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Article: [Letter: The importance of adrenergic neuronal uptake in termination of action; another view. Response to i. s. de la lande].

Kalsner, S

1975 Volume 12, Issue 5, Page(s) 316–322

MeSH term(s)	Animals ; Catecholamines/metabolism ; Cocaine/pharmacology ; Nerve Endings/metabolism ; Neurons/metabolism ; Sympathetic Nervous System/metabolism
Chemical Substances	Catecholamines ; Cocaine (I5Y540LHVR)
Language	English
Publishing date	1975
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	125104-1
ISSN	0303-6847 ; 0302-2765
ISSN	0303-6847 ; 0302-2765
DOI	10.1159/000158068
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Zs.A 513: Show issues

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Article: Autoregulation of neurotransmitter release at autonomic nerve terminals: a questionable theory.

Kalsner, S

Journal of autonomic pharmacology

2001 Volume 20, Issue 5-6, Page(s) 271–279

Abstract: ... on transmitter release. 5. Future efforts should be directed to exploring the mechanism(s) of antagonist action ...

Abstract	1. The evidence for feedback regulation of neurotransmitter release by means of autoreceptors is questioned. 2. Autoreceptor function must meet the expectations for feedback loops. However, this concordance has not been observed in most neuroeffector systems. 3. The characteristics of per pulse transmitter release with changes in the parameters of stimulation in several autonomic systems do not support the ongoing operation of negative feedback loop mediated by locally released transmitter. Also, the effects of antagonists and agonists often do not comply with feedback expectations. 4. Evidence is provided that agonists and antagonists act at different loci to achieve their inhibiting and potentiating effects on transmitter release. 5. Future efforts should be directed to exploring the mechanism(s) of antagonist action and to a system-by-system analysis of the evidence for and against autoreceptor operation.
MeSH term(s)	Animals ; Autonomic Pathways/metabolism ; Autoreceptors/agonists ; Autoreceptors/antagonists & inhibitors ; Autoreceptors/physiology ; Feedback ; Homeostasis ; Humans ; Nerve Endings/metabolism ; Neurotransmitter Agents/metabolism
Chemical Substances	Autoreceptors ; Neurotransmitter Agents
Language	English
Publishing date	2001-05-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	604626-5
ISSN	1365-2680 ; 0144-1795
ISSN (online)	1365-2680
ISSN	0144-1795
DOI	10.1046/j.1365-2680.2000.00191.x
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Zs.A 1604: Show issues

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Article: Autoreceptors do not regulate routinely neurotransmitter release: focus on adrenergic systems.

Kalsner, S

Journal of neurochemistry

2001 Volume 78, Issue 4, Page(s) 676–684

Abstract: The theory that neurotransmitter release is regulated locally at the individual terminals of neurons has achieved a rapid and seemingly secure status in our understanding of neuronal function both in the periphery and in the central nervous system. This ... ...

Abstract	The theory that neurotransmitter release is regulated locally at the individual terminals of neurons has achieved a rapid and seemingly secure status in our understanding of neuronal function both in the periphery and in the central nervous system. This concept of negative feedback control through the monitoring of the perineuronal concentration of previously released transmitter has been extended to a multiplicity of transmitters and utilized to explain the mechanisms of action of diverse classes of drugs, ranging from antihypertensives to antidepressants. It is my view that negative feedback by terminal and by somadendritic receptors cannot account for the existing body of experimental work. Analyses of the profiles of action of agonists and antagonists, and of the per pulse release of transmitter in the absence of drugs in a variety if peripheral organ systems, as well as in superfused brain slices, demonstrates the need for alternate interpretations of the available data. Evidence is provided that the actions of agonists to inhibit transmitter release and that of antagonists to enhance release occur at different cellular loci and that the purported unitary action of these two classes that is so central to the validity of presynaptic theory is unsupportable.
MeSH term(s)	Adrenergic alpha-Antagonists/pharmacology ; Animals ; Autoreceptors/metabolism ; Epinephrine/pharmacology ; Feedback ; Mice ; Mice, Transgenic ; Neurotransmitter Agents/metabolism ; Norepinephrine/pharmacology ; Presynaptic Terminals/physiology ; Receptors, Adrenergic/genetics ; Receptors, Adrenergic/metabolism ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology ; Yohimbine/pharmacology
Chemical Substances	Adrenergic alpha-Antagonists ; Autoreceptors ; Neurotransmitter Agents ; Receptors, Adrenergic ; Yohimbine (2Y49VWD90Q) ; Norepinephrine (X4W3ENH1CV) ; Epinephrine (YKH834O4BH)
Language	English
Publishing date	2001-06-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1046/j.1471-4159.2001.00483.x
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Article: The question of feedback at the somadendritic region and antidepressant drug action.

