Effects of amino and ammonio derivatives of adenosine on smooth muscle preparations and mouse neuroblastoma adenylate cyclase

1985 ◽  
Vol 63 (1) ◽  
pp. 58-61 ◽  
Author(s):  
H. P. Baer ◽  
M. Morr
Keyword(s):  
Smooth Muscle ◽  
Adenylate Cyclase ◽  
Adenosine Receptors ◽  
Smooth Muscles ◽  
Mouse Neuroblastoma ◽  
Derivatives Of ◽  
Stimulation Of

Several amino- and ammonio-substituted derivatives of adenosine were tested as effectors of adenosine receptors in different smooth muscle preparations and mouse neuroblastoma adenylate cyclase. The compounds did not affect adenosine receptors in smooth muscles. N6-[3-(trimethylammonio)propyl]adenosine was a weak stimulator of adenylate cyclase, and 3′-amino-3′-deoxyadenosine and 3′-rnonomethylamino-3′-deoxyadenosine antagonized the stimulation of adenylate cyclase by 2-chloroadenosine.

Effect of Na-K adenosinetriphosphatase activity on relaxation of canine tracheal smooth muscle

1988 ◽  
Vol 64 (2) ◽  
pp. 635-641 ◽  
Author(s):  
S. J. Gunst ◽  
J. Q. Stropp
Keyword(s):  
Smooth Muscle ◽  
Adenylate Cyclase ◽  
Atpase Activity ◽  
Prostaglandin E2 ◽  
Sodium Nitroprusside ◽  
Tracheal Smooth Muscle ◽  
Free Medium ◽  
Inhibitory Effects ◽  
Ca2 Channels ◽  
Stimulation Of

The effect of Na-K adenosinetriphosphatase (ATPase) on relaxation induced by isoproterenol, prostaglandin E2, sodium nitroprusside, and forskolin, a specific stimulant of adenylate cyclase, was investigated in canine tracheal smooth muscle strips. Relaxation in response to isoproterenol, prostaglandin E2, and forskolin was significantly decreased after inhibition of the Na-K ATPase by ouabain or a potassium-free medium, but relaxation to sodium nitroprusside was not affected. Relaxation to isoproterenol was greater in muscles contracted by 5-hydroxytryptamine than in those contracted by acetylcholine. The stimulation of Na-K ATPase activity with potassium also caused differences in relaxation between tissues contracted with 5-hydroxytryptamine or acetylcholine. Relaxation caused by isoproterenol by activation of the Na-K-ATPase was also decreased by the Ca2+-channel antagonists, verapamil and diltiazem. The results suggest 1) Na-K ATPase activity modulates relaxation caused by isoproterenol, prostaglandin E2, and forskolin in canine tracheal smooth muscle, 2) isoproterenol or activation of the Na-K ATPase may cause relaxation partly by reducing Ca2+ influx through potential-dependent Ca2+ channels, and 3) the differences in the inhibitory effects of isoproterenol and Na-K ATPase activity on muscles contracted by acetylcholine and 5-hydroxytryptamine could be due to differences between these contractile agents in their dependence on extracellular Ca2+ for activation.

Vascular α-adrenoceptors: from the gene to the human

1995 ◽  
Vol 73 (5) ◽  
pp. 533-543 ◽  
Author(s):  
David B. Bylund ◽  
John W. Regan ◽  
James E. Faber ◽  
J. Paul Hieble ◽  
Christopher R. Triggle ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Blood Vessel ◽  
Adenylate Cyclase ◽  
Inositol Phosphate ◽  
Second Messenger ◽  
Molecular Techniques ◽  
Cellular Growth ◽  
Site Directed Mutagenesis ◽  
Intracellular Loop ◽  
Stimulation Of

