PubMed Health⌕ Search

Biomedical subjects

E Zelcer

Publications and source records attributed to E Zelcer.

10 recordsLinked to original sources
PubMed1984

Electrical and mechanical activity in the lower esophageal sphincter of the cat.

Transmembrane electrical activity was correlated to isometric contractile activity for strips of circularly oriented smooth muscle from the feline lower esophageal sphincter (LES). Strips first were identified mechanically as being from the LES, and then either their cellular electrical activities were monitored with microelectrodes or their mechanical activities were monitored with force-displacement transducers. The mean resting membrane potential was -40.6 +/- 1.1 (SE) mV. Transmural electrical stimulation (0.2-8 Hz) induced only hyperpolarizations that were graded and increased as the frequency of stimulation increased. Mechanically, all strips developed tone spontaneously. Electrical stimulation induced only relaxations that likewise were graded and varied directly with the frequency of stimulation. When compared quantitatively, there was a correlation between the integral of the hyperpolarization and the integral of the relaxation. Thus, the tension exerted by LES smooth muscle appears to be related to the amount of current crossing the membrane of the smooth muscle cells.

Animals↗
PubMed1982

Spontaneous electrical activity in pressurized small mesenteric arteries.

Spontaneous electrical activity was recorded intracellularly in vitro from smooth muscle cells of guinea pig small pressurized mesenteric arteries. Spontaneous action potentials were recorded at 37 degrees C at frequencies of 30-55/min. Each action potential consisted of a prepotential (pacemaker potential) followed by a spike of variable amplitude (10-35 mV). This activity was not blocked by tetrodotoxin (TTX) or guanethidine, indicating it was myogenic in origin. Sympathetic nerve stimulation (single 0.5-ms field stimuli) could evoke action potentials in between the spontaneous action potentials and could drive the activity, this effect was blocked by TTX. Addition of the vasodilator adenosine (10(-6) to 10(-4) M) reversibly decreased action potential amplitude and frequency. Lowering the temperature to 35 degrees C for 1-3 min during a single impalement decreased spontaneous action potential frequency. Spontaneous activity was abolished after longer periods at 35 degrees C. The spontaneous activity recorded in vitro at 37 degrees C and 5 or 40 mm Hg inflation pressure was similar to that previously reported from guinea pig and rat mesenteric arteries in vivo. Such activity might be important in the normal physiological control of arterial tone.

Adenosine↗
PubMed1981

Electron-microscopic studies on reaggregate cultures of vascular smooth muscle cells from normotensive and spontaneously hypertensive rats.

Vascular smooth muscle cells were taken from the aortae of the WKY (normotensive) and SHR (spontaneously hypertensive) strains of rat by enzymatic dispersion and put into reaggregate culture. Initially the cells became individual spheroids having average diameters of 10 micrometers and surfaces that were either rough or smooth. The cells were far more complex than they appeared on their surfaces; after one day in culture, there was considerable internal variation in these cells. All the cells, whether WKY or SHR, lost the bulk of their cytoplasmic contents (including myofilaments, many mitochondria, and vesicular structures) in the early stages of culture and eventually became flattened. After 14 days in culture, these modified cells collected to form reaggregates that were commonly roughly spherical and several hundred micrometers in diameter. These reaggregates consisted of peripheral regions made up of several layers of flattened cells overlying cores formed by glia-like networks of cells similar in cytological appearance to the cells at the periphery. The meshes formed in this way contained cellular debris derived from dead cells or extrusion of cellular contents. It appears that SHR cells are quicker to form reaggregates than are WKY cells. Yet the SHR cells retained a rounded conformation after five days, whereas the WKY cells were more flattened and formed a more discrete aggregate at this stage of culture. However, by the fourteenth day of culture, differences between the two cell strains were not so pronounced, as far as could be judged by observations made with scanning and transmission electron microscopy. Both WKY and SHR cells at 14 days appeared highly secretory, possessing large Golgi systems as well as numerous ER cisternae and mitochondria. SHR cells produced greater amounts of connective tissue at all stages of culture than did WKY cells, indicating that a similar difference may contribute to the hypertension which develops naturally in situ in SHR animals.

Animals↗
PubMed1981

Ionic dependence of electrical activity in small mesenteric arteries of guinea-pigs.