Kalsner, S

Brain research bulletin

2000 Volume 52, Issue 6, Page(s) 467–473

Abstract: Presynaptic receptor theory has been expanded to encompass the regulation of the firing rate of serotonergic neurons through negative feedback mediated by the somadendritic release of transmitter. This has encouraged hypotheses as to the mechanisms of ... ...

Abstract	Presynaptic receptor theory has been expanded to encompass the regulation of the firing rate of serotonergic neurons through negative feedback mediated by the somadendritic release of transmitter. This has encouraged hypotheses as to the mechanisms of action of several classes of antidepressants and anxiolytics. One conspicuous example is the attribution of the clinical efficacy of 5-HT uptake inhibitors, such as fluoxetine and paroxetine, to desensitization of somadendritic 5-HT autoreceptors. An examination of the available evidence, mainly observations made with agonists, antagonists, monoamine oxidase inhibitors and uptake blockers, taken along with the theoretical expectations for a negative feedback loop, and the operational characteristics of inactivation pathways, indicates that negative feedback does not function at somadendritic sites to set firing rate or transmitter density, and suggests that the process may not function at all physiologically. The attribution of the effectiveness of neuroactive drugs to desensitization of raphe 5-HT inhibitory receptors, or to other interactions with feedback, is highly speculative and unlikely.
MeSH term(s)	Animals ; Antidepressive Agents/pharmacology ; Dendrites/drug effects ; Dendrites/metabolism ; Feedback/drug effects ; Feedback/physiology ; Humans ; Receptors, Serotonin/drug effects ; Receptors, Serotonin/metabolism ; Synapses/drug effects ; Synapses/metabolism
Chemical Substances	Antidepressive Agents ; Receptors, Serotonin
Language	English
Publishing date	2000-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	197620-5
ISSN	1873-2747 ; 0361-9230
ISSN (online)	1873-2747
ISSN	0361-9230
DOI	10.1016/s0361-9230(00)00289-6
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Zs.A 1243: Show issues

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Article: Surface properties from the S-layer of Clostridium thermosaccharolyticum D120-70 and Clostridium thermohydrosulfuricum L111-69.

Sára, M / Kalsner, I / Sleytr, U B

Archives of microbiology

1988 Volume 149, Issue 6, Page(s) 527–533

Abstract: ... polycationized ferritin, showed that the S-layers of two closely related clostridia Clostridium ... carboxyl groups are exposed on the S-layer surface of both strains. Amino-specific, bifunctional agents ... crosslinked both S-layer lattices. Studies with carbodiimides revealed that only the S-layer surface of C ...

