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Biomedical subjects

E E Daniel

Publications and source records attributed to E E Daniel.

At least 343 records · Page 19Linked to original sources
PubMed1982

Improved electrical coupling in uterine smooth muscle is associated with increased numbers of gap junctions at parturition.

We have studied some passive electrical properties of uterine smooth muscle to determine whether a change in electrical parameters accompanies gap junction formation at delivery. The length constant of the longitudinal myometrium increased from 2.6 +/- 0.8 mm (X +/- SD) before term to 3.7 +/- 1 mm in tissues from delivering animals. The basis of the change was a 33% decrease in internal resistance and a 46% increase in membrane resistance. Axial current flow in an electrical syncytium such as myometrium is impeded by the cytoplasm of individual cells plus the junctions between cells. Measurement of the longitudinal impedance indicated that the specific resistance of the myoplasmic component was constant at 319 +/- 113 omega . cm before term and 340 +/- 93 omega . cm at delivery. However, a decrease in junctional resistance was apparent from 323 +/- 161 omega . cm to 134 +/- 64 omega . cm at delivery. 1.5-2 d after delivery, the junctional resistance was increased, as was the myoplasmic resistance. Thin-section electron microscopy of some of the same muscle samples showed that gap junctions were present in significantly greater numbers in the delivering tissues. Therefore, our results support the hypothesis that gap junction formation at delivery is associated with improved electrical coupling of uterine smooth muscle.

Action Potentials↗
PubMed1982

Effects of glutaraldehyde fixative osmolarities on smooth muscle cell volume, and osmotic reactivity of the cells after fixation.

The contribution of glutaraldehyde (GA) to the effective osmolarity of GA fixatives, the osmotic reactivity of the cells after fixation in GA, and also the duration of fixation in GA on cell volume, were investigated using cultured smooth muscle cells (SMC) and spiral aortic strips. Four fixation procedures were studied. We found that GA contributes to the total effective osmolarity of the fixatives, and that the type of buffers used for the fixatives can also affect the cell volume differently during GA fixation. After GA fixation, the cells were still osmotically reactive, regardless of the buffer types for making up the GA fixatives, so that the osmolarity of the wash buffer after GA fixation is important. However, OsO4 eliminates osmotic responses, thus the osmolarity of OsO4 fixative and wash buffer have negligible influence on the cell volume. Longer fixation time up to 4 h had no effect of the cell volume.

Aldehydes↗
PubMed1982

Changes of gap junctions in myometrium of guinea pig at parturition and abortion.

Myometrial tissues from guinea pigs were quantitatively examined for gap junctions in electron micrographs. Small numbers of gap junctions were present between smooth muscle cells in myometria of pregnant guinea pigs at days 50 and 65 of gestation. The junctions increased in number and size at parturition on day 69 and decreased again to control levels 24 h after parturition. A similar increase in junctions occurred when abortion was induced by 16,16-dimethylprostaglandin E2 (PGE2) on day 65. There were no consistent or significant differences in number of gap junctions from myometrium taken over sites of placental attachment and from other sites. These results together with previous studies suggest that an increase in myometrial gap junction area is associated with and may be essential for parturition in guinea pigs, but the control of their development may differ from that in other mammals.

Abortion, Induced↗
PubMed1982

Pharmacological study of the contractile activity of leukotriene C4 and D4 on isolated human airway smooth muscle.

