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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The density of muscarinic receptor sites, choline acetyltransferase (ChAT), and acetylcholinesterase (AChE) activity in the myocardium of the Dahl salt-sensitive (DS) and salt-resistant (DR) rat was investigated. Both normotensive and hypertensive (as a result of 8.0% NaCl added to the diet) DS rats displayed a lower concentration of muscarinic receptors and less ChAT and AChE activity in myocardial tissue than normotensive DR rats. Lower receptor site density and enzyme activity in the myocardial of the DS line may reflect decreased vagal tone. If true, this may produce dificits in the ability to appropriately adjust heart rate (HR) in response to elevations in blood pressure (BP). Therefore, the present results may be viewed as exacerbational factors in the pathogenesis of hypertension in the DS line.
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PMID:Myocardial cholinergic receptor sites and enzyme activity in the Dahl model of essential hypertension. 672 89

Specific histochemical techniques for the demonstration of catecholamines and acetylcholinesterase (ACE) have been used to compare densities of innervation of the proximal and distal regions of pial arteries in the rat brain. The most distal parts, so called "arterial bordering zones" have very scarce noradrenergic innervation while the proximal parts of the vessels have an abundant noradrenergic nerve supply. ACE-positive fibers are distributed evenly. It is suggested that the preferential injuring of the brain tissue in acute hypertension characteristic of the arterial bordering zones might be due to deficiency in noradrenergic innervation of the pial arteries in these regions.
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PMID:[Regional characteristics of the noradrenergic and cholinergic innervation of the vessels of the brain surface]. 737 Apr 7

Previous work from this laboratory revealed in increased canine pancreatic intraductal pressure following cholinesterase inhibitor intoxication. The pressure was negatively correlated with serum butyrylcholinesterase (BChE) activity, suggesting that BChE activity mediated the pressure rise. This study uses a histochemical technique to investigate the tissue cholinesterase activity of the canine pancreatic sphincters and the effect of a cholinesterase inhibitor (ChEI) on tissue cholinesterase activity. In five control dogs, serial sections of the major and minor spincters were stained for acetylcholinesterase (AChE) and BChE activity. Four treated dogs were given the ChEI, O,O-diethyl-O- (2-isopropyl-6-methyl-4-pyrimidinyl) phosphoro-thioate, 25 mg/kg, one hour prior to excising the ampullae. In the control dogs, BChE activity is present in the periampullary nerves and the pancreatic smooth muscle sphincters. AChE activity is present in nerves but not in smooth muscle. In the treated group, following a dose of ChEI known to cause ductal hypertension, BChE activity was absent in the pancreatic sphincters but AChE activity was preserved in the periampullary nerves. These data suggest that the pancreatic ductal hypertension that occurs following ChEI administration is due to a selective reduction in pancreatic smooth muscle BChE activity.
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PMID:A study of the cholinesterases of the canine pancreatic sphincters and the relationship between reduced butyrylcholinesterase activity and pancreatic ductal hypertension. 743 91

Using a sensory stimulation (startle) paradigm in normotensive and hypertensive rats, we evaluated the contribution of central cholinergic mechanisms to the pathology of hypertension. In normotensive Wistar-Kyoto (WKY) rats, transient airpuff stimuli elicit a complex startle reaction consisting of several behavioral and autonomic components. These include jumping (motor response), an increase in blood pressure (pressor response), an early-trial decrease in heart rate (bradycardia) and a later-trial increase in heart rate (tachycardia). Intracerebroventricular (i.c.v.) administration of cholinergic compounds to WKY rats primarily altered the bradycardia component. Thus, depletion of brain acetylcholine with hemicholinium-3 (5 micrograms/kg i.c.v.) abolished bradycardia responses without significantly affecting the motor response, tachycardia or pretest cardiovascular base-line parameters. Furthermore, enhancement of brain acetylcholine with acetylcholinesterase inhibition (physostigmine, 50 micrograms/kg i.c.v.) enhanced bradycardia in WKY rats. The nonspecific muscarinic antagonist scopolamine and the M1 muscarinic receptor antagonist pirenzepine, but neither the M2 muscarinic antagonist methoctramine nor the nicotinic antagonist hexamethonium, attenuated bradycardia. We conclude that a central M1 muscarinic receptor participates in the control of startle-associated bradycardia in the WKY rat. The spontaneously hypertensive rat does not normally exhibit startle-associated bradycardia. Because i.c.v. physostigmine revealed early-trial bradycardia in this strain, we conclude that a selective central cholinergic deficit contributes to a suppression of startle-associated bradycardia in the spontaneously hypertensive rats.
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PMID:A unique central cholinergic deficit in the spontaneously hypertensive rat: physostigmine reveals a bradycardia associated with sensory stimulation. 813 21

