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Biomedical subjects

E E Daniel

Publications and source records attributed to E E Daniel.

At least 271 records · Page 15Linked to original sources
PubMed1986

Ultrastructural studies on the neuromuscular control of human tracheal and bronchial muscle.

This study presents an ultrastructural analysis of neural and myogenic control of smooth muscle in human trachea, in small (approximately fourth to seventh order) bronchi. A moderate frequency of gap junctions between smooth muscle cells and a sparse innervation was observed in trachea. In contrast, small junctions without identifiable gaps were identified in bronchi along with a dense, sometimes close innervation of muscle. Most profiles of nerve varicosities in both types of airways were of two types: (1) those containing mostly small agranular and few or no large granular vesicles; and (2) nerves (probably adrenergic) with some small granular vesicles along with other vesicles present in bronchi. In the bronchi some mast cells were found near nerve profiles and in close proximity to smooth muscle. These morphological findings suggest that tracheal muscle may be organized for more neural and less myogenic control of activity. Interactions between mast cells, nerves and muscles in bronchi could influence airway function. These findings imply that a single type of airway muscle may not adequately represent the structural and functional properties of human airway.

Bronchi↗
PubMed1986

The origin of airway hyperresponsiveness.

Consideration of the origin of airway hyperresponsiveness appears central to understanding the origin of asthma. Subjects with and without asthma differ both in the ease with which airway narrowing is produced by inhalation of histamine or methacholine and in the ability to demonstrate a maximal response to these agents. The latter appears, on present evidence, to be due to an added mechanism in asthma rather than the absence of a potent inhibitory process. Airway hyperresponsiveness is probably acquired during life as a result of airway reactions to various stimuli, although genetic factors such as atopy are likely to predispose the person to develop hyperresponsiveness. Environmental stimuli include inhaled allergens, chemical sensitizers, airway infections, immunization, and ozone. Allergen-induced airway hyperresponsiveness occurs in association with late-phase asthmatic responses. This and ozone-induced hyperresponsiveness have been demonstrated to be associated with release of chemical mediators and the cellular phase of inflammation. Their effect does not appear to be accounted for by increase in airway epithelial permeability, decrease in airway caliber, reflex bronchoconstriction, or beta-adrenoceptor blockade. The mechanism(s) responsible for the induced hyperresponsiveness are unknown but may involve airway epithelial damage, edema in and around the airway walls, stimulation of the noncholinergic excitatory or inhibition of the nonadrenergic inhibitory systems, or a change in function of airway smooth muscle. Airway hyperresponsiveness can be transient or persistent. Transient increases in responsiveness are almost certainly associated with mediator release and inflammation. It is not known whether persistent hyperresponsiveness is due to the same process, fired, for example, by leaky mediator-releasing cells and/or to some persisting change in neurogenic or smooth muscle function.

Allergens↗
PubMed1986

Subcellular membrane properties in vascular and non-vascular smooth muscles of Dahl hypertensive rats.

Subcellular membrane fractions were isolated from mesenteric arteries and vas deferens of salt-resistant and salt-sensitive Dahl rats on low-salt (0.4% NaCl) high-salt (8.0% NaCl) diets. Only the salt-sensitive Dahl rats on the high-salt diet developed sustained high blood pressure (BP) after 5 weeks of the high-salt diet. Protein contents, membrane associated enzyme activities, calcium ion (Ca2+) binding and ATP-dependent CA2+ transport were compared in fractions isolated from all four groups. No obvious changes were observed, except for minor enhancement in magnesium ion (Mg2+)- and CA2+ ATPase activities of mesenteric arterial membranes isolated from salt-sensitive Dahl rats on high-salt diet compared to those from other groups of rats. The membrane fractions from vas deferens of salt-sensitive Dahl rats on the high-salt diet, on the other hand, showed decreased ATP-dependent Ca2+ transport compared to those from salt-sensitive Dahl rats on the low-salt diet. No difference was observed in membrane fractions isolated from salt-resistant Dahl rats on high-salt diet compared to those on low-salt diet. The significance of these observations are discussed in relation to the findings previously obtained from corresponding smooth muscle tissues of spontaneous hypertensive rats (SHR).