Abstract	Labelling experiments using a positively charged topographical marker for electron microscopy, polycationized ferritin, showed that the S-layers of two closely related clostridia Clostridium thermohydrosulfuricum L111-69 and C. thermosaccharolyticum D120-70 do not exhibit a net negative charge, as usually observed for bacterial cell surfaces. Chemical modification of reactive sites confirmed that amino and carboxyl groups are exposed on the S-layer surface of both strains. Amino-specific, bifunctional agents crosslinked both S-layer lattices. Studies with carbodiimides revealed that only the S-layer surface of C. thermohydrosulfuricum L111-69 had amino and carboxyl groups closely enough aligned to permit electrostatic interactions between the constituent protomers. The regular structure of this S-layer lattice was lost upon converting the carboxyl groups into neutral groups by amidation. Disintegration of both S-layer lattices occurred upon N-acetylation or N-succinylation of the free amino groups. Adhesion experiments showed that in neutral and weakly alkaline environment whole cells of C. thermosaccharolyticum D120-70 exhibited a stronger tendency to bind to charged surfaces than whole cells of C. thermohydrosulfuricum L111-69, but showed a lower tendency to bind to hydrophobic materials.
MeSH term(s)	Cell Wall/ultrastructure ; Clostridium/ultrastructure ; Freeze Etching ; Membrane Glycoproteins/isolation & purification ; Microscopy, Electron ; Species Specificity
Chemical Substances	Membrane Glycoproteins
Language	English
Publishing date	1988
Publishing country	Germany
Document type	Journal Article
ZDB-ID	124824-8
ISSN	1432-072X ; 0302-8933
ISSN (online)	1432-072X
ISSN	0302-8933
DOI	10.1007/bf00446756
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Zs.A 805: Show issues

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Article: Vasodilator action of calcium antagonists in coronary arteries in vitro.

Kalsner, S

The Journal of pharmacology and experimental therapeutics

1997 Volume 281, Issue 2, Page(s) 634–642

Abstract: ... antagonists on arterial tone may be the consequence of antagonism at vascular smooth muscle cell site(s ...

Abstract	Calcium antagonists have routinely been assumed to inhibit the contractions of arterial smooth muscle through block of membrane channels. The effects of nifedipine and diltiazem on contractions were examined in in vitro preparations of cattle coronary artery, one of the key therapeutic targets of calcium antagonists, to determine if alternate mechanisms of action are involved. Contractions elicited in calcium-free Krebs, in the presence of U 46619, to potassium channel inhibitors (4-aminopyridine and tetraethylammonium) and to a Na(+)-K(+)-ATPase inhibitor (ouabain), were antagonized by low concentrations of nifedipine (3 x 10(-9)-3 x 10(-8) M) and by diltiazem (3 x 10(-8) and 1 x 10(-7) M). Contractions produced in calcium-free Krebs to KCl (50 mM) were antagonized similarly by calcium antagonists. Contractions to depolarizing agents in calcium-free Krebs were antagonized at lower concentrations of nifedipine than comparably elicited responses in Krebs containing 2.3 mM calcium. In addition, higher concentrations of nifedipine were required to antagonize contractions to extracellular calcium, produced in preparations maintained in calcium-free Krebs in the presence of KCl (50 mM), than were needed to block contractions to KCl or to potassium channel inhibitors elicited in calcium-free Krebs. Pretreatment of preparations in calcium-free Krebs with ryanodine (30 microM) did not reduce the nifedipine-sensitive contractions elicited in calcium-free Krebs. It is concluded that at least some of the therapeutic effects of calcium antagonists on arterial tone may be the consequence of antagonism at vascular smooth muscle cell site(s) at which calcium is released or interacts, rather than of block of calcium entry through membrane L channels.
MeSH term(s)	Animals ; Arteries/drug effects ; Arteries/physiology ; Calcium/metabolism ; Calcium Channel Blockers/pharmacology ; Cattle ; Coronary Vessels/drug effects ; Coronary Vessels/physiology ; Diltiazem/pharmacology ; In Vitro Techniques ; Nifedipine/pharmacology ; Potassium Channel Blockers ; Ryanodine/pharmacology ; Vasodilation/drug effects
Chemical Substances	Calcium Channel Blockers ; Potassium Channel Blockers ; Ryanodine (15662-33-6) ; Diltiazem (EE92BBP03H) ; Nifedipine (I9ZF7L6G2L) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	1997-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
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Article: Coronary artery spasm. Multiple causes and multiple roles in heart disease.

