Biomedical subjects

K Huber

Publications and source records attributed to K Huber.

At least 109 records · Page 6Linked to original sources

PubMed1998

TrkB and neurotrophin-4 are important for development and maintenance of sympathetic preganglionic neurons innervating the adrenal medulla.

The adrenal medulla receives its major presynaptic input from sympathetic preganglionic neurons that are located in the intermediolateral (IML) column of the thoracic spinal cord. The neurotrophic factor concept would predict that these IML neurons receive trophic support from chromaffin cells in the adrenal medulla. We show here that adrenal chromaffin cells in the adult rat store neurotrophin (NT)-4, but do not synthesize or store detectable levels of BDNF or NT-3, respectively. Preganglionic neurons to the adrenal medulla identified by retrograde tracing with fast blue or Fluoro-Gold (FG) express TrkB mRNA. After unilateral destruction of the adrenal medulla, 24% of IML neurons, i.e., all neurons that are preganglionic to the adrenal medulla in spinal cord segments T7-T10, disappear. Administration of NT-4 in gelfoams (6 microgram) implanted into the medullectomized adrenal gland rescued all preganglionic neurons as evidenced by their presence after 4 weeks. NT-3 and cytochrome C were not effective. The action of NT-4 is accompanied by massive sprouting of axons in the vicinity of the NT-4 source as monitored by staining for acetylcholinesterase and synaptophysin immunoreactivity, suggesting that NT-4 may enlarge the terminal field of preganglionic nerves and enhance their access to trophic factors. Analysis of TrkB-deficient mice revealed degenerative changes in axon terminals on chromaffin cells. Furthermore, numbers of FG-labeled IML neurons in spinal cord segments T7-T10 of NT-4-deficient adult mice were significantly reduced. These data are consistent with the notion that NT-4 from chromaffin cells operates through TrkB receptors to regulate development and maintenance of the preganglionic innervation of the adrenal medulla.

Adrenal Medulla↗

PubMed1998

Inherited platelet glycoprotein polymorphisms and a risk for coronary heart disease in young central Europeans.

Among central Europeans polymorphisms of GPIIIa, GPIb, GPIIb, and GPIa named human platelet antigen-1 (HPA-1), -2, -3, and -5 are the clinically most relevant systems in which alloimmunization occurs. These genetically determined polymorphisms of glycoproteins may render platelets sensible for plaque formation and thus could increase risk for coronary artery disease (CAD). We therefore determined gene frequencies of HPA-1, -2, -3, and -5 in European patients suffering from CAD (n = 92; median age, 46 years) or CAD accompanied by diabetes mellitus (DM) (n = 30; median age, 60 years, DM I/II, 5/25) and compared the data obtained with those in DM patients without CAD (n = 80; median age, 43 years; DM I/II, 53/27) and a control group (newborns, n = 906). Triglyceride and cholesterin levels as well as the percentage of smokers was significantly higher in the CAD group compared with the diabetics without DM (p < 0.005). No significant difference of the frequencies of any HPA-type between CAD patients with or without DM, diabetics, or controls could be detected. This was also true when evaluating a subgroup of patients aged 45 years or younger. To include a mutual influence of the described HPA-polymorphisms, we condensed the four HPA genotypes to joint glycoprotein variants. Again the same frequencies were found in patient groups and controls, when analyzing the five most common condensed joint glycoprotein variants. The analysis of the combined published studies shows that the pooled HPA-1 allele frequencies are identical in controls and CAD patients. Thus, no significant association between the polymorphisms of any of the studied HPA systems and the development of CAD can be found in central Europeans.

Adolescent↗

PubMed1998

Restoration of coronary blood flow by single bolus injection of the GPIIb/IIIa receptor antagonist c7E3 Fab in a patient with acute myocardial infarction of recent onset.

It has been debated that primary coronary angioplasty could be more effective if immediate antithrombotic therapy would contribute to a faster recanalization of the infarct-related artery. This is the first report of a patient who presented at the emergency department with acute anterolateral myocardial infarction, in whom a single bolus injection of c7E3 Fab (0.25 mg/kg body weight) led to complete reperfusion of the infarct-related coronary artery during organization time for planned acute coronary angioplasty. Pain relief 15 min after initiation of therapy and ST-segment resolution of > 50%, as well as occurrence of idioventricular rhythm 30 min thereafter, were suggestive of successful recanalization before the coronary intervention was started. Diagnostic coronary angiography at 90 min revealed TIMI-grade 3 flow in the infarct-related coronary artery with only moderate luminal irregularities. Bolus administration of c7E3 Fab could be effective for dissolving platelet-rich thrombi in the early stage of acute myocardial infarction (AMI) and may therefore represent a promising "bridging" therapy in patients with AMI elected for primary coronary angioplasty.

