Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety-three patients 65 years of age or older were studied to determine the incidence of dysrhymia following administration of 1 of 2 cholinesterase inhibitors, neostigmine or pyridostigmine. The ECG was then continuously monitored for 90 minutes. Neostigmine was associated with a higher incidence of dysrhythmia than was pyridostigmine. Neostigmine administered to patients with pre-existing coronary artery disease and/or conduction defects and to patients with hypertension was associated with a significantly higher incidence of dysrhythmia than was pyridostigmine when administered to patients with the same conditions. The incidence of dysrhythmia in patients who received a halogenated anesthetic was 5 times greater after neostigmine than after pyridostigmine.
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PMID:Cardiac dysrhythmia following reversal of neuromuscular blocking agents in geriatric patients. 56 56

The practice of dietetic therapy is unusual today for patients suffering from renal failure without hypertension and reduction of glomerular filtration rate. Specific treatment is needed, however, for arterial hypertension, uremia, calculus and uralith disease. Experiments in rats showed, that a lot of uremic symptoms following poorly functioning kidneys are partly at least caused by disturbances in amino acid metabolism. Uremia patients with dysfunctioning plasma protein metabolism (transferrin, complement, cholinesterase, prealbumin and retinolbinding protein) need oral, respectively parenteral substitution of essential amino acids. This substitution is very important under catabolic stress conditions in uremic syndrome with and without vividialysis treatment.
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PMID:[Nutrition problems in kidney diseases]. 96 82

This study was undertaken to investigate the possibility that mechanisms other than cholinesterase (ChE) inhibition account for the acute toxicity of organophosphorus insecticide. Both the P = O type insecticide (direct ChE inhibitors: chlorfenvinphos and dichlorvos) and the P = S type insecticide (indirect ChE inhibitors: diazinon and fenthion) were employed. Rats treated with lethal doses of intravenous and oral P = O type insecticides and oral P = S type insecticides exhibited typical signs of anti-ChE poisoning along with marked inhibition of brain and erythrocyte ChE activity. In contrast, rats given lethal doses of intravenous P = S type insecticides exhibited tonic convulsions and opisthotonos, with only slight inhibition of ChE activities. When P = O type insecticides were intravenously administered to anesthetized and conscious rats, animals exhibited typical anti-ChE poisoning signs in cardiorespiration: hypertension and apnea which were antagonized by atropine. After administration of lethal doses of P = O type insecticides, breathing disappeared before the cessation of heart beats. Rats receiving lethal doses of intravenous P = S type insecticides did not show hypertension, but exhibited transient cessation of breathing and heart beats. Breathing was observed after the disappearance of heart beats. The electroencephalogram (EEG) was characterized by spike and wave complexes. The EEG and cardiorespiratory changes were not antagonized by atropine. It was concluded that lethality following intravenous P = S type insecticides may be independent of ChE inhibition.
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PMID:Differences in the mode of lethality produced through intravenous and oral administration of organophosphorus insecticides in rats. 185 19

This study sought to determine whether release of acetylcholine (ACh) within the C1 area of nucleus reticularis rostroventrolateralis (RVL) contributes to the tonic maintenance of arterial pressure (AP) in the rat. The activity of choline acetyltransferase (ChAT), the biosynthetic enzyme for ACh, varied 5.5-fold in micropunches of the 6 medullary regions examined. ChAT activity in the C1 area (179 +/- 35 nmol [14C]ACh formed/mg protein/60 min; n = 4) was intermediate between that of the hypoglossal nucleus (249 +/- 38; highest) and the pyramids (45 +/- 11; lowest) and equivalent to that found in the parietal cortex (147 +/- 15). Release of [3H]ACh from C1 area micropunches was increased by raising extracellular K+ concentrations (5-55 mM) and was entirely Ca2(+)-dependent. Muscarinic receptor binding density was assessed using [3H]quinuclidinyl benzylate ([3H]QNB) as ligand and a recently developed 'electronic micropunch' technique which allows measurement of quench-corrected [3H]QNB binding within corresponding cylinders of tissue obtained by the mechanical micropunch cannula. [3H]QNB binding density varied 2.6-fold: lateral reticular nucleus pars lateralis greater than C1 area greater than nucleus ambiguus = hypoglossal nucleus = pyramid = oral spinal trigeminal nucleus. In urethane-anesthetized rats, inhibition of ACh synthesis by hemicholinium-3 (HC-3, 3 nmol/50 nl), or blockade of muscarinic receptors by scopolamine (SCOP, 3 nmol/50 nl), reduced resting mean AP by 18-24 mm Hg following bilateral microinjection into the C1 area. These concentrations of HC-3 and SCOP were sufficient to attenuate by 70-80% the increase in local cholinergic neurotransmission elicited by the cholinesterase inhibitor physostigmine given systemically. High concentrations of SCOP (30-150 nmol/50 nl) lowered AP by 46-60 mm Hg. Similarly, bilateral microinjections of GABA (10 nmol/50 nl) into the C1 area markedly reduced mean AP by 51 +/- 6 mm Hg to levels normally found after transection of the spinal cord. Thus, a substantial portion of tonic sympathetic activity may be driven by activation of muscarinic receptors in the C1 area. In the spontaneously hypertensive rat (SHR), a genetic model of hypertension, neither spontaneous nor K(+)-evoked release of [3H]ACh from the C1 area differed from that of normotensive Wistar-Kyoto rats (WKY).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Synthesis, release and receptor binding of acetylcholine in the C1 area of the rostral ventrolateral medulla: contributions in regulating arterial pressure. 233 21