Kalsner, S

Biochemical pharmacology

1995 Volume 49, Issue 7, Page(s) 859–871

Abstract: Myocardial infarction and sudden cardiac death may be initiated by a sudden intense localized contraction of coronary artery smooth muscle. When this event occurs around a vulnerable eccentric lipid-filled plaque, rupture and extrusion of plaque contents ...

Abstract	Myocardial infarction and sudden cardiac death may be initiated by a sudden intense localized contraction of coronary artery smooth muscle. When this event occurs around a vulnerable eccentric lipid-filled plaque, rupture and extrusion of plaque contents and exposure of collagen occur. This may sometimes be a silent and self-limiting event; other times it leads to thrombus formation. A second wave of spasm due to accumulated platelet and inflammatory mediators may compound the contractile consequences of the initiating event. Spasm involves intrinsic smooth muscle cell electrical mechanisms, hyper-responsive cells, and multiple agonists that synergize their actions, and the involvement of each mechanism varies at different times in the sequence of vascular occlusion. Study of spasm requires vascular systems that adequately model coronary artery responses of the ageing human heart. As previously emphasized, tissues obtained postmortem, and when possible from recipients during heart transplants, must be integral to theory building, alongside animal models, despite the experimental limitations such tissues impose. A multidisciplinary approach, at all levels of vascular physiology and pharmacology, will be necessary to understand coronary motor activity and human heart disease.
MeSH term(s)	Animals ; Coronary Disease/etiology ; Coronary Disease/physiopathology ; Coronary Thrombosis/etiology ; Endothelium, Vascular/physiopathology ; Humans ; Muscle, Smooth, Vascular/physiopathology ; Myocardial Infarction/etiology ; Spasm/etiology ; Vasoconstrictor Agents/adverse effects
Chemical Substances	Vasoconstrictor Agents
Language	English
Publishing date	1995-03-30
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/0006-2952(94)00447-t
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Article: Hypoxic relaxation in functionally intact cattle coronary artery segments involves K+ ATP channels.

Kalsner, S

The Journal of pharmacology and experimental therapeutics

1995 Volume 275, Issue 3, Page(s) 1219–1226

Abstract: Functionally intact coronary artery segments studied in vitro responded to 15 min of hypoxia with relaxations of preexisting contractions. The hypoxic relaxations were obtained in preparations routinely denuded of endothelium and were unaffected by ... ...

Abstract	Functionally intact coronary artery segments studied in vitro responded to 15 min of hypoxia with relaxations of preexisting contractions. The hypoxic relaxations were obtained in preparations routinely denuded of endothelium and were unaffected by tetrodotoxin, by indomethacin or by the blockers of calcium-dependent potassium channels, apamin and charybdotoxin. Relaxations from contractions to the calcium channel opener Bay K 8644 and to spontaneous tone were attenuated most by hypoxia, and those to carbamylcholine and 5-hydroxytryptamine were inhibited to an intermediate extent. Contractions to the thromboxane A2 analog U 46619, dependent largely on intracellular calcium, were the least reduced during 15 min of hypoxia. Pretreatment of contracted preparations with glibenclamide, the potent antagonist of ATP-dependent potassium channels, before exposure to 95% N2/5% CO2 significantly attenuated, but did not eliminate, hypoxic relaxations. Hypoxic relaxations from contractions to the calcium channel opener Bay K 8644 and to spontaneous tone were antagonized most by glibenclamide, and those to U 46619 were reduced the least. In the presence of the calcium channel antagonist nifedipine, tissues contracted with carbamylcholine or 5-hydroxytryptamine relaxed during hypoxia, but these relaxations were insensitive to glibenclamide. Contractions of cattle radial artery and rabbit aorta were variably reduced during hypoxia but were insensitive to glibenclamide. We conclude that K+ ATP channels participate in hypoxia-induced coronary artery smooth muscle relaxation and may do so particularly with contractions that utilize principally extracellular calcium.
MeSH term(s)	Adenosine/pharmacology ; Adenosine Triphosphate/physiology ; Animals ; Arteries/drug effects ; Arteries/physiopathology ; Calcium/metabolism ; Calcium Channel Blockers/pharmacology ; Cattle ; Coronary Vessels/drug effects ; Coronary Vessels/physiopathology ; Glyburide/pharmacology ; Guanidines/pharmacology ; Hypoxia/physiopathology ; In Vitro Techniques ; Indomethacin/pharmacology ; Muscle Relaxation ; Pinacidil ; Potassium Channel Blockers ; Potassium Channels/metabolism ; Rabbits ; Tetrodotoxin/pharmacology ; Vasodilator Agents/pharmacology
Chemical Substances	Calcium Channel Blockers ; Guanidines ; Potassium Channel Blockers ; Potassium Channels ; Vasodilator Agents ; Tetrodotoxin (4368-28-9) ; Pinacidil (7B0ZZH8P2W) ; Adenosine Triphosphate (8L70Q75FXE) ; Adenosine (K72T3FS567) ; Glyburide (SX6K58TVWC) ; Calcium (SY7Q814VUP) ; Indomethacin (XXE1CET956)
Language	English
Publishing date	1995-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
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Article: Non-neurogenic contractions in isolated coronary arteries by brief electrical pulses.