Abciximab↗

PubMed1998

Distinct populations of macrophages in the adult rat adrenal gland: a subpopulation with neurotrophin-4-like immunoreactivity.

Macrophages are widely distributed in lymphohaemopoietic and many other mammalian tissues, where they are mainly involved in host defence mechanisms, phagocytosis, wound repair, and secretion of growth factors. Increasing evidence suggests that secretory products of macrophages can influence adrenal gland functions. In the present study, we have used specific antibodies to ED1 (cytoplasmic antigen), ED2 (membrane antigen), ED8 (membrane antigen), and OX-6 (MHC class II/membrane antigen) as markers for macrophages to examine their distribution within the adult rat adrenal gland. ED2 and OX-6 recognize distinct subpopulations of adrenal gland macrophages, whereas macrophages immunoreactive (-ir) for ED1 and ED8 could not be detected. OX-6-ir macrophages were most numerous in the cortical reticularis and glomerulosa zones, while only few cells were found in the zona fasciculata and in the adrenal medulla. Macrophages immunoreactive for ED2 were restricted to the adrenal medulla. The majority of these macrophages were associated with vascular sinuses or chromaffin cells. By double-immunolabelling we found that most of ED2-ir medullary macrophages contain neurotrophin-4 (NT-4)-like ir. Attempts to clarify whether macrophages take up NT-4 from NT-4-ir chromaffin cells indicated that medullary macrophages are immunonegative for chromogranin A and neuropeptide Y, two major secretory products of chromaffin cells. In situ hybridizations and immunofluorescence showed expression of the neurotrophin receptor TrkA, but not TrkB in the adrenal medulla. In vitro studies indicated that NT-4, similar to nerve growth factor, can induce c-fos-ir in chromaffin cells. We conclude that chromaffin cells are putative targets for adrenal medullary NT-4, whose functions remain to be clarified.

Adrenal Cortex↗

PubMed1998

Decreased urinary apolipoprotein (a) excretion in patients with impaired renal function.

BACKGROUND: Plasma lipoprotein (a) [Lp(a)] levels are elevated in patients with kidney disease and are strongly associated with premature cardiovascular disease and stroke. METHODS: As the kidney is suggested to play an important role in apolipoprotein (a) [apo(a)] catabolism and as apo(a) fragments appear in urine, we determined plasma Lp(a) levels and urinary apo(a) excretion in relation to kidney function in a large cohort of renal patients. A total of 368 renal patients with normal or different degrees of impaired renal function and 163 healthy control subjects matched for age and sex were investigated. Plasma Lp(a) and urinary apo(a) were analysed immunochemically. RESULTS: Renal patients were found to have significantly elevated total cholesterol and low-density lipoprotein (LDL)-C values but lower high-density lipoprotein (HDL)-C values than control subjects. Plasma Lp(a) values were significantly higher only in patients with creatinine clearance < 70 mL min-1. There was a significant correlation between urinary apo(a) and plasma Lp(a) in patients and control subjects. Urinary apo(a) excretion was significantly lower in patients than in control subjects and showed no correlation with urinary protein excretion. CONCLUSION: Although it is unlikely that impaired renal excretion of apo(a) fragments largely contributes to increased plasma Lp(a) levels in patients suffering from impaired kidney function, these data suggest that urinary apo(a) excretion is significantly decreased in renal patients and that this might contribute to increased plasma Lp(a) levels in this patient group.

Aged↗

PubMed1998

Efficacy of thrombolytic therapy in pulmonary embolism determined by MION-enhanced MRA: an experimental study in rabbits.