Adrenoceptors can be subdivided into three major types, the α1-, α2-, and β-adrenoceptors. Each of these types can be further subdivided into three subtypes, based on pharmacological characteristics. Molecular cloning techniques have supported this subclassification. Recent data now suggest that α-adrenoceptor subtypes identified by pharmacological and molecular techniques correspond well, although species orthologs of several adrenoceptor subtypes have been identified. The secondary structure of the adrenoceptors has been elucidated and correlated with their interaction with second messenger molecules. α1-Adrenoceptors, β-adrenoceptors, and α2-adrenoceptors mediate their actions through stimulation of inositol phosphate release, stimulation of adenylate cyclase, and inhibition of adenylate cyclase, respectively. Site-directed mutagenesis and the preparation of chimeric receptors have located the site of receptor – second messenger interaction to the third intracellular loop for each of these adrenoceptors. While subtypes of each of these classes all interact with the same second messenger, studies with recombinant α2-adrenoceptors show subtype-related differences in receptor – second messenger interaction. Multiple α-adrenoceptor subtypes are expressed in vascular smooth muscle and are involved in various aspects of blood vessel function, including contraction, cellular growth, and proliferation. Various physiological factors can selectively influence responses to a particular subtype, and the relative roles of each subtype can vary between vascular beds and along an individual blood vessel as its caliber changes. Functional studies in blood vessels suggest the presence of additional α-adrenoceptor subtypes not yet identified via molecular techniques. Optimization of the therapeutic profile of an α-adrenoceptor antagonist may be possible via enhancement of selectivity for a particular subtype or by design of a specific profile of affinity for the individual subtypes.Key words: adrenoceptor subclassification, second messenger, G-proteins, vasoconstriction, smooth muscle proliferation.

Dissociation between adenosine receptors and adenylate cyclase in the smooth muscle of guinea pig myometrium

1989 ◽  
Vol 1 (4) ◽  
pp. 357-365 ◽  
Author(s):  
Merton A. Smith ◽  
Judith L. Silverstein ◽  
David P. Westfall ◽  
Iain L.O. Buxton
Keyword(s):  
Smooth Muscle ◽  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Adenosine Receptors

Release of nitric oxide by activation of nonadrenergic noncholinergic neurons of internal anal sphincter

1993 ◽  
Vol 264 (1) ◽  
pp. G7-G12 ◽  
Author(s):  
S. Chakder ◽  
S. Rattan
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Anal Sphincter ◽  
Internal Anal Sphincter ◽  
Smooth Muscles ◽  
Electrical Field Stimulation ◽  
Didelphis Virginiana ◽  
Inhibitory Neurons ◽  
No Release ◽  
Stimulation Of

The purpose of the present study was to investigate the direct release of nitric oxide (NO) in response to the stimulation of nonadrenergic noncholinergic (NANC) nerves. The studies were performed on isolated smooth muscle strips of the opossum (Didelphis virginiana) internal anal sphincter (IAS). Electrical field stimulation (EFS) using the appropriate parameters caused a frequency-dependent fall in the resting tone of the IAS. The release of NO was measured directly by the chemiluminescence method. The stimulation of NANC neurons by EFS and the nicotinic stimulant 1,1-dimethyl-4-phenylpiperazinium (DMPP) caused IAS relaxation with an accompanying release of NO. The release of NO and the fall in the resting tension of IAS in response to lower frequencies of EFS and DMPP were abolished by pretreatment of the smooth muscles with the neurotoxin tetrodotoxin and the NO-synthase inhibitor NG-nitro-L-arginine (L-NNA). The obliteration of the release of NO and the IAS relaxation in the presence of L-NNA reversed to control levels by the addition of the NO precursor L-arginine. The effect of L-NNA and L-arginine on NO release and IAS relaxation was stereoselective, since D-NNA and D-arginine had no significant effect. Vasoactive intestinal polypeptide also caused release of NO from IAS smooth muscle strips, which was abolished by L-NNA. However, isoproterenol and atrial natriuretic factor caused IAS relaxation without any increase in NO release. In conclusion, these studies demonstrate the direct release of NO in response to the stimulation of NANC inhibitory neurons of the gut.