Adenosine Triphosphate↗
PubMed1986

Receptors for neurotransmitters in opossum oesophagus muscularis mucosa.

Muscularis mucosa of the distal oesophagus of the opossum contains nerves which release acetylcholine and substance P(SP)-like material on field stimulation. The release of SP-like material appeared to be inhibited by the presence of exogenous muscarinic agonists and potentiated by muscarinic antagonists. Analysis of the postjunctional receptors involved using carbachol, McNeil A-343 (McN A-343), atropine and pirenzepine suggested that the receptors were not typical M2-muscarinic receptors. The potency of agonists and antagonists were consistent with some receptor properties resembling M1-muscarinic receptors. Prejunctional receptors to opiates, adenosine, agonists at alpha 2-adrenoceptors and prostaglandins were not detected. Receptors for tachykinins were present on the muscle in this tissue, but did not resemble clearly either SP-E or SP-P type receptors. They appear to be undifferentiated since most tachykinins were of similar potency. These results suggest that not all postjunctional muscarinic receptors in intestinal smooth muscle are M2 in type. There may be a gradation of types between M1 and M2.

Animals↗
PubMed1986

Maintenance of tone, role of arachidonate metabolites, and effects of sensitization in guinea pig trachea.

A study was made of the mechanisms underlying production of resting active tension in guinea pig tracheal smooth muscle and the changes with active sensitization to ovalbumin. The same types of tissues were also analyzed as to their responses to arachidonate. Responses for each tissue were expressed in relation to a scale between zero active tension and maximum active tension in response to carbachol. A variety of selective and nonselective inhibitors of cyclooxygenase or 5-lipoxygenase were shown to affect active tension in a manner consistent with the conclusion that a cyclooxygenase product, probably prostaglandin F(PGF2 alpha) and not thromboxanes was chiefly responsible. The inhibition of active tension produced by cyclooxygenase inhibition was shown to be related to the initial active tension, such that tissues with greater resting active tension had greater reductions in tone. No differences of major importance were found as to the mechanisms underlying tone production in control and sensitized tissues. The tension changes in response to exogenous arachidonate were also found to be dependent on the initial level of active tension; when this was low, tension increased, when it was high, tension decreased or did not change. Effects of inhibitors on these responses were again consistent with the conclusion that primarily excitant prostaglandins, not thromboxanes, were produced. Some suggestive evidence for production of excitatory and inhibitory nonprostaglandin metabolites was obtained. No difference of major importance between control and sensitized tissues was observed in the magnitude or underlying mechanism of production of active tension.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1986

Dense-cored membrane structures in rat myometrial smooth muscle cells: increase in number during parturition.

Membrane-bound structures containing electron-dense material were found in the cytoplasm of the smooth muscle cells of rat myometrium. Most of these structures were observed as membrane-bound vesicles with a variable diameter in the range of 50-90 nm. Some of these were present underneath the cell membranes among the clusters of caveolae and some were found deep in the interior of the smooth muscle cell. The number of such structures progressively increased with gestation reaching the maximum during parturition and decreasing to a minimal level 2 days postpartum, suggesting that the occurrence of these structures is of physiological relevance in parturition. Ovariectomy of the pregnant rats had no influence upon the temporal distribution of these structures within the gestation period, indicating that hormones of ovarian origin are not responsible for the maintenance of these structures during their disappearance after parturition.

Animals↗
PubMed1986

Mechanisms of response to antigen in isolated guinea pig trachea after active sensitization.