RATIONALE AND OBJECTIVES: This study determined whether contrast-enhanced magnetic resonance angiography could be used as a noninvasive imaging technique to determine the therapeutic effect and endpoint in thrombolysis of acute pulmonary embolism in an animal model. METHODS: New Zealand white rabbits (n = 18) were anesthetized and mechanically ventilated. Single (n = 12 emboli) or dual (n = 12 emboli in 6 animals) pulmonary emboli were created by injecting autologous thrombi through a right internal jugular venous approach. Three-dimensional time of flight (TOF) magnetic resonance angiograms were obtained after intravenous administration of 2 mg Fe of a long circulating monocrystalline iron oxide. Animals then received 5000 IU heparin and 1.3 mg recombinant tissue plasminogen activator/kg intravenously, and magnetic resonance angiography was repeated 30 minutes and 60 minutes after initiation of thrombolytic therapy. RESULTS: MION-enhanced magnetic resonance angiography accurately detected pulmonary emboli in all rabbits. Thrombolysis during the observation period was successful in 8 of the 18 animals. In animals with a single embolus, the revascularization rate was 50% (6 of 12 emboli). The rate was 33% (4 of 12 emboli) in animals with multiple emboli. Magnetic resonance angiography allowed determination of thrombus resolution or thrombus persistence. CONCLUSIONS: It was feasible to diagnose pulmonary embolism accurately in this experimental study and to monitor thrombolysis of pulmonary emboli by MION-enhanced magnetic resonance angiography.

Acute Disease↗

PubMed1998

Renal phosphate excretion in goats.

It was the aim of these experiments to characterize further the role of salivary glands and kidneys in phosphate (Pi) homeostasis of small ruminants. Renal clearance experiments were performed in five female, non-pregnant adult goats during infusions of physiological NaCl or isotonic phosphate solution. Basal plasma Pi concentrations of 1.6 +/- 0.3 mM (NaCl infusion) were associated with a renal resorption of the filtered Pi by 98.5-99.3% and Pi was excreted in the urine at a rate of 1.2-2.8 mumol/min. Elevating the plasma Pi levels up to 7.2 +/- 1.7 mM resulted in significant increases of Pi excretion. The mean plasma threshold for renal Pi excretion of these animals was high (4.3 +/- 1.0 mM) and thus substantially higher than the physiological range of plasma Pi. The maximal tubular resorption rate for Pi in goats was found to be higher than the respective values in monogastric animals. In relation to the enhanced Pi concentrations in plasma the salivary Pi concentrations increased simultaneously and reached a maximum level of about 66.3 mM at plasma levels between 4-6 mM. Indications for hormonal regulation mechanisms via parathyroid hormone (PTH) and calcitriol could not be detected during the infusion periods.

Animals↗

PubMed1998

Concentration of endogenous tPA antigen in coronary artery disease: relation to thrombotic events, aspirin treatment, hyperlipidemia, and multivessel disease.

Tissue plasminogen activator (tPA) is the major plasminogen activator responsible for dissolving blood clots found in blood vessels. However, elevated concentrations of tPA antigen were found to be related to adverse events in patients with coronary artery disease (CAD). Considerable controversy about the significance of these results exists. The goal of this cross-sectional study was to identify independent determinants for tPA antigen concentrations in patients with CAD, to possibly clarify the above paradoxical relationship. The baseline tPA antigen concentrations of 366 patients with angiographic evidence of coronary sclerosis were determined. Univariate analysis showed that age (P=0.013), angiographic extent of disease (P<0.001), presence of angina at rest (P<0.001), diabetes mellitus (P=0.004), hypercholesterolemia (P=0. 045), hypertriglyceridemia (P=0.015), and chronic intake of nitrates (P<0.001) were significantly and positively related to tPA antigen concentration, while the chronic intake of aspirin was inversely related to tPA antigen (P<0.001). In addition, plasminogen activator inhibitor type 1 (PAI-1) activity was found to be significantly and positively associated with tPA antigen concentration (P<0.001). A multivariate analysis identified chronic low-dose aspirin therapy (P<0.001), PAI-1 activity (P<0.001), hypertriglyceridemia (P=0.005), the type of angina (P=0.026), multivessel disease (P=0.041), and hypercholesterolemia (P=0.043) as significant and independent determinants of tPA antigen. While hypertriglyceridemia and hypercholesterolemia both are related to the underlying disease, the type of angina and the number of involved vessels are linked to the severity and extent of disease, and all of them are indicators of a prothrombotic state found during the progression of CAD. In contrary, low-dose aspirin rather would decrease the likelihood of thrombotic events. The relation of tPA antigen to PAI-1 activity furthermore underlines the relation between tPA antigen concentration and a prothrombotic state. Therefore, the positive or-in case of aspirin therapy-negative correlation of these parameters with tPA antigen concentration would indicate that thrombus formation and simultaneous endothelial cell activation might be major determinants for tPA antigen concentration in CAD.

