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

A lot of over 60 atherosclerotics with clinical manifestations of senile depressive illness was studied comparatively with a lot of subjects of the same age with essential arterial hypertension (EAH). As concerns the behaviour of the catecholamine content in CSF and blood, the total catecholamines are approxiately equal in the two lots, but with a clear difference of the catecholamine fractions. The CSF catecholamines behaviour in old atherosclerotics is characterized by the presence of increased values of noradrenaline (NA) and of adrenaline (A), with increased statistical significance, but without modifications of the adrenaline percentage (A %) from the total catecholamines, comparatively to the values found in normal subjects. The serotonin (5-HT) content of the CSF in men with atherosclerotic senile depressive illness was lower even than in subjects with coronary atherosclerosis. In atherosclerosis protides modifications precede the histologic changes. In CSF, GLU, ALA, TYR increase in old subjects. In blood, GLU, ALA, TYR, HIS, LEU, SER increase in the same subjects. ARG decreases with age. THR is higher in men than in women. In the urine of all the men as well as of all the women of more than 60 years, GLN and ALA have increased values. LYS increases with age. GLN and ARG are higher in men than in women.
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PMID:Pattern of the cerebrospinal fluid (CSF) and blood biogenic amines and of the CSF, blood and urine amino acids as pathogenetic ground of the senile depressive illness. 677 91

The blood pressure of spontaneously hypertensive rats (SHR) was measured by tail-plethysmography. Feeding SHR a diet supplemented with 0.6 g% L-tyrosine, for 15 weeks after weaning, resulted in a slower increase of blood pressure than in rats fed the control diet (no tyrosine added). The blood pressure stabilized, after about 8 weeks, at values lower by about 10 mm Hg than in the control SHR group. Diets with a higher content of free L-tyrosine (1.2 or 2.4 g%) produced no greater hypotensive effects, despite the fact that the plasma level of the amino acid, at the time of blood pressure measurements, was related to the tyrosine content of the diet. In addition, providing 2.4 g% free L-tyrosine to the diet of SHR with established hypertension, produced within a few days a decrease of blood pressure similar to the one recorded in rats fed the tyrosine-supplemented diet during the whole period of development of hypertension. A maximal effect of L-tyrosine, in decreasing the blood pressure of SHR, is thus obtained at relatively low concentrations of the amino acid in the diet, and after a short period of consumption. However, this effect is rather small, and rapidly reversed upon removing free L-tyrosine from the diet.
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PMID:Development of hypertension in spontaneously hypertensive rats fed L-tyrosine-supplemented diets. 684 71

Content of tryptophane, tyrosine, serotonin, noradrenaline, adrenaline and dopamine was studied in blood serum and various brain regions of rats with genetically determined spontaneous form of hypertension. The arterial pressure of these animals was shown to depend on activity of noradrenaline-, serotonin- and dopaminergic systems of brain. Oppositely directed alterations in content of dopamine and noradrenaline were observed in various brain regions apparently as a result of changes in activity of the enzymes involved in the amines synthesis and degradation.
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PMID:[Biogenic monoamines and their precursors in rats with spontaneous arterial hypertension]. 685 37

alpha-Methyl-p-tyrosine is an orally active inhibitor of catecholamine synthesis which inhibits the hydroxylation of tyrosine to dopa. At dosages of 600 to 3500 mg daily it is effective in controlling the hypertensive episodes and symptoms of catecholamine excess in phaeochromocytoma during preparation for surgery. Limited published experience suggests that it is effective in controlling hypertension and symptoms in malignant phaeochromocytoma, but further long term experience is needed. Concomitant administration of phenoxybenzamine and propranolol may be desirable in some patients and treatment with phentolamine is usually necessary to control hypertension during manipulation of the tumour.
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PMID:alpha-Methyl-p-tyrosine: a review of its pharmacology and clinical use. 700 39