Synthetic leukotriene C4(LTC4) and leukotriene D4(LTD4) were examined on isolated human tracheal and bronchial smooth muscle. Both LTC4 and LTD4 produced slowly developing contraction of trachealis and bronchus which were submaximal (70-85% of the carbachol maximum) and were not blocked by 1.0 microM atropine, 5.0 microM mepyramine, or 5.6 microM indomethacin. The EC50's for LTC4 and LTD4 were 10.3 and 1.8 nM on trachealis and 1.8 and 1.7 nM on bronchus, respectively. LTD4 was in excess of 20 000 times more potent than acetylcholine on some bronchial and tracheal tissues. Similar differences in potency were obtained in some tissues when LTC4 and LTD4 were compared with histamine. Tissues pretreated for 30 min with 2.0-4.0 microM FPL-55712 were less reactive to LTC4 and LTD4 than untreated control tissues. Established contractions to LTC4 and LTD4 persisted despite washing with fresh Krebs solution, were partially reversed by FPL-55712 (0.5-10 microM) and the Ca2+ channel blocker D-600 (5-10 microM), but were completely reversed by the catecholamine adrenaline (1.0 microM) and by high concentrations of FPL-55712 (greater than 20 microM). The marked potency of the leukotrienes on human tracheal and bronchial smooth muscle suggests an important role for these lipoxygenase products in respiratory disease.

Bronchi↗
PubMed1982

The effects of substance P and met5-enkephalin in dog ileum.

Substance P initiated tonic contraction of dog ileum when administered in doses from 1 pg to 20 micrograms intraarterially (ED50 = 67 ng). Low doses acted to excite cholinergic postganglionic neurones since atropine or tetrodotoxin (TTX) increased the ED50 of substance P about 25-fold, while hexamethonium and local field stimulation had only a small effect to increase the ED50. Also atropine and tetrodotoxin effects were not additive. Higher doses apparently acted to stimulate smooth muscle directly, but no evidence was obtained that local field stimulation could release substance P to act on smooth muscle. Substance P tachyphylaxis prevented substance P actions on cholinergic nerves, but it did not affect responses to intraaterial acetylcholine or block distal inhibition from proximal distention or field stimulation. Met-enkephalin given intraarterially, was also excitatory in doses from 1 ng to 20 micrograms; the amplitude of tonic and phasic contractions produced was significantly decreased by TTX and atropine but was not diminished by hexamethonium or substance P tachyphylaxis. Partial tachyphylaxis to met-enkephalin was produced but was not diminished by hexamethonium or substance P tachyphylaxis. Partial tachyphylaxis to met-enkephalin was produced without affecting the ED50 for substance P. We conclude that substance P acts in small amounts on receptors in myenteric nerves to release acetylcholine by a mechanism, presumably involving postganglionic cholinergic nerves, while met-enkephalin also apparently may act at least in part through a similar TTX- and atropine-sensitive mechanism. These peptides also caused activation of other receptors, probably on smooth muscle by noncholinergic. TTX-insensitive mechanisms. Also the receptors for each peptide which are located on nerves were distinct and independent since tachyphylaxis could be produced to each without affecting the response to the other.

Acetylcholine↗
PubMed1982

Cholinergic control of canine antral immunoreactive gastrin release and motility.

We used acute anesthetized dogs to investigate the role of cholinergic receptors in the relationship between antral immunoreactive (I) gastrin release and antral motility. Electrical stimulation of extrinsic nerves via the cervical vagus or the nerve of Latarjet appeared to increase I gastrin release and antral motility by separate pathways as blockade of muscarinic receptors, i.e., atropinization inhibited motility but did not alter I gastrin release. On the other hand, blockade of nicotinic receptors by hexamethonium treatment obliterated I gastrin release induced by stimulation of the extrinsic nerves but only reduced motility. Field stimulation of intrinsic nerves via serosal electrodes also increased both I gastrin release and local motility. Since hexamethonium treatment only slightly reduced both I gastrin release and motility and atropinization eliminated both during field stimulation, the presence of a muscarinic receptor in the final pathway for each is proposed. Atropine eliminated carbachol-induced I gastrin release and motility increases, even in the presence of nerve blockade by tetrodotoxin. This suggests that this muscarinic receptor is on the smooth muscle cell itself and possibly on the gastrin cell. However a proposed role of the somatostatin cell in controlling gastrin release is also consistent with these data. Thus, both an intrinsic cholinergic and a separate extrinsic noncholinergic pathway are involved in antral release of I gastrin but initiation of motility appears to involve a final common pathway terminating in a muscarinic receptor on the smooth muscle cell.