To study acute organophosphorus (OP) poisoning cases, 190 OP-intoxicated cases admitted to Civil Hospital, Ahmedabad, were investigated in depth. The group consisted of subjects ranging from 11 to 60 years of age, with the maximum number of cases in the age group 21-30 years and a male-to-female ratio of 2.1:1. Most of the subjects (71.61%) were partially educated, 24.2% of the cases were illiterate, and only 4.2% of the cases were highly educated. Socioeconomically, 21.1% of the subjects were of low economic status, 52.6% were low middle class, 16.8% were upper middle class, and only 9.5% were upper class. With regard to marital status of the subjects, 98 cases were married and 92 were unmarried. About 67.4% of the cases had the intention of committing suicide, 16.8% of the cases were the result of occupational exposure, and 15.8% of the cases were from accidental poisoning. Social and domestic problems (37.5%), marital friction (15.6%), financial stress (15.6%), love affairs (14.1%), job problems (10.9%), chronic illness (4.7%), and failure in examination (1.6%) were observed as the precipitating factors. Muscarinic manifestations such as vomiting (96.8%), nausea (82.1%), miosis (64.2%), excessive salivation (61.1%), and blurred vision (54.7%) and CNS manifestations such as giddiness (93.7%), headache (84.2%), disturbances of consciousness (44.2%), and typical pungent odor from mouth and clothes (77.9%) were the main presenting symptoms. Cardiac manifestations such as sinus tachycardia (25.3%), sinus bradycardia (6.3%), and depression of ST segments with T-wave inversion (6.3%) were observed electrocardiographically, with hypertension (10.5%) and muscular twitching in some (2.1%) cases. Biochemical changes such as albuminuria (12.6%) and azotemia (18.9%) with inhibition of acetylcholinesterase enzyme activity in blood were recorded in 78.9% of the cases. About 89.5% of the cases recovered completely, 4.2% of the cases absconded after partial recovery, and 6.3% of the cases died. The mortality rate (6.3%) depended on various factors such as the organophosphorus compound consumed, the amount ingested, the time interval for hospitalization, and the general health of the patient. Chances of recovery were higher when the patient was hospitalized at the earliest indication.
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PMID:A clinical, biochemical, neurobehavioral, and sociopsychological study of 190 patients admitted to hospital as a result of acute organophosphorus poisoning. 832 67

The influence of pregnancy-induced hypertension (pre-eclampsia) on muscarinic cholinergic receptors and on acetylcholinesterase (AChE) activity was investigated using frozen sections of the umbilical artery and vein. Pre-eclamptic patients undergoing Caesarean delivery and normotensive pregnant control woman undergoing Caesarean delivery with similar parity, gestation length and age were examined. Muscarinic cholinergic receptors were assayed in frozen sections of the umbilical artery and vein by a radioligand binding assay technique, using [3H]-N-methyl scopolamine (NMS) as a ligand. AChE was demonstrated with a histochemical technique associated with microdensitometry. [3H]-NMS was specifically bound to sections of both umbilical artery and vein in a manner consistent with the labelling of muscarinic cholinergic receptors. The affinity of the radioligand was similar in the two vessels, whereas the maximum density of binding sites (Bmax) was higher in the umbilical vein than in the artery. A faint AChE reactivity was observed in the tunica media of both umbilical artery and vein. In pre-eclampsia, a loss of [3H]-NMS binding sites not accompanied by changes in the affinity of radioligand was found. The decrease of muscarinic cholinergic receptors involved to a greater extent the umbilical artery than the vein. No differences in AChE activity were found at the level of umbilical artery and vein between control and pre-eclamptic subjects. These findings suggest that pre-eclampsia is characterized by a loss of muscarinic cholinergic receptors in the umbilical circulation not accompanied by changes of the acetylcholine catabolizing enzyme AChE. It is possible that the decreased density of vascular muscarinic cholinergic receptors in pregnancy-induced hypertension contribute to the increased resistance of the umbilical circulation occurring in pre-eclampsia.
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PMID:Muscarinic cholinergic receptors and acetylcholinesterase activity in umbilical artery and vein in pregnancy-induced hypertension (pre-eclampsia). 938 71

The acetylcholinesterase inhibitor, soman, induces marked and sustained hypertension and tachycardia associated with a convulsive syndrome in rats. The aims of the present study were to distinguish between the cardiovascular and convulsant effects of soman and to determine whether the maintenance of the soman-induced hypertension and tachycardia depends solely on a central muscarinic effect. To this end, using a computerised analysis of blood pressure (BP) in conscious freely moving rats, we examined the consequences on the increase in mean BP (MBP) and heart rate (HR) induced by soman (60 micrograms/kg, i.v.) of 1) a pre-treatment with the anticonvulsant drug diazepam (3 mg/kg, i.v.) and 2) atropine sulphate (10 mg/kg, i.v.) administered 10 or 60 min after the intoxication. Pretreatment with diazepam prevented the convulsions, assessed by electroencephalogram (EEG) recording, but modified neither the magnitude nor the kinetics of the pressor and tachycardic effects of soman (delta MBP = 74 +/- 2 and 73 +/- 5 mmHg, delta HR = 69 +/- 10 and 79 +/- 7 bpm, maximum MBP = 186 +/- 3 and 182 +/- 6 mmHg, maximum HR = 545 +/- 9 and 522 +/- 16 bpm in solvent- (n = 8) and diazepam- (n = 8) pre-treated rats, respectively). Whatever its time of administration, atropine sulphate fully and immediately reversed the rise in BP induced by soman. The soman-induced tachycardia was also suppressed by atropine administered 10 min after soman whereas it persisted when atropine was injected 60 min after the intoxication. These results show that the cardiovascular effects of soman can occur independently of the convulsive syndrome and that the maintenance of the soman-induced hypertension depends entirely on a permanent central muscarinic stimulation.
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PMID:Soman-induced hypertension in conscious rats is mediated by prolonged central muscarinic stimulation. 1045 88

