carp].

Using microelectrode technique, studies have been made on electrophysiological indices (amplitude of AP, amplitude of the plateau, latent period of AP, duration of maximal depolarization, duration of repolarization at different levels) of cells of isolated atrium and ventricles of the carp during both the spontaneous activity and electrical stimulation. The obtained amplitude-temporal parameters were compared to those of the heart in the frog R. temporaria. It was found that the amplitude of AP, the amplitude of the plateau and the duration of the latent period of AP in both the atrium and ventricles of the carp significantly (p less than 0.01) differ from the corresponding indices of the frog. On the contrary, the duration of maximal depolarization and repolarization in cells from homologous parts of the heart is very close in the species investigated.

Action Potentials↗
PubMed1977

[Prognostic value of the state of the heart atria in determination of the time of sinus rhythm preservation after correction of auricular fibrillation].

Data are presented from atrial vectorcardiograms of 130 patients with different forms of auricular fibrillation including an analysis of their parameters and a study of the catamnestic data following the elimination of auricular fibrillation, which permitted to develop prognostic criteria for determining the period of sinus rhythm preservation after this type of arrhythmia had been eliminated.

Adolescent↗
PubMed1977

[Study of the electric activity of the heart atria in auricular fibrillation with the aid of the instrumental correlation analysis].

The autocorrelation funtion of the electrocardiographic signal in the V1 lead is approximated by the formula of an attenuated consinusoid. Parameters are singled out (median period, attenuation factor) to characterize the atrial activity. A procedure for recording the auto correlation function is described and optimal conditions of its registration are studied. First results following clinical application of the method are reported.

Action Potentials↗
PubMed1991

Interaction of the neuromuscular blocking drug atracurium with muscarinic acetylcholine receptors.

On isolated rat heart atria, atracurium competitively antagonized the negative chronotropic effect of methylfurmethide, shifting the concentration-response curve to the right without diminishing the agonist's maximal effect; Kd calculated from dose ratios was 3.0 mumol/l. On the longitudinal muscle of rat ileum, atracurium antagonized the effect of methylfurmethide in a non-competitive manner; at 50 mumol/l atracurium, the maximum response to methylfurmethide was diminished by about 50%. Atracurium antagonized the binding of (3H)quinuclidinyl benzilate [3H)QNB) to muscarinic binding sites in the atria, ileal longitudinal muscle and cerebellum with IC50 values of 5-8 mumol/l, and in brain cortex of 25 mumol/l. Atracurium was little efficient, however, in antagonizing the binding of N-(3H-methyl) scopolamine [3H)NMS) to muscarinic binding sites. Complete blockade was not achieved at concentrations up to 1 mmol/l. Concentrations required to diminish the binding by 50% were 10 - 1000 times higher for (3H)NMS than for (3H)QNB. Atracurium brought about the dissociation of (3H)QNB-receptor complexes, but its effect was considerably stronger at a concentration of 30 mumol/l than at 1 mmol/l. Atracurium slowed down the dissociation of (3H)QNB-receptor complexes observed after the addition of atropine. The effects of atracurium on the dissociation of (3H)NMS-receptor complexes were similar to those on (3H)QNB-receptor complexes, but a high concentration of atracurium (1 mmol/l) produced a transient increase in (3H)NMS binding preceding its subsequent dissociation. Although the observations of the antagonism by atracurium of the effect of methylfurmethide on the heart atria, and of the inhibition of the specific binding of (3H)QNB to the atria, ileal smooth muscle, cerebellum and brain cortex are compatible with the assumption of a competitive interaction, the discrepancy between the effects of atracurium on the binding of (3H)QNB and (3H)NMS indicates that atracurium does not bind to the same binding site as (3H)QNB and (3H)NMS. It appears that most effects of atracurium on muscarinic receptors are allosteric and that both negative and positive cooperatives play a role in interactions between atracurium and muscarinic ligands.

Animals↗
PubMedDate not supplied

[A comparative study of the stereoselectivity of cholinoreceptors].

Muscarine-sensitive cholinoreceptors (M-ChR) of higher vertebrates exhibit high stereoselectivity which is also revealed with respect to enantiomers of a very potent muscarinomimetic methyldilvasen (F-2268), the stereospecific index (SSI) being about 100. M-ChRs in the neuronal membrane of the gastropod mollusc Planorbarius corneus and in the hearts of the bivalve molluscs Mercenaria stimpsoni and Anadara broughtoni are highly sensitive to methyldilvasen (10(-9)-10(-10) M), but their sensitivity to its enantiomers is identical. In heart atria of the tortoise Testudo horsfieldi, frog Rana temporaria, and fishes Siluris glanis, Cyprinus carpio, as well as in ventricles of tadpoles, high SSI was revealed. These data are consistent with a hypothesis that during evolution of vertebrates no significant changes took place in the active center of M-ChR. Possibly, the lack of stereoselectivity in the investigated molluscan M-ChRs, together with their other peculiarities (they are not blocked by atropine), indicate "immaturity" of these receptors.