Animals↗
PubMed1982

Ovarian hormones are not necessary for postpartum regression of gap junctions.

We tested the hypothesis that gap junction degradation in myometrium after parturition in rats requires an ovarian hormone. Compared with unoperated or sham-operated controls, ovariectomy on day 21 slightly delayed parturition (nearly all animals delivered on day 23 instead of day 22). It also significantly reduced the number and membrane area occupied by gap junctions in delivering animals. However, it did not alter the disappearance of gap junctions which occurs less than 24 h after parturition or disassociate gap junction disappearance from parturition. These results do not support the hypothesis of a necessary role for ovaries in gap junctions degradation after parturition and suggest that events associated with parturition may initiate this event.

Animals↗
PubMed1982

Calcium-channel antagonist binding to isolated vascular smooth muscle membranes.

The binding characteristics of the calcium-channel antagonist nitrendipine, an analog of nifedipine, have been measured in plasma membrane enriched microsomal fractions from the canine thoracic aorta, canine mesenteric artery, and rat mesenteric artery. The dissociation constants, KD, for the high-affinity binding sites were, respectively, 0.308, 0.254, and 0.101 nM and Bmax values for binding capacity were 20.3, 25.0, and 18.0 fmol/mg of microsomal protein. Studies with isolated tissues, in which the sensitivity of the high potassium mechanical response to nitrendipine was determined, indicate that the apparent KD for nitrendipine in the canine mesenteric artery, as reflected by the IC50 (mean inhibition constant) value, is 4.5-5.3 nM and for the rat mesenteric artery 2.5-6.6 nM.

Animals↗
PubMed1982

Chloride removal selectively inhibits phasic contractions of guinea pig ileal longitudinal smooth muscle.

Removal of external chloride selectively and reversibly inhibits the phasic responses of the guinea pig ileal longitudinal muscle to high potassium and cholinergic stimulation. The binding of calcium to a relatively superficial pool is affected by chloride removal. Alterations in anionic composition of bathing solution affects the availability of calcium for excitation--contraction (E--C) coupling in smooth muscle.

Animals↗
PubMed1982

Ca2+ dependence of calcium uptake by rat myometrium plasma membrane-enriched fraction.

ATP-dependent Ca uptake by rat myometrium plasma membrane fraction occurs only in the presence of magnesium. Studies of the membrane protein-concentration dependence of the ATP-dependent Ca uptake showed that at 33 micrograms protein/ml the uptake increased linearly with time up to 2 min and deviated from linearity at longer times. Studies of the Ca2+ concentration dependence of initial Ca-uptake velocity (reaction time 2 min) of the uptake reaction showed that 1) ATP-dependent Ca uptake increased with increasing Ca2+ concentration from 0.1 to 1 microM, and a further increase in Ca2+ concentration above 1 microM did not enhance the uptake further and 2) the Ca-uptake dependence on Ca2+ concentration was nonhyperbolic with a Hill coefficient of 1.3-1.7 and half saturation occurring at 0.4-0.5 microM Ca2+. These data suggest that the ATP-dependent Ca movement by rat myometrium plasma membranes may play a very important role in smooth muscle relaxation. Physiological implications of the nonhyperbolic kinetics are also discussed.

Adenosine Triphosphate↗
PubMed1982

Control of human airway smooth muscle: in vitro studies.