Adult↗

PubMed1998

Diagnostic challenges of hepatitis C virus infections.

In less than 10 years, tremendous progress has been made in our understanding of the biology of hepatitis C virus. Since it was defined as the causal agent of most hepatitis non-A, non-B infections in 1989, clinical laboratories now have access to powerful new techniques for the diagnosis of infection and control of therapy. Identification of the specific virus strain in the patients as well as measurement of the individual viral load and the prediction of a possible therapeutic success have become routine procedures. This effort is warranted because the treatment options are still limited, with alpha-interferon being the only approved drug. No new treatment regimens have emerged yet from the wealth of data from subtyping and quantitating.

Journal Article↗

PubMed1998

Pain management for dermatologic laser surgery: a nursing perspective.

Pain after laser surgery is one of the most commonly experienced patient problems. It is a pervasive part of laser treatment and a problem with which nurses and physicians are expected to deal. The nurse's most important role is preoperative patient teaching. Prior to undergoing the prescribed treatment, patients must have a realistic understanding of the laser procedure, including the expected sensations associated with the surgery. Education will not only correct misconceptions and reduce anxiety, but will also allow patients to play an active role in their surgery and to optimize fully from pain-reducing techniques and strategies.

Humans↗

PubMed1998

Effect of antihypertensive treatment with doxazosin on insulin sensitivity and fibrinolytic parameters.

The effects of the selective alpha-1-adrenoceptor antagonist doxazosin on metabolic and fibrinolytic parameters were studied in hypertensive patients with various degrees of fasting plasma insulin levels (Group A: 22.5 +/- 3 microU/ml, Group B: 8.1 +/- 1.5 microU/ml; p <0.01) to disclose a potential link between a doxazosin-induced alteration of insulin and/or lipid metabolism and possible changes of these parameters on the fibrinolytic system. Doxazosin treatment resulted in a dose-dependent reduction of basal insulin levels in group A to 16 +/- 3 microU/ml; p <0.05. This finding was paralleled by a dose-dependent increase in t-PAmass concentration in the same patient group (basal t-PAmass from 9.7 +/- 1 to 15.5 +/- 2 ng/ml; p <0.05). As PAI-1 "active" as well as total antigen levels were not altered in parallel, the net effect on the endogenous fibrinolytic system is an increase of the fibrinolytic potential.

Antihypertensive Agents↗

PubMed1998

Plasma Lp(a) levels are increased in patients with chronic thromboembolic pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a disease resulting from the thromboembolic obstruction of the segmental and/or large size pulmonary arteries, subsequently leading to pulmonary arterial hypertension. Incomplete resolution of acute pulmonary emboli and thrombus organization are believed to be important for the development of the disease. Primary pulmonary hypertension (PPH) is a further disease that at present is poorly understood but shows a clinical picture similar to CTEPH. Since lipoprotein(a) [Lp(a)]. a genetically determined risk factor for atherosclerosis and thrombosis, has been found increased in plasma of patients with deep vein thrombosis and pulmonary embolism, we measured plasma Lp(a) levels in 40 patients with CTEPH and 50 patients with PPH and compared them to 50 matched controls. The median for Lp(a) plasma levels was significantly higher in CTEPH patients (26.6 mg/dl) than in PPH patients (9.6 mg/dl) and controls (7.2 mg/dl). Increased plasma Lp(a) could, therefore. play a significant role in the mechanisms of ongoing thrombosis and thrombus organization in CTEPH, while its possible role in PPH can be limited to a small number of patients.

Adult↗

PubMed1997

Increased prevalence of a polymorphism in the gene coding for human prothrombin in patients with coronary heart disease.