To assess the relationship between sympathetic nerve function and sodium intake, we examined norepinephrine (NE) turnover in several cardiovascular tissues and the brain stem of rabbits maintained for 3 weeks on high (86 mEQ), normal (14 mEQ), and low (0.2 mEQ/day) sodium diet. None of the diets changed the blood pressure significantly. Plasma renin activity became high in the low sodium group and low in the high sodium group at the end of the treatment. NE turnover was measured from the rate of decline of tissue NE concentration after administration of alpha-methyl-p-tyrosine. Variation of sodium intake exerted opposite effects on NE turnover in the periphery and in the central nervous system; increasing sodium intake caused an increase in NE turnover in the thoracic aorta, mesenteric vein, and left ventricle, and a decrease in the hypothalamus, midbrain, and pons medulla. But in the mesenteric vein, and left ventricle, and a decrease in the hypothalamus, midbrain, and pons medulla. But in the mesenteric artery and abdominal aorta it was not affected by dietary sodium manipulation. The results show the varying influence of sodium balance on the central and peripheral noradrenergic neuron activity.
Hypertension
PMID:Effect of high and low sodium intake on norepinephrine turnover in the cardiovascular tissues and brain stem of the rabbit. 706 88

Sodium restriction is not the only nutritional measure likely to prove valuable in the treatment and prevention of hypertension. The hypotensive effects of central adrenergic stimulation can be promoted by supplementary tyrosine, insulin potentiation (as with GTF), and (possibly) high-dose pyridoxine. Insulin potentiators (GTF) and prostaglandin precursors (essential fatty acids) should have direct relaxant effects on vascular muscle. A high potassium, low sodium diet, coenzyme Q, and prevention of cadmium toxicity (as with dietary selenium) may act to offset renally-mediated pressor influences. Functional combinations of these measures might prove to be substantially effective, in which case they would offer considerable advantages over potentially toxic drug therapies.
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PMID:Prospects for nutritional control of hypertension. 721 48

The in vivo binding of [3H]spiroperidol was measured in discrete areas of the brain in 7-, 9- and 16-week-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto (WKY) controls. An increase in the [3H]spiroperidol binding in the striatum, tuberculum olfactorium and frontal cortex but not in the cerebellum was detected at all ages in SHR. The increase was more pronounced in 7- than in 9- or 16-week-old SHR. In vitro data indicated an increase in Bmax but no variation in Kd in the striatum of 7-week-old SHR. Moreover no difference was detectable in the dopaminergic cell bodies (A9, A10). This increase was specific to [3H]spiroperidol binding sites since no difference was observed in the in vivo binding of [3H]QNB and [3H]LSD in the same brain regions. No variation in dopamine level or dopamine utilization, as estimated by measuring the disappearance of the amine induced by alpha-methyl-p-tyrosine, was observed. The DOPA accumulation after injection of the DOPA decarboxylase inhibitor NSD 1015 was greater in the tuberculum olfactorium from 7-week-old SHR. An increase in [3H]spiroperidol binding sites was also observed in the striatum and tuberculum olfactorium after 7 weeks of DOCA-salt treatment. These results suggest that dopaminergic neurons might be implicated in the onset of hypertension in the rat.
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PMID:Central dopaminergic neurons during development of genetic and DOCA-salt hypertension in the rat. 722 85

