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P Aaronson

Publications and source records attributed to P Aaronson.

10 recordsLinked to original sources
PubMed1990

Effects of phenylephrine in single isolated smooth muscle cells of rabbit and guinea pig taenia caeci.

Spontaneous transient and evoked outward currents were studied using the whole cell patch-clamp technique with freshly dispersed smooth muscle cells isolated from rabbit and guinea pig taenia caeci. Phenylephrine induced a low amplitude sustained outward current in both tissues. Simultaneously, the frequency and amplitude of spontaneous transient outward currents were increased. However, there were differences between the effects of phenylephrine on the evoked outward currents recorded from smooth muscle cells of rabbit (reduction) and guinea pig (enhancement) taenia caeci.

Animals↗
PubMed1988

Evolutionary development of systems.

The number of HMOs and their enrollment has increased since the inception of managed care and is expected to continue to expand. The dynamic growth in this area has raised concerns whether there are systems available which can handle their needs. Capabilities need to handle the complexities inherent in multiple benefit plans and provider relations.

Health Maintenance Organizations↗
PubMed1986

Calcium activation of vascular smooth muscle. State of the art lecture.

Tension development in arterial smooth muscle is regulated by variations of calcium concentration in the submicromolar range. The receptor for Ca2+ is calmodulin, which through stimulation of myosin light chain kinase can activate sequentially two apparently different contractile states. A third possible contractile state may be related to C-kinase activation. These contractile states are thought to have different Ca2+ sensitivities. Ca2+ is supplied from two major sources: the sarcoplasmic reticulum and the extracellular space. The release of sarcoplasmic reticulum Ca2+ is mediated by the intracellular messenger inositol-1,4,5-trisphosphate (IP3) and perhaps by Ca2+ itself. These two messengers have the potential for amplification; for example, IP3 may release some Ca2+ that may subsequently cause Ca2+-induced Ca2+ release. The entry of Ca2+ from the extracellular space into the cytoplasm is mediated by a Ca2+ leak and by excitable Ca2+ channels and is modulated by a Ca2+ buffer barrier consisting of the superficial sarcoplasmic reticulum. Two types of adenosine 5'-triphosphate-driven Ca2+ pumps in the sarcoplasmic reticulum and plasmalemma are responsible for returning the cytoplasmic Ca2+ concentration to resting level after contraction and for maintaining Ca2+ homeostasis during the life of the cells.

Actin Cytoskeleton↗
PubMed1982

Effects of Na readmission on cellular 45Ca fluxes in Na-depleted guinea pig taenia coli.

The removal of Na from the medium causes a cellular Ca uptake in the smooth muscle of the guinea pig taenia coli which is rapidly reversed if medium Na is readmitted. This net extrusion was characterized in tissues which were first Na-depleted in a zero-Na (sucrose) solution. Li was able to substitute for Na in mediating this effect. K was also able to mimic Na in this respect if the depolarization-mediated Ca influx caused by the isotonic K solution was blocked with 10(-5) M D -600. The net Ca extrusion upon Na readmission was due to a small decrease in Ca influx, as well as a marked increase in the transmembrane Ca efflux rate, as revealed by 45Ca washout experiments. The increased 45Ca efflux upon Na readmission could be mimicked by Li, K, choline and tris. We conclude that the Na/Ca-exchange hypothesis is insufficient to explain these data, in that both Ca extrusion and 45Ca efflux can be stimulated in the absence of a Na gradient, or in the absence of any monovalent cationic gradient. These observations are discussed in terms of a possible intracellular competition of Ca and monovalent cations for anionic binding sites, as well as with regard to a possible direct stimulation of a plasmalemmal CaATPase by monovalent cations.

Animals↗
PubMed1982

Calcium fluxes in isolated rabbit aorta and guinea pig tenia coli.