An in vitro study of neural and myogenic control of human tracheal smooth muscle was undertaken. Over 80% of these had active tension and 13% had phasic contractile activity. Tonic and phasic activities were not reversed by indomethacin, 5,8,11,14-eicosatetraynoic acid, methysergide, mepyramine, atropine, or tetrodotoxin (TTX) but were blocked by the calcium antagonist verapamil. In some quiescent strips, tonic and/or phasic activity was induced by exposure to potassium-conductance blockers such as 4-aminopyridine (4-AP) and tetraethylammonium chloride (TEA). Electrical (field) stimulation resulted in frequency-dependent biphasic responses: an initial atropine-sensitive cholinergic contraction followed by a nonadrenergic relaxation. This biphasic response to low stimulus parameters (less than 0.5 ms, less than 15 Hz) was blocked by TTX and scorpion venom and enhanced by 4-AP and TEA, consistent with a neural mechanism. Relaxation responses to longer pulse durations (0.5-1 ms) were not blocked by TTX despite abolition of contraction nor were they enhanced by 4-AP and TEA, suggesting a nonneural mechanism. ATP, adenosine, arachidonate metabolites, histamine, 5-hydroxytryptamine, neurotensin, or vasoactive intestinal polypeptide were ruled out as possible nonadrenergic mediators. The nature and physiological significance of the nonneural inhibitory response remains unknown.

4-Aminopyridine↗
PubMed1982

Role of smooth muscle alpha 1-receptors in nonspecific bronchial responsiveness in asthma.

It has been postulated that the wide range of bronchial hyperresponsiveness to nonspecific stimuli, such as methacholine, found in asthmatics could be due to increased alpha-adrenergic receptor activity in the airways. We examined alpha 1- receptor responsiveness by comparing the responses obtained after inhaling the alpha 1-agonist phenylephrine (2 to 32 mg/ml) with the responses obtained after inhaling buffered saline in 10 asthmatics in whom the provocation concentration of methacholine causing a 20% fall in the forced expiratory volume in one second (FEV1) ranged from 0.13 to 9.19 mg/ml. Subjects were pretreated with inhaled atropine (3 mg nebulized during tidal breathing) and inhaled propranolol (3 mg nebulized during tidal breathing) to exclude cholinergic and beta receptor activity influencing bronchial smooth muscle responsiveness. After pretreatment drugs, the mean value for FEV1 before phenylephrine inhalations did not differ significantly from that before the control inhalations of saline. There was no significant change in FEV1 after phenylephrine compared with that after saline, suggesting that bronchial smooth muscle alpha 1-adrenergic receptor activity was not present. We conclude that increased bronchial smooth muscle alpha 1-receptor activity is not the primary abnormality producing the variability between asthmatics in nonspecific bronchial hyperresponsiveness.

Adult↗
PubMed1982

Isolation and properties of plasma membrane from smooth muscle.

A generalized approach to obtain relatively pure fractions of plasma membrane from smooth muscle tissues for studying calcium transport is described. The use of various markers for cellular membranes to establish the purity of various fractions is critically considered. Plasma membranes from rat myometrium have been isolated in a purity estimated to be 95-99%. Plasma membrane purifications to 70-80% have been achieved from rat mesenteric arteries and veins, canine tracheal smooth muscle, rabbit intestinal muscle, rat vas deferens, rat fundus, and dog gastric corpus. The ATP-dependent transport of Ca is correlated with the distribution of plasma membrane markers. Ca gradient of greater than 1000-fold have been achieved. ATP-dependent active Ca transport by plasma membranes could sometimes be stimulated by oxalate or phosphate. Anion activation of Ca active transport is not a marker for endoplasmic reticulum. In some smooth muscles (e.g., rat vas deferens) ATP-dependent Ca uptake did not correlate exclusively with the distribution of plasma membrane markers. Instead, the correlation seemed to be with NADPH-cytochrome reductase EC 1.6.2.5 activity (putative endoplasmic reticulum marker) as well as with plasma membrane markers. In all smooth muscles, active Ca transport appears to be a property of the plasma membrane; in some it may also be a property of the endoplasmic reticulum. Mitochondria actively transport Ca, but in most systems studied to date, the Km for Ca2+ for this transport is higher than that for plasma membrane. Thus the plasma membrane may be the major physiological mechanism of active transport for Ca out of cytoplasm of smooth muscle cells. In two plasma membrane fractions (from rat myometrium and mesenteric arteries) it has been possible to demonstrate the existence of an Na-Ca exchange system. Its contribution to lowering cytoplasmic Ca is unknown.