Animals↗
PubMed1975

The mechanism of the positive chronotropic action of diethyl ether on rat atria.

Diethyl ether elicited a dose-dependent increase in the intrinsic frequency of contraction of isolated rat atrial preparations. The maximum effect (plus 34 per cent) occurred with 230 mg ether/100 ml medium. This ether concentration corresponds to a partial pressure of 29.2 mm Hg or 3 MAC. The positive chronotropic action of ether was not reduced in atria obtained from rats pretreated with reserpine (4 mg/kg, ip) although this treatment markedly reduced the effect of tyramine on frequency of contraction. The positive chronotropic response to 0.01 muM isoproterenol was inhibited by the beta-adrenergic antagonist 0.3 mgM dl-propranolol but remained unimpaired in the presence of 0.3 mgM d-propranolol (a much weaker antagonist). In contrast, the atrial response to ether was similar in the presence of either d- or dl-propranolol. Atropine, in concentrations that completely blocked the negative chronotropic action of acetylcholine, did not increase the frequency of contraction, suggesting that the positive chronotropic effect of ether is not due to an atropine-like activity of ether. Our results indicate that the positive chronotropic effect of ether on isolated rat atrial preparations is not mediated via catecholamine release, nor does it represent direct stimulation of beta-adrenergic receptors or block of cholinergic receptors. (Key words: Anesthetics, volatile, diethyl ether; Heart, atria, diethyl ether.).

Adrenergic beta-Antagonists↗
PubMed1991

Atrial natriuretic peptide hormonal system in plants.

To determine if atrial natriuretic peptides are present in plants as well as animals, where they are important for water and sodium metabolism, the leaves and stems of the Florida Beauty (Dracena godseffiana) were examined. The N-terminus consisting of amino acids (a.a.) 1-98 (i.e., pro ANF 1-98), the mid portion of the N-terminus (a.a. 31-67; pro ANF 31-67), and C-terminus (a.a. 99-126; ANF) of the 126 a.a. atrial natriuretic factor (ANF) prohormone were all present in the leaves and stems of this plant. The concentrations of pro ANF 1-98, pro ANF 31-67 and ANF-like peptides of 120 +/- 20, 123 +/- 21, and 129 +/- 20 ng/g of plant tissue in leaves and 109 +/- 20, 96 +/- 21, and 124 +/- 18 ng/g of tissue, respectively, in the stems were lower (P less than 0.05) than their concentrations in rat (Rattus norvegicus) heart atria of 196 +/- 40, 192 +/- 28, and 189 +/- 15 ng/g of tissue respectively, but higher (P less than 0.001) than their respective concentrations of 4.3 +/- 1.4, 4.1 +/- 1.2, and 3.9 +/- 1 ng/g of rat heart ventricular tissue. We conclude that the atrial natriuretic peptide-like hormonal system is present in the plant kingdom as well as in the animal kingdom.

Animals↗
PubMed1990

Positive cooperativity in the binding of alcuronium and N-methylscopolamine to muscarinic acetylcholine receptors.

The effect of the neuromuscular blocker alcuronium on the binding of N-[3H]-methylscopolamine [( 3H]NMS) and l-[3H]quinuclidinylbenzilate ([3H]QNB) to muscarinic binding sites in rat heart atria, longitudinal smooth muscle of the ileum, cerebral cortex, cerebellum, and submaxillary glands was measured using filtration techniques. In the presence of 10(-5) M alcuronium, the binding of [3H]NMS (which was present at a subsaturating concentration of 2 x 10(-10) M) was increased 5.3-fold in the atria and smooth muscle and 3-fold in the cerebellum; no increase was observed in the brain cortex and salivary glands. The binding of [3H]NMS was inhibited at 10(-3) M and higher concentrations of alcuronium. The rates of [3H]NMS association to and dissociation from muscarinic binding sites in the atria were diminished by 10(-5) M alcuronium. Scatchard plots of [3H]NMS binding data obtained with and without 10(-5) M alcuronium indicated that the maximum number of binding sites was not altered by the drug, whereas the apparent Kd for [3H]NMS was diminished. In contrast to [3H] NMS, the effects of alcuronium on the binding of [3H]QNB were only inhibitory. The concentration of alcuronium required to diminish the binding of [3H]QNB by 50% (IC50) was 4-7 microM in the atria, ileal smooth muscle, and the cerebellum, 140 microM in the brain cortex, and 1200 microM in the parotid gland. The results suggest that the binding of low concentrations of alcuronium to muscarinic receptors in the heart, ileal smooth muscle, and cerebellum allosterically increases the affinity of muscarinic receptors towards [3H]NMS, although not [3H]QNB. At high concentrations, alcuronium inhibits the binding of muscarinic ligands, presumably by competition for the classical muscarinic binding site. Positive cooperativity induced by alcuronium appears to be specific for the m2 (cardiac) subtype of muscarinic receptors.

Alcuronium↗