The in vivo time course of cholinesterase inhibition was measured in brain, lung, spleen, hind limb skeletal muscle, diaphragm, intestine, kidney, heart, liver, and plasma of rats receiving 90 micrograms/kg soman, im. This dose of soman produced severe respiratory depression and transient hypertension, but no significant changes in the cardiac output or heart rate of anesthetized rats. The rate and maximal extent of in vivo cholinesterase inhibition by soman varied widely among the tissues. Although cardiac output was unchanged by soman administration, the blood flow in heart, brain, and lung (bronchial arterial flow and arteriovenous shunts) was increased, whereas blood flow in spleen, kidney, and skeletal muscle was decreased. The relative importance of tissue blood flow, tissue levels of cholinesterase and acetylcholinesterase, and tissue levels of soman-detoxifying enzymes (diisopropyl-fluorophosphatase and carboxylesterase) in determining the in vivo rate and maximal extent of cholinesterase inhibition was examined by multiple regression analysis. The best multiple regression model for the maximal extent of cholinesterase inhibition could explain only 63% of the observed variation. The best multiple regression model for the in vivo rate of cholinesterase inhibition contained three independent variables (blood flow, carboxylesterase, and cholinesterase) and could account for 94% of the observed variation. Of these three variables blood flow was the most important, accounting for 79% of the variation in the in vivo rate of cholinesterase inhibition. This suggests that it may be possible to use a flow-limited physiological pharmacokinetic model to describe the kinetics of in vivo cholinesterase inhibition by soman.
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PMID:The effects of blood flow and detoxification on in vivo cholinesterase inhibition by soman in rats. 356 32

Central cholinergic control of pulse rate and blood pressure has seldom been studied in humans. In the current study we contrasted the cardiovascular effects of the centrally acting cholinesterase inhibitor physostigmine, which increases central and peripheral acetylcholine levels, with those of saline placebo and with those of the non-centrally acting cholinesterase inhibitor neostigmine, which only increases peripheral acetylcholine levels. We found that physostigmine, in contrast to neostigmine and saline, caused significant and often profound increases in pulse rate and blood pressure levels in humans. Thus, we conclude that acetylcholine may have a role in central cardiovascular regulation in humans. We also found that administration of physostigmine may cause net increases in pulse of up to 74 beats/minute, systolic blood pressure increases of up to 50 mm Hg, and diastolic increases of up to 45 mm Hg. Such increases could be dangerous in elderly patients with concomitant cerebrovascular or coronary circulation disorders.
Hypertension
PMID:Central cardiovascular effects of physostigmine in humans. 398 55