A number of genetic risk factors for the development of coronary heart disease has been identified in the past. Some of these represent polymorphisms in genes of proteins which are associated with the process of blood clotting. We investigated the distribution of a recently described G/A polymorphism in the 3'untranslated region of the human prothrombin gene (nt 20210) in 98 patients (19 female age: 53 + 12 SD years and 79 male, age: 49 + 8.5 SD years) with coronary heart disease and in 102 healthy newborns by enzymatic amplification of the genomic DNA carrying the polymorphic site and by subsequent restriction digest. The diagnosis of coronary heart disease was established by coronary angiography in all patients. The frequency of the A allele in the healthy newborns was 0.98% (0.2%-3.5%; CI 0.95) with the G/A genotype occurring in 1.96% (0.24%-6.9%; CI 0.95). In the group of patients with coronary heart disease the G/A genotype was found in 5.1% (1.7%-11.4%; CI 0.95). 94.9% of the patients studied showed a G/G genotype. The A/A genotype was neither detected in the newborns nor in the patients with coronary heart disease. This preliminary study strongly suggest that the presence of the G/A polymorphism in the 3'untranslated region of the gene coding for human prothrombin is associated with the occurrence of coronary heart disease.

Adult↗

PubMed1997

Evaluation of bedside prothrombin time and activated partial thromboplastin time measurement by coagulation analyzer CoaguCheck Plus in various clinical settings.

In the present study CoaguCheck Plus (CCP), a coagulation test system using whole blood, was evaluated with respect to its comparability with widely distributed conventional routine coagulation assays. A correlation of r = 0.997 (p < 0.0001) was found between INR of CCP-prothrombin time (CCP-PT) and Thrombotest (KC-1 analyzer) in patients on oral anticoagulant therapy. A correlation of r = 0.899 (p < 0.001) between CCP-aPTT and Actin ES aPTT (STA analyzer) was found in heparinized patients. Impaired hepatic hepatic coagulation factor synthesis in liver cirrhosis patients was detected by CCP-PT with a sensitivity of 0.75 and by Normotest (STA analyzer) with a sensitivity of 0.92. Those patients with normal CCP-PT values and liver disease had, only mild reductions (> 30% of normals) in coagulation factors II, V, VII or X. CCP-aPTT was also performed in patients with a deficiency in the so called endogenous coagulation factors VIII, IX, XI and XII. CCP-aPTT showed a sensitivity similar to that of Actin FS aPTT in the detection even of mild deficiencies in factors VIII, IX and XII; factor XI deficiency was however detected only in patients with severe (< 12% of normals) disease; lupus anticoagulants were detected with a high sensitivity.

Blood Coagulation Tests↗

PubMed1997

Expression of fibroblast growth factor-2 in hypoglossal motoneurons is stimulated by peripheral nerve injury.

We have studied the expression of basic fibroblast growth factor 2 (FGF-2) and FGF receptor 1 (FGFR1) in the hypoglossal motor system during degeneration and regeneration by using an RNase protection assay, in situ hybridization, and Western blot analysis. The FGF-2 transcript was found to be weakly expressed in the hypoglossal motoneurons of the adult rat. Both peripheral transection and crush injury of the hypoglossal nerve resulted in a marked up-regulation of the FGF-2 mRNA in motoneurons of the hypoglossal nucleus (with a peak at 10 and 11 days postlesion) as well as in the proximal and distal nerve stumps. The FGFR1 transcript was strongly expressed by hypoglossal motoneurons of unlesioned rats. Neither axotomy nor crush lesion of the hypoglossal nerve revealed any alteration of the expression level and cellular localization in the hypoglossal nucleus, but they did result in a significant increase of the FGFR1 mRNA level in the proximal and distal nerve stump. Western blot analysis of the hypoglossal nucleus revealed the presence of the 21 kD and 23 kD isoforms and of a weak expression of the 18 kD isoform. Hypoglossal nerve transection resulted in a complete down-regulation of the FGF-2 protein 3 days after lesion. After 14 days, however, the level of the three isoforms was increased above the control level. The regulation of FGF-2 in hypoglossal motoneurons after experimental nerve injury is in agreement with the idea of a lesion-related function of FGF-2. Together with previously reported neurotrophic effects, these results suggest that FGF-2 provides trophic support for lesioned motoneurons. At the injury site, FGF-2 could be involved in the regulation of the myelination.

Animals↗

PubMed1997

[Follow-up studies of routine health screening in Vorarlberg 1986-1994].