The regulation of blood vessel diameter is under the control of the autonomic nervous system (as well as hormones and metabolites), sympathetic nerve stimulation evoking depolarizing post-synaptic potentials. Excitatory junction potentials (EJPs) were recorded from vascular smooth muscle cells of guinea-pig small mesenteric arteries (pressurized) following nerve stimulation. Repetitive stimulation (greater than 5Hz) led to summation of EJPs, which evoked spikes and vasoconstriction. Replacing extracellular Na+ with choline (plus atropine) resulted in a decrease in EJP amplitude, but spike amplitude and maximum rate of rise (+Vmax) were unaffected. Decreasing the Ca2+ concentration produced decreases in EJP amplitude and spike +Vmax. Verapamil and bepridil, agents that depress Ca2+ influx in vascular and visceral smooth muscle, depolarized the membrane and depressed EJPs and spikes at higher concentrations (10(-5) M and 5 X 10(-6) M, respectively). The data indicate that EJPs are dependent on external Na+ and Ca2+ ions, and that spikes are dependent on Ca2+. Thus, neuromuscular transmission in this muscle is similar to that in non-vascular smooth muscles, such as intestinal muscles and vas deferens.

Animals↗
PubMed1981

Angiotensin induction of active responses in cultured reaggregates of rat aortic smooth muscle cells.

Electrical activity was studied in cultured reaggregates of vascular smooth muscle cells prepared from the aortas of normotensive (WKY) and spontaneously hypertensive (SHR) rats. There were no significant differences between the resting membrane potentials of WKY (- 44.7 +/- 0.5 mV) and SHR (- 45.6 +/- 0.5 mV) reaggregates. Electrical field stimulation elicited active responses that consisted of two components: an initial spike component (amplitude, 30-40 mV; +Vmax 1-3 V/s) and a plateau component (amplitude, 10-30 mV; duration 3-5s; +Vmax, 0.1-0.3 V/s). Often the spike component was absent. Both components of the response were abolished by verapamil, Mn++, and Na+-free solutions indicating that Na+ and Ca++ currents may be associated with them. Addition of 10 mM TEA increased the duration of the response, and addition of 0.5 mM BaCl2 to the TEA solution increased the duration even further. The spike component always occurred in the presence of TEA and Ba++. No differences were observed between responses in WKY and SHR reaggregates. A bolus of angiotensin II (AII) (bolus concentration of 1 micro M) elicited a transient depolarization. In some cells an active membrane response was triggered by the depolarization and sometimes included the spike component. Replacing all the Na+ in the solution with either Tris or choline resulted in loss of the response to AII, and in some cells a hyperpolarization was actually seen on addition of the AII. The response to AII was insensitive to verapamil (up to 10(-5) M), but was blocked by 1 mM MnCl2. Reaggregates from both WKY and SHR animals gave similar responses to AII. The data indicates that cultured reaggregates of vascular smooth muscle are electrically excitable and are sensitive to angiotensin. Therefore functional angiotensin receptors must be present in the cultured cells.

Angiotensin II↗
PubMed1979

Electrical coupling in rat myometrium during pregnancy.

Gap junctions were found in rat myometrium only during parturition of abortion. A comparison was made between the values of the length constants obtained from longitudinally cut strips of rat myometrium at the midterm stage of pregnancy and during parturition. No significant difference was found between these values. No significant difference was found between length constants measured in myometrium from rats near term (22 days) and those during parturition, or between midterm myometrium and myometrium taken from animals aborting at midterm following ovariectomy. It was concluded that the appearance of gap junctions in parturient myometrium does not alter the spread of passive current in the longitudinal axis of the cells in these tissues. It is suggested that gap junctions are not required for spread of passive current, and that other structures may provide an alternate path.

Animals↗
PubMed1979

Electrical coupling in the circular muscles of dog jejunum.

Two distinct layers of circular muscle have previously been demonstrated in dog jejunum, the main circular layer containing many gap junction contacts, and an inner dense muscle layer where no gap junctions have been found. Length constants were determined for these muscle layers and no significant difference was found between these values. The main circular muscle cells had lower membrane potentials and may have had abnormally low space constants owing to injury. It was concluded that the absence of gap junctions in the inner dense layer does not reduce the spread of passive current as might be expected of electrically isolated cells, and it is suggested that an alternate pathway for passive current exists in this layer.

Animals↗