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

Serotonin levels and turnover were analyzed in discrete forebrain and mesencephalic nuclei of young (4-week-old) and adult (14-week-old) spontaneously hypertensive rats and age-matched normotensive control Wistar Kyoto rats. Most changes observed were age-dependent, and occurred only in young, early hypertensive rats. Both serotonin levels and the accumulation rate of 5-hydroxy-tryptophan after L-amino acid decarboxylase inhibition were higher in the nuclei periventricularis and paraventricularis of the hypothalamus of young hypertensive rats than in controls. In addition, 4-week-old spontaneously hypertensive rats showed higher 5-hydroxytryptophan accumulation rates in the nuclei supraopticus and dorsomedialis of the hypothalamus than controls. The only difference in serotonin metabolism found in adult hypertensive rats was high serotonin concentration in the median eminence of the hypertensive animals. Our results suggest the presence of anatomically specific, age-dependent alterations in serotonin metabolism, localized to selected hypothalamic nuclei in young hypertensive rats. These data support a role for the hypothalamic serotonin in the development of the spontaneous (genetic) hypertension in the rat.
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PMID:Serotonin turnover in discrete hypothalamic nuclei and mesencephalic raphe nuclei of young and adult spontaneously hypertensive rats. 242 65

Behavioral state instability in growth-retarded fetuses might be related to a decrease in serotonine production. Tryptophan maternal and cord blood values after elective cesarean section have been investigated by means of high performance liquid chromatography in 20 growth-retarded fetuses due to pregnancy-induced hypertension (PIH) and 20 normal pregnancies as control group. The feto-maternal ratio of tryptophan is significantly higher in normal fetuses than in PIH growth-retarded fetuses (p less than 0.001). Behavioral states have been determined 1 week and just before cesarean section. Values of 1F, 2F, 3F and 4F differ in the 2 groups (p less than 0.001). A higher percentage of non-coincidences (p less than 0.001) and state interruptions (p less than 0.001) is found in PIH fetuses. A significant correlation is demonstrated between the increase of non-coincidences and decrease in the feto-maternal Trp ratio (p less than 0.001).
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PMID:Tryptophan availability and fetal behavioral states. 248 11

Hypertension developed within 5 weeks in uninephrectomized rats administered deoxycorticosterone acetate (DOCA, 30 mg/kg, s.c., weekly) and given isotonic saline to drink. Chronic dietary administration of tryptophan (50 g/kg food) reduced intake of saline solution and prevented the elevation of systolic blood pressure induced by treatment with DOCA alone. Treatment with tryptophan also protected against the reduction in urinary concentrating ability during a 24 h dehydration that is characteristic of DOCA-treated rats. Other tests were carried out to assess the responsiveness to the beta-adrenergic agonist, isoproterenol. The tests included measurement of drinking and heart rate following acute administration of isoproterenol. The characteristically depressed drinking response of DOCA-treated rats to acute administration of isoproterenol was returned to that of untreated controls by chronic treatment with tryptophan. However, the reduced chronotropic response of the heart of DOCA-treated rats to administration of isoproterenol was unaffected. The cardiac hypertrophy characteristic of DOCA-treatment was attenuated significantly by chronic treatment with tryptophan. These results suggest that tryptophan provides significant protection against the development of DOCA-induced hypertension, polydipsia, and cardiac hypertrophy in rats. The mechanism by which tryptophan protects is unknown and requires additional study.
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PMID:Prevention of DOCA-induced hypertension in rats by chronic treatment with tryptophan. 295 Oct 40

Malnutrition is frequently associated with advanced cirrhosis. To investigate the role of portal hypertension in nutritional impairment, we developed an animal model to isolate and characterize the effects of chronic intestinal venous hypertension on intestinal nutrient absorption. We performed mesenteric arteriovenous anastomosis combined with portal vein banding in rats. Hepatic architecture and excretory function (bile flow and bile salt output) were unaltered, while severe and persistent intestinal venous hypertension was produced. We then measured in vivo absorption rates of three test nutrients (vitamin D3, valine, and tryptophan) and water. Vitamin D3 absorption was significantly impaired by intestinal congestion, while amino acid absorption was unaffected. Splanchnic hypertensive rats absorbed less water than controls. We conclude that chronic intestinal venous hypertension alone selectively impairs nutrient absorption.
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PMID:Selective impairment of nutrient absorption from intestines with chronic venous hypertension. 300 45