Kalsner, S

Cardiovascular research

1994 Volume 28, Issue 12, Page(s) 1843–1853

Abstract: ... a single ten thousandth of a second pulse) with long lasting [150(SEM 18.5) s] contractions ...

Abstract	Objective: The aim was to describe a novel form of non-neurogenic coronary artery contraction. Methods: Superfused cattle coronary artery preparations in vitro were placed between platinum electrodes and stimulated. Results: The preparations responded to exceedingly brief transmural stimulation (a single ten thousandth of a second pulse) with long lasting [150(SEM 18.5) s] contractions. These previously undescribed contractions were not reduced by neural blockade nor did they involve free radicals, prostaglandins, or the endothelium. In contrast to the rapid loss of responses to KCl in zero calcium Krebs solution, responses to stimulation were only progressively diminished over many minutes, suggesting involvement of internal calcium stores. The L channel calcium antagonists nifedipine and diltiazem markedly reduced contractions to KCl but did not materially alter those to 1, 5, or 10 stimulation pulses, nor did the T channel antagonist tetramethrin, further supporting the involvement of stored calcium in contractions to stimulation. Evidence was obtained that neither Na+/K(+)-ATPase nor the Na+/Ca+ exchanger are involved in the contractions to stimulation. Ryanodine in zero calcium Krebs solution potentiated contractions to stimulation with 10 pulses and also to endothelin, but depressed contractions to U 46619. Conclusions: Stimulation at excitation parameters well below those associated with neurotransmitter release activates a highly effective contraction sequence that may use a ryanodine insensitive pool of bound calcium. This novel process may have physiological and pathophysiological relevance and provides a means of activating contraction in a coronary artery and studying its time course and contributory components, without the complicating participation of an agonist drug.
MeSH term(s)	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid ; Animals ; Calcium/metabolism ; Cattle ; Coronary Vessels/physiology ; Diltiazem/pharmacology ; Electric Stimulation ; In Vitro Techniques ; Insecticides/pharmacology ; Muscle Contraction/drug effects ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/physiology ; Nifedipine/pharmacology ; Prostaglandin Endoperoxides, Synthetic/pharmacology ; Pyrethrins/pharmacology ; Ryanodine/pharmacology ; Thromboxane A2/analogs & derivatives ; Thromboxane A2/pharmacology ; Vasoconstrictor Agents/pharmacology
Chemical Substances	Insecticides ; Prostaglandin Endoperoxides, Synthetic ; Pyrethrins ; Vasoconstrictor Agents ; Ryanodine (15662-33-6) ; Thromboxane A2 (57576-52-0) ; 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid (76898-47-0) ; Diltiazem (EE92BBP03H) ; Nifedipine (I9ZF7L6G2L) ; Calcium (SY7Q814VUP) ; tetramethrin (Z72930Q46K)
Language	English
Publishing date	1994-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/28.12.1843
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Zs.A 565: Show issues

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Article: Propranolol antagonizes coronary artery relaxation by a potassium channel opener.