Electrical properties of smooth muscle cell membrane of opossum esophagus

1985 ◽  
Vol 248 (3) ◽  
pp. G342-G346 ◽  
Author(s):  
M. S. Kannan ◽  
L. P. Jager ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Electrical Properties ◽  
Cell Membrane ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Smooth Muscles ◽  
Mechanical Activity ◽  
Circular Smooth Muscle ◽  
Stimulation Of ◽  
Muscle Cell Membrane

The electrical properties of the circular smooth muscle layer from the North American opossum esophagus (body) were studied in vitro by microelectrode recording techniques, both at rest and during stimulation of intramural inhibitory nerves. All observations were made at 37 degrees C in an Abe-Tomita partitioned bath on muscle strips dissected 2 cm orad of the lower esophageal sphincter. At rest, the potential of the smooth muscle cell membrane was -49 +/- 4 mV (mean +/- SE); the length constant and the time constant were 2.0 +/- 0.6 mm and 120 +/- 16 ms, respectively. The inhibitory junction potential (IJP) elicited by stimulation of intramural nerves was followed by a "rebound" or "off" response, characterized by a membrane depolarization on which spikes were superimposed and concomitant mechanical activity of the preparation that usually caused dislocation of the recording microelectrode. The maximal IJP amplitude was 35 mV, and the response reversed at a membrane polarization to -90 mV, suggesting that the IJP was due to an increase of the permeability toward potassium ions. The invariability of the IJP latency at different distances from the stimulating electrodes (1.25-4 mm) suggests that the latency is largely due to diffusion of transmitter from nerve varicosities to postsynaptic receptor sites. Depending on the rate, prolonged stimulation caused fusion of IJP or a continuous hyperpolarization of the membrane. The hyperpolarization faded with time, but off responses were only observed after terminating stimulation. The passive electrical properties of the membrane are comparable with those of other gastrointestinal smooth muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium and angiotensin tachyphylaxis in rat uterine smooth muscle

1975 ◽  
Vol 228 (5) ◽  
pp. 1423-1430 ◽  
Author(s):  
RJ Freer
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscles ◽  
Rabbit Aorta ◽  
Rat Uterus ◽  
Uterine Smooth Muscle ◽  
Normal Tissues ◽  
High Concentrations ◽  
The Relationship ◽  
Very High ◽  
Stimulation Of

Studies were carried out to investigate the relationship between extracellular Ca++ and the ability of a particular smooth muscle to develop tachyphylaxis to angiotensin II (AII). Stimulation of rat uterus by AII was found to be dependent on extracellular Ca++. Placing the tissue in 0 Ca++ completely blocked AII-induced contractions as did the presence of the "Ca++ antagonists" verapamil (10- minus 5M), SKF 525-A (10- MINUS 5M), tetracaine (10- minus 4M), Mn++ (8 times 10- minus 3M), or La-3+ (10- minus 3M). In addition, it is no longer possible to produce tachyphylaxis to AII in deplorazed rat uterus under conditions of pH and Ca++ concentration in which a normally polarized preparation would be unresponsive. Verapamil, on the other hand, was an even more effective antagonist of AII in depolarized preparations (ID50 of 10- minus 8M) than in normal tissues (ID50 of 2.0 times 10- minus 7M). Like the rat uterus, the smooth muscle of the guinea pig ileum also develops tachyphylaxis to AII, and the effect of this peptide was also blocked by 10- minus 5 M verapamil. Rabbit aorta, however, was found to be relatively resistant to both development of tachyphylaxis under conditions of low Ca++ and low pH and also to inhibition by even very high concentrations of verapamil (10- minus 4M). The results of these studies suggest that the Ca++ site involved in the tachyphylactic response to AII may be a physiologically important one in those smooth muscles in which movement of extracellular Ca++ contributes to the inward ion currents during excitation. Verapamil, however, appears to act at a common step in the excitation-contraction sequence in rat uterus. A working model of the interaction of AII with rat uterine smooth muscle is presented.

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