To determine the effect of the duration and severity of hypertension on arterial wall metabolism 28 enzyme activities and several macromolecular complexes were histochemically studied in normotensive (WK), moderately (SHR) and strongly hypertensive (SP-SHR) rats at various ages. The results indicate that the abnormalities of 5' nucleotidase, acid esterase, cholinesterase and Alk.P. appeared in prehypertensive 4 w.old SHR. The posthypertensive changes, fluctuating in relation to the duration of hypertension, concerned: the pentose pathway, Krebs cycle and glycolosis -linked dehydrogenases; lysosomal enzymes; glycogen-phosphorylase and MAO; glycosaminoglycan and glycoprotein content. The structural and metabolic response presented several local and regional differences. The metabolic changes were greater in the aorta than in the caudal and femoral arteries. The comparison between SHR and SP-SHR indicates that the blood pressure (BP) at 170 mm Hg seems well tolerated during a long period of time. Severe lesions such as degeneration and failure of lipolytic activity in aortic smooth muscle cells (SMC), notable and early (8 mo.) in SP-SHR with 240 mm Hg were less intense and appeared later (13 mo.) in SHR with 190 mm Hg. The level of hypertension, rather than its duration, appears as a determining factor of posthypertensive vascular damage.
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PMID:Enzyme-histochemical changes in arteries of genetically hypertensive rats (SHR, SP-SHR). 632 44

Chemical stimulation of brain cholinergic neurons in many species can produce hypertension. Recent studies in this laboratory have demonstrated that clonidine inhibits this central cholinergic pressor response by inhibiting the biosynthesis of brain acetylcholine. This study was designed to determine whether methyldopa, like clonidine, could inhibit brain cholinergic neurons involved in cardiovascular regulation in freely-moving spontaneously hypertensive rats (SHR). Intravenous (i.v.) injection of methyldopa (50-200 mg/kg) produced a dose-related fall in blood pressure (29/15-54/33 mm Hg) in SHR. Intracerebroventricular (i.c.v.) injection of hemicholinium-3 (HC-3) in SHR evoked a fall in arterial pressure through inhibition of acetylcholine synthesis. Doses of HC-3 (10 micrograms, or 15 micrograms, i.c.v.) and methyldopa (50 mg/kg, i.v.) were administered to produce small reductions in arterial pressure in SHR (7-14 mm Hg diastolic, respectively). When the two agents were injected simultaneously, however, a greater than additive response was obtained (p less than 0.05). Central injection of echothiophate (a long-acting cholinesterase inhibitor) to potentiate brain cholinergic activity resulted in a sustained hypertensive response (greater than 40 mm Hg) in SHR for at least 150 minutes. Simultaneous injection of or pretreatment with methyldopa (100 mg/kg, i.v.) inhibited the pressor response to echothiophate over a time course similar to its antihypertensive response in untreated SHR. Methyldopa, however, was completely ineffective in altering the hypertensive response to central injection of carbachol (1 microgram, i.c.v.). This difference in methyldopa susceptibility between the indirect-acting (echothiophate) and direct-acting (carbachol) cholinergic agonists may be related to an inhibiting effect of methyldopa on brain acetylcholine release.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Effect of methyldopa on brain cholinergic neurons involved in cardiovascular regulation. A study in conscious spontaneously hypertensive rats. 650 Jun 69

Little is known about the function of cholinesterase activity present in the walls of cerebral microvessels. It has been shown that systemically administered physostigmine, a cholinesterase inhibitor that penetrates the blood-brain barrier, causes barrier opening. This has led to suggestions that perivascular cholinesterase is involved in the maintenance of morphological blood-brain barrier function. The present study demonstrates that the physostigmine-induced barrier opening is fully attributable to the acute hypertension and hypercapnia the agent gives rise to. Thus, it is discussed whether the enzyme activity may function as an enzymatic barrier to cholinergic agents.
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PMID:Perivascular cholinesterase and morphological blood-brain barrier function. 651 93

Succinyldicholine-induced asphyxia in awake calves led to massive catecholamine release by the adrenal medulla. Hypertension and bradyarrhythmias resulted. Electroencephalograms recorded during periods of succinyldicholine-induced apnoea indicated that calves were probably conscious and under psychic stress for at least 4 min after the onset of apnoea. Electroencephalographic signs indicative of decreased consciousness became evident in one calf only after 4,8 min of apnoea but were absent in 3 calves subjected to maximum periods of apnoea of 4,1; 3,2 and 4,4 min. The latter 3 calves all recovered with no apparent neurological deficit after intravenous injection of plasma pseudocholinesterase.
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PMID:Haemodynamic and neurological responses of ventilated and apnoeic calves to succinyldicholine. 734 77


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