Studies utilizing 45Ca have been helpful in analyzing the Ca control system in smooth muscle. Activation of rabbit aortic alpha receptors stimulates Ca influx and a release of Ca from superficial binding sites. Membrane depolarization by high K causes an influx, but no release. However, the influx pathways activated by alpha agonists and membrane depolarization are different and independent, because the maximal Ca influxes induced by each type of stimulation are additive. The cellular Ca pools that release Ca during pharmacological activation are shared by several agonists; release of cellular Ca by one agent after abolition of Ca influx inhibits Ca release by a second, different agonist. U44069, a stable prostaglandin H2 analog, induces both Ca influx and release. The extracellular Ca source for initial influx exchanges more slowly than free interstitial Ca, and may be located within the glycocalyx or on the outer membrane surface. An Na-Ca exchange process has been suggested as the important determinant of the transmembrane electrochemical Ca gradient. However, manipulation of the Na gradient by Na pump inhibition and Na substitution has provided data showing that Na-Ca exchange is a nonspecific process not directly involved in regulating [Ca]i. It is more likely that Ca extrusion is dependent on an ATPase in smooth muscle.

Animals↗
PubMed1981

Effects of sodium gradient manipulation upon cellular calcium, 45Ca fluxes and cellular sodium in the guinea-pig taenia coli.

1. Sucrose and choline were utilized as NaCl substitutes in order to investigate Na-Ca interactions in the smooth muscle of the guinea-pig taenia coli.2. Progressive substitution of NaCl by sucrose caused a progressive increase in cellular exchangeable Ca. This uptake, which amounted to about 300 mumole Ca/kg tissue upon total Na replacement, reached a plateau within 20 min. Complete substitution of NaCl by choline chloride caused cellular Ca to increase rapidly to an initial peak, and then decrease to a stable plateau which was also about 300 mumole/kg above control.3. Replacement of NaCl by either sucrose or choline chloride caused a transient increase in the Ca influx rate, which was measured using a 3 min pulse labelling with (45)Ca. This increase was more pronounced in choline chloride.4. NaCl substitution by either sucrose or choline chloride caused a decrease in the (45)Ca efflux rate. Two exponential components of transmembrane (45)Ca efflux were found in control and Na-free media.5. Treatment of tissues with 3 x 10(-5)m-ouabain did not significantly affect the cellular Ca content after 80 min, at which time the Na and K gradients were largely dissipated.6. Removal of medium K caused a slower dissipation of the Na and K gradients. This treatment decreased cellular Ca, did not affect the Ca influx rate, and increased the (45)Ca efflux rate.7. Tissues were incubated in depolarizing media containing 10(-4)m-ouabain in order to remove the Na gradient. Subsequent measurement of cellular Na indicated the absence of a significant fraction of bound Na.8. The ratio [Na](o)/[Na](i) had a value of 6.3 in control medium, and decreased as [Na](o) was progressively lowered by sucrose substitution, reaching a value of < 1 in a medium containing 5 mm-Na.9. These experiments provide evidence that a Na-Ca exchange carrier does not play an important role in regulation of tension in this muscle, and also indicate that the Ca gradient is not solely dependent on the Na gradient in guinea-pig taenia coli.

Animals↗
PubMed1980

Ca2+ movements in smooth muscle.

We describe the Ca2+ movements in smooth muscle cells at rest and during activation and relaxation as deduced from transplasmalemmal Ca2+ fluxes and contractile respnses. The general picture which emerges is: the resting cell has a [Ca2+]cyt below 10(-7) M and large gradients are poised across both the cell membrane and intracellular membranes. Excitation opens up Ca2+ channels which are linked to receptors and, if depolarization occurs, to other channels not linked to specific receptors but capable of sensing the membrane potential. Receptor activation also leads to release of Ca2+ from a limited intracellular Ca2+ pool which is superficially located because it has to be refilled from the outside. Relaxation is effected by Ca2+ accumulation by another intracellular Ca2+ pool, very likely sarcoplasmic reticulum, which does not release Ca2+ during activation. The sarcoplasmic reticulum Ca2+ pump can also decrease initial activation of the myofilaments. Elevation of cAMP levels may inhibit contraction by stimulating the sarcoplasmic reticulum Ca-ATPase. An enormous amount of research is still required to prove the above scheme and to localize and quantitate the various intracellular Ca2+ pools.

Animals↗