Adenosine Triphosphate↗
PubMed1981

Biochemical abnormalities of venous plasma membrane fraction isolated from spontaneously hypertensive rats.

Alkaline phosphatase activity and Ca2+ accumulation were examined in the isolated plasma membrane fractions from small arteries and veins of spontaneously hypertensive (SHR) and normotensive (WKY). Increased Ca2+ binding by plasma membrane fractions from veins, decreased ATP-dependent Ca2+ accumulation by those from arteries and increased alkaline phosphatase activity in both fractions from SHR were observed. We conclude that biochemical abnormalities in vascular smooth muscle cell membrane cannot be explained solely as adaptive changes induced by elevated blood pressure.

Animals↗
PubMed1981

Disorganised electrical activity in a child with idiopathic intestinal pseudo-obstruction.

This report presents the findings of investigation of a child with idiopathic intestinal pseudo-obstruction (IIP). Functional abnormalities of the smooth muscle of the gastrointestinal tract were disclosed by electrical recordings from the gut obtained after laparotomy. In vitro analysis of tissue and ultrastructure were undertaken and a possible aetiology of the disorder in this patient based on these findings is presented.

Action Potentials↗
PubMed1981

Initiation of migrating myoelectric complexes in human subjects: role of duodenal acidification and plasma motilin.

The hypothesis that acid, emptied intermittently from the stomach during fasting, might initiate the duodenal phase of the migrating motor complex was tested in normal human subjects. In addition, the relationship between plasma motilin concentrations and the initiation of migrating motor complexes was examined. Migrating complexes occurred spontaneously in the absence of acid in the duodenal bulb and in the presence of duodenal bulb neutralization with sodium bicarbonate. Thus duodenal bulb acidification is not necessary for initiation of the duodenal phase of the migrating motor complexes. Furthermore, cyclical increases in plasma motilin concentrations were not closely correlated with the initiation of the gastric phase of maximal activity of the migrating motor complexes. However, motilin concentrations were decreased significantly following onset of the duodenal phase III. We conclude that neither duodenal acidification nor increases in motilin concentration are necessary to initiate migrating motor complexes in man.

Adult↗
PubMed1981

Changes in plasma motilin concentration in response to manipulation of intragastric and intraduoduenal contents in man.

Immunoreactive plasma motilin concentrations were studied following a variety of stimuli in 24 healthy fasting subjects. Plasma motilin was measured by a radioimmunoassay using antibody GP 71 (J. C. Brown) and natural porcine motilin as standard. Basal motilin levels ranged from undetectable to 365 pg/mL. Antral and intraduodenal infusion of 50 mL o.1 N HCl (pH 1.2) at 5 mL/min failed to alter significantly plasma motilin levels but duodenal acid infusions at 17 mL/min caused a significant increase (70.8 +/- 29.5 pg/mL, mean +/- SEM; n = 6), maximal at 40 min. Duodenal alkalinization with 50 mL 0.3 M Tris buffer (pH 8.0) infused at 5 mL/min produced no change in plasma motilin. A mixed meal did not affect plasma motilin levels. Ingestion of 60 g fat significantly increased plasma motilin (n = 13; maximal increase 150.3 +/- 43.3 pg/mL at 30 min) but duodenal infusions of fat failed to increase plasma motilin levels. These results suggest that motilin secretion induced by fat requires that the fat be present initially within the stomach for secretion to occur. We conclude that ingested fat is a potent stimulus of motilin release. As duodenal acidification (50 mL 0.1 N HCl over 10 min) induces duodenal activity resembling migrating motor complexes but does not release motilin, our data argue against the release of motilin following duodenal acidification as a trigger for the initiation of these complexes in man.

Adult↗