Many women with cerebrospinal fluid shunts are now reaching reproductive age. Clinical management of pregnant patients with hydrocephalus should include preconception counseling and CT scan or MRI. A family pedigree should also be established for counseling on the risk of recurrence of the woman's condition or another neural tube defect. Electrophoresis of acetylcholinesterase in the amniotic fluid can provide the diagnosis of open neural tube defect between 13 and 24 weeks gestation. Shunt malfunction may occur during pregnancy in 50 % of cases. Management requires well-planned, a combined neurosurgical and obstetrical approach. Vaginal delivery is possible in asymptomatic mothers. Cesarean section is recommended for neurologically unstable patients. Prophylactic antibiotics are recommended for labor and delivery to avoid shunt infection. Epidural analgesia is contraindicated in patients with intracranial hypertension. Some complications of complementary treatment for cerebral tumors in childhood are briefly reported.
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PMID:[Hydrocephalus during pregnancy with or without neurosurgical history in childhood. Practical advice for management]. 1084 53

Our laboratory has found that the organophosphate pesticide chlorpyrifos elicits an elevation in blood pressure that persists for approximately 24 hr after exposure. Since organophosphate pesticides inhibit acetylcholinesterase activity and cause cholinergic stimulation in the central nervous system and peripheral tissues, we suspect that the hypertensive response from chlorpyrifos is elicited by activation of pressor areas in the brain stem, specifically muscarinic receptors which are known to mediate hypertensive responses. Oxotremorine, a muscarinic agonist, should elicit a blood pressure response similar to organophosphate pesticides. This study used radiotelemetry to assess the effects of oxotremorine on blood pressure, heart rate, core temperature, QA interval (a measure of cardiac contractility), and motor activity in the male, Long-Evans rat. Subcutaneous co-administration of 0.2 mg/kg oxotremorine with 1.0 mg/kg methyl scopolamine (i.e., to block oxotremorine's peripheral effects) caused a marked elevation in blood pressure that developed concomitantly with a 2 degrees decrease in core temperature, 60 beats/min. increase in heart rate, increase in cardiac contractility but no change in motor activity. Overall, blood pressure increased by 19 mmHg from baseline and the response persisted for approximately 12 hr after injection. Methyl scopolamine alone increased heart rate but had no effect on blood pressure, core temperature, and motor activity. Oxotremorine injected without methyl scopolamine led to a relatively minor increase in blood pressure and hypothermia. Overall, central muscarinic stimulation with oxotremorine and methyl scopolamine leads to a vigorous hypertensive response that is associated with increased cardiac contractility, suggesting an increase in cardiac output. Combined central and peripheral cholinergic stimulation following oxotremorine without methyl scopolamine, as would also occur with exposure to chlorpyrifos and other organophosphate pesticides, did not elicit as much of a hypertensive response. This would suggest pathways other than those controlled directly with muscarinic receptors are operative in the development of chlorpyrifos-induced hypertension.
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PMID:Peripheral versus central muscarinic effects on blood pressure, cardiac contractility, heart rate, and body temperature in the rat monitored by radiotelemetry. 1148 8

The past decade has seen a renewed interest in vascular dementia. The search for a causal relationship between a vascular event or a vascular cerebral lesion and dementia has led to new classification schemes which no longer consider vascular dementia a homogeneous entity but acknowledge the diversity of the clinical and morphological substrates of this syndrome. Deviation from the term "multi-infarct dementia" is only one but many consequencies of these recent developments. Etiologically, vascular dementia may result from cerebral small vessel disease leading to extensive leucencephalopathy or lacunes or may be the consequence of strategically located infarcts or multiple infarcts in large vessel territories. It may also be the consequence of global cerebral hypoperfusion, intracerebral hemorrhage or other mechanisms such as vasculitis. There is no definitive medical or surgical treatment for vascular dementia. Thus, it appears that stroke prevention offers the most immediate and substantial solution to reduce the morbidity and mortality. This is best substantiated for treatment of arterial hypertension. Once vascular dementia occurs control of vascular risk factors may be useful but this contention will require larger scale studies to provide more definite proof. A number of metabolically active drugs has been used for the treatment of cognitive symptoms in vascular dementia. Yet, the data are conflicting und the effects described modest at most. There is epidemiological evidence for a more than incidental co-existence between vascular and primary degenerative dementia which suggests that therapies found to be effective in Alzheimer's disease may also prove beneficial at least in subgroups of vascular dementia. Lately, this concept is tested by several studies on the efficacy of acetylcholinesterase inhibitors in vascular dementia.
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PMID:[Vascular dementia]. 1192 78


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