A study was made of the responses of guinea pig tracheal muscle in vitro after sensitization by either subcutaneous or intraperitoneal administration of antigens. No difference was observed in the responses of strips from either group to cumulative or single doses of antigen. The responses of the tracheal muscle to antigen were analyzed as to magnitude (relative to maximal carbachol responses), time to peak contraction, and time to half decay. Pyrilamine, an H1-receptor antagonist, slowed the onset of contraction and decay. The latter result suggested a role for histamine in controlling the release of or the response to other mediators and the former was consistent with previous evidence that histamine release augments the initial response. An inhibitor of 5'-lipoxygenase and cyclooxygenase (5,8,11,14-eicosatetraynoic acid), indomethacin, and the slow-reacting substance of anaphylaxis (SRS-A) antagonist FPL-55712 all shortened the time to half decay of the contraction, presumably by different mechanisms. The release and actions of leukotrienes may have been limited by eicosatetraynoic acid and FPL55712, respectively, but the action of indomethacin suggests a modulating role for prostanoids in leukotriene action or release. Nordihydroguaiaretic acid both reduced the maximum response and accelerated decay of this response, suggesting that the maximum response depends upon leukotriene release. Cromoglycate, methysergide, and an inhibitor of thromboxane synthetase were without effect. Both tetrodotoxin and atropine delayed the time to peak contraction and tetrodotoxin also delayed the decay of the contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Control of gap junction formation in canine trachea by arachidonic acid metabolites.

This study examined whether the synthesis of the metabolites of arachidonic acid (AA) was involved in gap junction formation by 4-aminopyridine (4-AP) treatment in vitro in canine trachealis. Studies were made of the effects on gap junction formation of putative inhibitors of the cyclooxygenase and of both this and the lipoxygenase pathway of AA metabolism and the direct effects of prostaglandins (PG) E2 and I2. The number of gap junctions of similar size was increased after brief exposure to 4-AP. After indomethacin (IDM), 4-AP treatment decreased the number of gap junctions but did not affect their size. Pretreatment with 5,8,11,14-eicosatetraynoic acid or nordihydroguiaretic acid, putative inhibitors of cyclooxygenase and lipoxygenase enzymes, inhibited both the 4-AP-induced increase and decrease in the number of gap junctions. FPL 55712, a putative antagonist of leukotriene C4, did not alter either the number or the size of gap junctions when added alone or in combination with IDM. AA alone increased the number of gap junctions, but after IDM, AA decreased the number of gap junctions compared with the controls. Incubation of trachealis strips in vitro for 30 min with PGE2 increased the number of gap junctions by about threefold along with an increase in the size of the gap junctions. Similar incubation with PGI2, however, increased the number of gap junctions by approximately 60% without any change in the size. In the course of some control experiments, an interaction between carbachol and alcohol was observed such that alcohol caused an IDM-sensitive relaxation of carbachol-induced contractions, which was not observed when serotonin was the contractile agent. These results strongly suggest that PGE2 and PGI2 increase the formation of gap junctions in canine trachealis and that these prostanoids are released by 4-AP treatment. Leukotrienes may also be inhibitory in the formation of gap junctions, but FPL 55712 did not affect either the increase or the decrease in gap junctions after 4-AP.

4-Aminopyridine↗
PubMed1986

Substance P: a potent inhibitor of the canine small intestine in vivo.

Intra-arterially administered substance P inhibited neurally activated contractions of the circular muscle of canine small intestine in vivo (lowest effective dose approximately 10(-13) mol). Excitation of intestine required higher (10(-10) mol) doses. The inhibitory effect required functioning nerves, since tetrodotoxin treatment eliminated it. However, inhibition of neurogenic contraction by substance P was unaffected by nicotinic or opiate receptor antagonists or by catecholamine depletion but was reduced by a selective substance P antagonist. Since the inhibition by substance P was also greatly reduced by treatment with atropine or pirenzepine and acetylcholine given intra-arterially produced a similar inhibitory response, stimulation of release of acetylcholine to inhibitory muscarinic receptors on nerves appeared to be the mechanism of this action. Direct smooth muscle effects were ruled out; substance P did not inhibit contractions to intra-arterial acetylcholine or those following tetrodotoxin. In vitro in ileal strips, no inhibition by substance P of any contractile response was found. We propose that the local release of substance P into the myenteric plexus produces inhibition and suggest that this constitutes a physiological function of the neuropeptide. This action may be absent in vitro.