The influence of stress on the metabolism of adrenaline (A) and noradrenaline (NA) in the prosencephalon (PC) and rhombencephalon (RC) of SHR and normotensive Wistar rats (WR) was studied. After intraperitoneal injection of 3H-tyrosine, radioactivity of 3H-adrenaline (3H-A), 3H-noradrenaline (3H-NA), total 3H-3-methoxy-4-hydroxyphenylglycol (3H-MHPG), total 3H-3,4-dihydroxyphenylglycol (3H-DHPG) and 3H-vanillylmandelic acid (3H-VMA) was measured in PC and RC of SHR and WR, non-stressed or subjected to running stress. Stress induced a significant decrease of 3H-A level in PC and RC of 8-week-old SHR while no stress-related changes in 3H-NA level were found in either part of the brain of SHR. In RC, 3H-A level was lower in older than in younger non-stressed SHR and decreased further after stress. In all SHR, stress enhanced formation of total 3H-MHPG and/or 3H-DHPG in PC, while increased 3H-VMA level was found only in PC of 24-week-old and in RC of 8-week-old stressed SHR. The results suggest that the decrease of the level of 3H-A in the brain of SHR is involved in their reaction to stress and may depend on increased metabolism mainly to glycols but also to VMA. The lower 3H-NA and 3H-A levels in the prosencephalon of non-stressed young and older SHR, concomitant with unaltered or elevated formation of their metabolites, may suggest higher release of the transmitters involved in the pathogenesis of spontaneous hypertension.
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PMID:Metabolism of 3H-catecholamines in the brain of spontaneously hypersensitive rats (SHR) after running stress. 724 96

The metabolism of 3H-catecholamines after i.p. injection of 3H-tyrosine was studied in the heart and adrenals of spontaneously hypertensive (SHR) and normotensive Wistar (NCR) rats at rest and following running stress. In the heart of 8-week-old NCR a sharp stress-induced increase of the levels of 3H-A and 3H-DA with an elevation of the levels of their metabolites was observed. In contrast, there was no stress-related change in the levels of 3H-NA, 3H-A and 3H-VMA in the hearts of young SHR, while the 3H-DA level, though increased after stress, remained still lower than in the age-matched NCR. In the phase of established hypertension (24 weeks) lower levels of 3H-NA and 3H-A in the heart already present at rest, as compared with NCR, remained lower after stress but the elevation of the level of their metabolites 3H-VMA and 3H-MA, was similar in both strains. In the adrenals of 8-week-old SHR the basal 3H-A level was already higher than in NCR. Stress provoked a marked decrease of adrenal 3H-A accompanied by increased formation of 3H-MA and an increase in the levels of 3H-NA and 3H-DA, more pronounced in SHR than NCR. In the phase of advanced hypertension a further elevation of 3H-A and 3H-MA and an increase of basal 3H-DA level in the adrenals were found at rest. The decreased levels of 3H-catecholamines in the heart of stressed young and non-stressed older SHR may indicate an increase in their rate of release and/or their impaired synthesis. An increased basal level of 3H-A in the adrenals of SHR concomitant with the development of hypertension, may reflect an increased synthesis and/or decreased release, as evidenced by the proportionally lower increase of its extraneuronal metabolite 3H-MA. The adrenal response to stress, more intense in SHR than in NCR, may be considered as due to enhanced release of 3H-A from the gland.
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PMID:Metabolism of 3H-catecholamines in the heart and adrenals of spontaneously hypertensive rats (SHR) after running stress. 727 Feb 17

The effects of injection of a peptidase-resistant analog of methionine-enkephalin, [D-ala2]-methionine-enkephalin, on blood pressure (BP), heart rate, and vasopressin release were studied in spontaneously hypertensive rats (SHR). Intravenous injection of [D-Ala2]-methionine-enkephalin (DAME) increased BP in both SHR and normotensive Wistar-Kyoto (WKY) controls, with a significantly greater increase in hypertensive rats. Intracerebroventricular injection of DAME produced a biphasic increase in BP and an increase in heart rate in both groups. The initial pressor effect was significantly greater in the SHR, Plasma vasopressin levels in SHR were depressed relative to both untreated hypertensive rats and animals given vehicle control injections. Intravenous pretreatment with a vasopressin vasopressor antagonist, [l-(beta-mercapto-beta-beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine] arginine-vasopressin, did not block either component of the central enkephalin response in hypertensive rats. These date indicate that central enkephalin injection does not release vasopressin and that SHR are hyperresponsive to enkephalin. It is concluded that pressor systems other than that of vasopressin mediate the enkephalin-induced cardiovascular effects.
Hypertension
PMID:Vasopressin release does not contribute to pressor action of enkephalin in SHR. 730 4


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