In this longitudinal study we observed a sample of people who participated in the general health screening program in Vorarlberg between 1986 and 1994. The aim was to analyse the changes in the parameters, body-mass index, diastolic and systolic blood pressure, blood glucose, cholesterol, gamma-GT and triglycerides of 1205 women and 718 men over this period. Using the baseline values recorded in 1986 as reference the sample was divided into groups with normal, slightly increased and highly increased values for the parameters. On average, the risk factors of people with highly increased baseline values decreased on both a short-term (1986-1988), and a long-term basis (1986-1994). The only exception was the body-mass index, which showed a slight reduction in the first two years and a slight increase in the long run. The normal baseline values rose in all the variables within the period of observation. Sex differences must be considered with regard to body-mass index, cholesterol and triglycerides, age differences are significant with regard to body-mass index, systolic blood pressure and cholesterol. The results of the study point to the usefulness of regular participation in general health screening programs. They show, in particular, that the risk factors for civilization-induced diseases diminish visibly in the group of highly endangered people.

Adult↗

PubMed1997

Urinary apo(a) discriminates coronary artery disease patients from controls.

Increased plasma lipoprotein (a) (Lp(a)) levels are associated with premature cardiovascular diseases and stroke. Since Lp(a) immune reactivity is found in urine we compared urinary apolipoprotein (a) (apo(a)) with plasma Lp(a) levels in 116 patients suffering from angiographically proven coronary artery diseases with that of 109 controls. Urinary apo(a) investigated by immuno blotting, revealed a distinct apo(a) fragmentation pattern with molecular weights between 50 and 160 kDa. Apolipoprotein B however was not secreted into urine. Lp(a) and apo(a) were measured by a fluorescence immuno assay. Within single individuals, urinary apo(a) levels correlated significantly with creatinine (Rho, 0.98; P < 0.0005). Medians and 25/75 percentiles of urinary apo(a) in coronary artery disease (CAD) patients were 5.70, 3.25 and 10.35 microg/dl and in controls 2.64, 1.43 and 3.50 microg/dl respectively. At cut-off levels of 30 mg/dl for plasma Lp(a) and 10 microg/dl of urinary apo(a) respectively, both paramenters showed comparable sensitivities (33.8% vs. 26.7%), yet the specificity (76.1% vs. 91.7%) and the positive predictive value (60.0% vs.76.4%) of urinary apo(a) were much higher. In receiver-operating characteristic plots, urinary apo(a) was much more sensitive at high specificities i.e. greater than 60% as compared to Lp(a). Urinary secretion of apo(a) fragments normalized to creatinine is stable in a given individual and significantly associated with coronary artery disease.

Apolipoproteins A↗

PubMed1997

Reduced acetylcholinesterase (AChE) activity in adrenal medulla and loss of sympathetic preganglionic neurons in TrkA-deficient, but not TrkB-deficient, mice.

TrkA high-affinity receptors are essential for the normal development of sympathetic paravertebral neurons and subpopulations of sensory neurons. Paravertebral sympathetic neurons and chromaffin cells of the adrenal medulla share an ontogenetic origin, responsiveness to NGF, and expression of TrkA. Which aspects of development of the adrenal medulla might be regulated via TrkA are unknown. In the present study we demonstrate that mice deficient for TrkA, but not the neurotrophin receptor TrkB, show an early postnatal progressive reduction of acetylcholinesterase (AChE) enzymatic activity in the adrenal medulla and in preganglionic sympathetic neurons within the thoracic spinal cord, which are also significantly reduced in number. Quantitative determinations of specific AChE activity revealed a massive decrease (-62%) in the adrenal gland and a lesser, but still pronounced, reduction in the thoracic spinal cord (-40%). Other markers of the adrenal medulla and its innervation, including various neuropeptides, chromogranin B, secretogranin II, amine transporters, the catecholamine-synthesizing enzymes tyrosine hydroxylase and PNMT, synaptophysin, and L1, essentially were unchanged. Interestingly, AChE immunoreactivity appeared unaltered, too. Preganglionic sympathetic neurons, in contrast to adrenal medullary cells, do not express TrkA. They must, therefore, be affected indirectly by the TrkA knock-out, possibly via a retrograde signal from chromaffin cells. Our results suggest that signaling via TrkA, but not TrkB, may be involved in the postnatal regulation of AChE activity in the adrenal medulla and its preganglionic nerves.

Acetylcholinesterase↗