Acetylcholine↗
PubMed1986

Succinyl trialanine p-nitroanilide hydrolytic activity in blood vessels of the rat.

Succinyl trialanine p-nitroanilide [Suc-(Ala)3-pNA] hydrolytic activity, an enzymatic activity related to elastase, in vascular wall was detected and partially characterized. Subcellular distribution of this activity closely paralleled that of plasma membrane marker enzymes, 5'-nucleotidase, and phosphodiesterase I, suggesting its association with the vascular muscle plasma membranes. The same distribution of elastolytic activity was observed. Hydrolytic activity toward Suc-(Ala)3-pNA was inhibited by EDTA, ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid but not by trypsin inhibitor. Enzyme activities were different not only between aortic muscle extracts from young and mature rats, but also among the extracts from elastic and muscular arteries, specific activity being higher in the aortas of young animals or in elastic arteries, respectively. The activity studied [Suc-(Ala)3-pNAase] in vascular wall may play a role in vascular connective tissue metabolism as well as function.

Aging↗
PubMed1986

Calmodulin stimulation of plasmalemmal Ca2+-pump of canine aortic smooth muscle.

Plasma-membrane-enriched fractions of canine aortic smooth muscle possess an ATP-supported Ca2+ accumulation which has an absolute requirement for Mg2+ and a high affinity for Ca2+ (Km approximately 0.5 microM). The rate of ATP-supported Ca2+ transport is not affected by several calmodulin antagonists, but is stimulated by exogenously added calmodulin. The maximal effect of calmodulin on the rate of ATP-dependent Ca2+ transport (at 5.0 microM Ca2+) occurs at 10 micrograms/ml calmodulin and represents an approximately 3-fold stimulation. This calmodulin stimulation of Ca2+ transport does not require pretreatment of the membranes by EGTA and is an intrinsic property of the plasma membranes. A high-affinity Ca2+-ATPase (Km for Ca2+ approximately 0.5 microM) is also present in the aortic smooth muscle plasma membrane. This high-affinity Ca2+-ATPase does not require Mg2+ for catalytic activity, but is in fact inhibited by increasing Mg2+ concentrations. Calmodulin at concentrations effective for the stimulation of the ATP-dependent Ca2+ transport has no effect on the high-affinity Ca2+-ATPase activity or on the basal ATPase activity stimulated by 5 mM Mg2+ or Ca2+. Our results indicate that isolated plasma membranes of canine aortic smooth muscle contain no endogenous calmodulin. The ability of exogenously added calmodulin to stimulate the rate of ATP-dependent Ca2+ transport by vascular smooth muscle plasma membranes suggests that calmodulin may play a role in lowering the cytoplasmic concentration of ionized calcium during vasodilatation. An Mg2+-independent, but not an Mg2+-dependent high-affinity Ca2+-ATPase, was identified in the plasma membranes. This may be separate from the plasmalemmal Ca2+-pump.

5'-Nucleotidase↗
PubMed1986

Determination of molecular size of alpha-1 and alpha-2 adrenoceptors in rat mesenteric artery by radiation inactivation.

Radiation inactivation of alpha-1 and alpha-2 adrenoceptors in the purified plasma membranes of rat mesenteric artery has been performed with high energy electrons at -45 to -55 degrees C. Alpha-1 and alpha-2 adrenoceptor inactivation was monitored with [3H] prazosin and [3H]yohimbine binding, respectively. Internal endogenous and external standards of known molecular weight were used in these studies to determine the molecular size. The average value of D37 for the [3H]prazosin binding site was 6.75 +/- 0.62 Mrad (n = 4) with an estimated molecular size of 122,921 +/- 11,329 Daltons. However, the average value of D37 for the [3H] yohimbine binding site was higher (D37 = 10.05 +/- 0.91 Mrad) and accordingly the molecular size of this binding site was less than the [3H]prazosin binding sites (molecular weight = 82,540 +/- 7478 Daltons; n = 4). Irradiation did not change the dissociation constant of either radioligand, suggesting that the loss of the radioligand binding sites after radiation is due to receptor protein inactivation. These results confirm our earlier finding that [3H]prazosin and [3H]yohimbine bind to two distinct sites in the plasma membranes of rat mesenteric artery. Whether both of these sites are the subunits of a common macromolecule of alpha adrenoceptor on vascular smooth muscle in rat mesenteric artery cannot be concluded from these results. This report is the first one in the literature on the molecular size of alpha-1 and alpha-2 binding sites in vascular smooth muscle.