Kalsner, S

Life sciences

1994 Volume 55, Issue 14, Page(s) 1109–1121

Abstract: Coronary artery preparations from cattle hearts responded with stable contractions to the thromboxane A2 analogue, U 46619. These contractions were progressively reduced by increasing concentrations of the prototypical potassium channel opener pinacidil ( ...

Abstract	Coronary artery preparations from cattle hearts responded with stable contractions to the thromboxane A2 analogue, U 46619. These contractions were progressively reduced by increasing concentrations of the prototypical potassium channel opener pinacidil (3.8 x 10(-8) to 1.1 x 10(-4) M). Pinacidil-induced relaxations were antagonized significantly by d,l-propranolol (1.2 x 10(-6) to 1.2 x 10(-5) M). Forskolin-induced relaxations of coronary preparations were also antagonized by d,l-propranolol, but those to nitroprusside were not. d-Propranolol also antagonized relaxations to pinacidil but only when used in higher concentrations than the I-isomer. Nadolol and metoprolol, two other beta receptor antagonists with differing profiles of action, also antagonized to some extent the vasodilator action of pinacidil. The known potassium channel antagonist, glibenclamide, shifted the concentration-relaxation curve for pinacidil to the right, but d,l-propranolol produced an additional antagonistic effect in the presence of glibenclamide. Relaxations of contracted tracheal ring preparations of guinea pig by pinacidil, however, were not antagonized by d,l-propranolol, suggesting specificity for vascular tissue. Isoproterenol increased significantly the cyclic AMP levels in coronary tissue, but pinacidil had no such effect, ruling out an adrenergic component to pinacidil action. Pinacidil increased the efflux of 86Rb in isolated coronary preparations, and this effect was blunted by propranolol. It is concluded that beta receptor antagonists inhibit relaxations to a potassium channel opener by a mechanism independent of beta adrenergic receptors and that this effect may have therapeutic implications.
MeSH term(s)	Adrenergic beta-Agonists/pharmacology ; Adrenergic beta-Antagonists/pharmacology ; Animals ; Biological Transport ; Cattle ; Colforsin/pharmacology ; Coronary Vessels/drug effects ; Coronary Vessels/physiology ; Cyclic AMP/metabolism ; Drug Interactions ; Glyburide/pharmacology ; Guanidines/antagonists & inhibitors ; Guanidines/pharmacology ; Guinea Pigs ; In Vitro Techniques ; Muscle Relaxation/drug effects ; Muscle, Smooth/drug effects ; Muscle, Smooth/physiology ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/physiology ; Nitroprusside/pharmacology ; Pinacidil ; Potassium Channels/drug effects ; Propranolol/pharmacology ; Rubidium Radioisotopes/pharmacokinetics ; Trachea/drug effects ; Trachea/physiology ; Vasodilator Agents/antagonists & inhibitors ; Vasodilator Agents/pharmacology
Chemical Substances	Adrenergic beta-Agonists ; Adrenergic beta-Antagonists ; Guanidines ; Potassium Channels ; Rubidium Radioisotopes ; Vasodilator Agents ; Nitroprusside (169D1260KM) ; Colforsin (1F7A44V6OU) ; Pinacidil (7B0ZZH8P2W) ; Propranolol (9Y8NXQ24VQ) ; Cyclic AMP (E0399OZS9N) ; Glyburide (SX6K58TVWC)
Language	English
Publishing date	1994
Publishing country	Netherlands
Document type	Comparative Study ; Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/0024-3205(94)00239-8
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