Animals↗
PubMed1986

Framework of the enteric nerve plexuses: an immunocytochemical study in the guinea pig jejunum using an antiserum to S-100 protein.

Immunostained sections and whole-mount preparations of the layers of the guinea pig jejunum were investigated by an improved peroxidase-antiperoxidase method using an antiserum to S-100 protein. A delicate latticework of S-100 protein immunopositive glial cells was demonstrated extending in the longitudinal muscle layer, myenteric or Auerbach's plexus, circular muscle layer including the deep muscular plexus, submucous layer including the submucous or Meissner's plexus, lamina muscularis mucosae and lamina propria mucosae. The whole enteric nerve plexuses consisted of two subsystems; nerve plexuses of the muscular coat and those of the submucous and mucous coats. These two subsystems were joined to each other by thick, connecting branches perforating the inner circular muscle layer. Extrinsic nerves entering the myenteric plexus formed a specialized junctional structure containing S-100 protein immunopositive glial cells, whereas those entering the submucous plexus ran along the submucous arteries. We proposed the term enteroglial cells to designate the S-100 protein immunopositive cells which ensheathed the somata and processes of the enteric neurons. The frameworks of all structures in the enteric nerve plexuses from the largest ganglia to the thinnest nerve fasciculi were constructed of these enteroglial cells. A spectrum of the enteroglial cells was presented. Those in the myenteric and submucous ganglia were found similar to the astroglia of the central nervous system and to the satellite cells in the peripheral ganglia. Those in the primary and secondary fasciculi of the myenteric plexus formed a kind of neuropil together with the neuronal processes. Those in the tertiary fasciculi of the muscular coat formed the framework of the autonomic ground plexus. We tentatively concluded that the interstitial cells of Cajal contain an immunoreactivity for S-100 protein, and thus are glial in nature. The occurrence of specialized enteroglial cells with a neuron-like function was discussed in the autonomic ground plexus of the muscular coat. In the lamina propria mucosae, there was a fine latticework of the S-100 protein immunopositive enteroglial cells. This latticework corresponded to that of the interstitial cells of Cajal in the villous and periglandular plexuses.

Animals↗
PubMed1985

Peptide neurons in the canine small intestine.

The distributions of peptide-containing nerve fibers and cell bodies in the canine small intestine were determined with antibodies raised against seven peptides: enkephalin, gastrin-releasing peptide (GRP), neuropeptide Y, neurotensin, somatostatin, substance P, and vasoactive intestinal peptide (VIP). Immunoreactive nerve cell bodies and fibers were found for each peptide except neurotensin. In the muscle layers there were numerous substance P, VIP, and enkephalin fibers, fewer neuropeptide Y fibers, and very few GRP or somatostatin fibers. The mucosa contained many VIP and substance P fibers, moderate numbers of neuropeptide Y, somatostatin, and GRP fibers and rare enkephalin fibers. Nerve cell bodies reactive for each of the six neural peptides were located in both the myenteric and submucous plexuses. The distributions of nerve cell bodies and processes in the canine small intestine show many similarities with other mammals, for example, in the distributions of VIP, substance P, neuropeptide Y, and somatostatin nerves. There are some major differences, such as the presence in dogs of numerous submucosal nerve cell bodies with enkephalinlike immunoreactivity and of GRP-like immunoreactivity in submucous nerve cell bodies and mucosal fibers.

Animals↗
PubMed1985

Binding and degradation of angiotensin II by mesenteric artery subcellular membranes.

Rat mesenteric artery microsomes were previously reported to degrade 125I-angiotensin II (AII). It is now shown here that washing the membranes with EDTA and including EGTA in the assay media reduces the 125I-AII degradation to very low levels without reducing the specific binding of 125I-AII. Using EDTA wash and including 5 mM MgCl2 and 0.2 mM EGTA the following characteristics of the binding were observed: microscopic association rate constant (k1) = 1.3 to 2.2 X 10(5) M-1 s-1, microscopic dissociation rate constant (k-1) = 3.8 to 6.4 X 10(-4) s-1, equilibrium dissociation constant (Kd) = 1.8 nM and number of binding sites (Bmax) = 193 fmol/mg protein. The subcellular distribution of the specific binding of 125I-AII at 0.16 nM and 1.63 nM was studied along with the distribution of the marker enzymes. The specific binding paralleled the plasma membrane marker (5'-nucleotidase), but not the putative endoplasmic reticulum marker (NADPH-cyt. c-reductase) or the inner mitochondrial marker (cyt. c-oxidase). Thus the binding to the plasma membrane-enriched fraction F2 occurred with a similar affinity (Kd = 2.2 nM) but with higher number of binding sites (420 fmol/mg protein). This study establishes the 125I-AII binding method suitable for determining the changes in the angiotensin receptor characteristics in the pathophysiology of the vascular smooth muscle.

Angiotensin II↗
PubMed1985

The effect of inhaled hexamethonium bromide and atropine sulphate on airway responsiveness to histamine.

The degree of protection against inhaled histamine achieved by inhalation of the ganglion blocker hexamethonium bromide plus placebo, hexamethonium plus atropine sulphate, and placebo plus placebo was examined in six atopic subjects, four of whom had current asthma. Hexamethonium was administered until there was systemic evidence of ganglionic blockade with a postural drop in blood pressure of 31 +/- 7.5 mm Hg (mean +/- SD) (p = 0.01) and an increase in heart rate of 30 +/- 3.1 bpm (mean +/- SD) (p = 0.01). Atropine was inhaled in a dose (18 mg nebulized during tidal breathing) known to produce systemic inhibition of cardiac and salivary cholinergic (muscarinic) receptors. The airway effects were measured by FEV1. Hexamethonium caused bronchoconstriction in all four subjects with asthma, which was reversed by atropine. The mean provocation concentration of histamine to provoke a 20% fall in FEV1 was 2.97 mg/ml after premedication with placebo, it was not different at 2.84 mg/ml after hexamethonium alone, and it increased slightly to 5.31 mg/ml after both hexamethonium and atropine (p = 0.06). The results suggest that the main effect of inhaled histamine is not by reflex bronchoconstriction but rather through stimulation of H1-receptors on airway smooth muscle. Therefore, histamine hyperresponsiveness in asthma is not primarily caused by a defect in the parasympathetic nervous supply to the airway.

Adult↗
PubMed1985

Ultrastructural immunocytochemical distribution of VIP-like immunoreactivity in dog ileum.

The electron-immunocytochemical protein A-gold technique was employed to study the subcellular localization of vasoactive intestinal polypeptide-like material in dog ileum. The vasoactive intestinal polypeptide-like immunoreactivity was found within a population of large granular vesicles similar in structure in nerve varicosities of the myenteric plexus, the deep muscular plexus, the submucous plexus, the longitudinal muscular layer and the mucosa; none was found in nerve cell bodies. In the myenteric plexus, submucous plexus, the mucosa and the longitudinal muscular layer, varicosities containing similar large granular vesicles consistently remained unstained suggesting that within these plexuses morphologically indistinguishable by our technique large granular vesicles are not necessarily biochemically identical. In the deep muscular plexus, nearly all varicosities with large granular vesicles contained immunoreactivity for vasoactive intestinal polypeptide, but these varicosities often contained a few unstained large granular vesicles. This suggests that vasoactive intestinal polypeptide may share the same varicosity or the same vesicle with other neuropeptides present in this plexus (e.g., substance P or enkephalins) and that this plexus is a site where vasoactive intestinal polypeptide exerts its control over motility.

Animals↗