Diet clearly influences neurotransmission. This can be important in grossly undernourished children. It can also be important in children in whom normal homeostatic mechanisms governing food intake are bypassed. Subtle differences in behavior can occur with physiologic variation in food intake. Components of foods can also be used as drugs. Starvation can impair neuronal maturation and can have lasting effects upon behavior and intellectual performance. The extent of starvation's impact upon the brain depends upon whether undernutrition occurred during a critical phase in brain development. Short-term fasting has small, but significant, effects upon intellectual performance. Even when gross malnutrition is not present, subtle changes in diet may modulate brain function. Tryptophan, tyrosine, and choline in the diet are used as precursors for neuronal synthesis of serotonin, dopamine and norepinephrine, and acetylcholine, respectively. It is likely that the brain's sensitivity to certain components of the diet exists to permit monitoring of food intake by the central nervous system. Tryptophan, tyrosine, and choline may be useful in treatment of humans with sleep disorders, pain depression, mania, hypertension, shock, or dyskinesias. Other components of the diet that may affect behavior include food additives, sugar, and caffeine. Food additives may exacerbate hyperactive symptoms in a small proportion of children with attention deficit disorder. Given that there is little potential for harm and that there is a subpopulation that may respond, a trial of a diet that contains no food additives may be a valid diagnostic approach for children with attention deficit disorder who do not respond to stimulant therapy or for children for whom stimulant therapy is not desired. Refined sugar has been blamed for many behavioral abnormalities. Subtle effects of carbohydrate upon behavior have been reported, but the existing data do not support the hypothesis that sucrose or fructose exert special effects upon neurotransmission. Caffeine is easily detected as a stimulant by humans, but it has little effect upon cognitive function. Administration of large doses of vitamins has no beneficial effect in most humans with schizophrenia, attention deficit disorder, autism, Down's syndrome, or drug addiction. Large doses of niacinamide may even be harmful, as they may cause hepatic damage.
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PMID:Dietary influences on neurotransmission. 302 51

Chronic dietary administration of L-tryptophan (2.5 and 5.0 g/100 g food) to rats provided significant protection against the development of hypertension induced by bilateral encapsulation of the kidneys with latex envelopes. Lower doses of tryptophan (0.5 and 1.0 g/100 g food) attenuated the rate of elevation of blood pressure, but failed to maintain systolic blood pressures at levels significantly below that of untreated renal hypertensive controls. The body weight of the rats was not affected significantly by treatment with any dose of tryptophan used. Chronic treatment with tryptophan also protected against the reduced urinary concentrating ability during a 24-hour dehydration that characteristically accompanies renal encapsulation. A modest (5-8%) effect of treatment to reduce cardiac hypertrophy was also observed. The mechanism of the antihypertensive effect of tryptophan is not revealed by these studies although they rule out the possibilities that reduction in sodium intake and/or reduction in body weight may be important factors.
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PMID:Effect of chronic dietary treatment with L-tryptophan on the development of renal hypertension in rats. 335 43

The present study investigated the metabolism of serotonin (5-HT) in rats made hypertensive by treatment with DOCA/NaCl. 5-Hydroxytryptamine and its major metabolite, 5-hydroxyindoleacetic acid (5-HIAA) were significantly elevated in a number of regions of the brain in rats treated for 2 weeks with DOCA/NaCl. Elevations in levels of 5-HIAA were present with 4 weeks of treatment with DOCA/NaCl but levels of 5-HT were not altered. No changes in the metabolism of 5-HT were detectable with 5 weeks of treatment with DOCA/NaCl. Levels of tryptophan were also elevated in a number of regions of the brain by treatment with DOCA/NaCl. Alterations in norepinephrine (NE) in the brainstem were present with 2, 4 or 5 weeks of treatment with DOCA/NaCl. The neurochemical effects of muscimol, a GABA agonist, were also investigated in rats treated with DOCA/NaCl for 4 weeks. Significant increases in levels of 5-HIAA and 5-HT were present in rats treated with DOCA/NaCl but not in controls, 15 min after intraventricular administration of muscimol (1.0 microgram/300 g body weight). Sixty min after muscimol, 5-HIAA was increased in both rats treated with DOCA/NaCl and control rats, but 5-HT was only increased in the hypothalamus. Treatment with DOCA/NaCl produced changes in the metabolism of 5-HT that may be important in the genesis of hypertension, but are not required for the maintenance of elevated arterial pressure. A disturbance of GABA-5-HT interactions between GABA and 5-HT in brainstem sites may also contribute to the pathogenesis of hypertension induced by DOCA/NaCl.
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PMID:Central serotonergic alterations in deoxycorticosterone acetate/NaCl (DOCA/NaCl)-induced hypertension. 341 40

Chronic dietary administration of either l-tryptophan (5.0%) or nicotinic acid (5.0%) reduced the elevated blood pressure of rats with established, deoxycorticosterone-acetate (DOCA)-salt-induced hypertension without affecting either body weight or cardiac hypertrophy. In a second study, chronic dietary administration of nicotinic acid (2.5 and 5.0%) provided significant protection against the development of an elevated blood pressure in rats treated with DOCA salt. A modest (approximately 10%) reduction in cardiac hypertrophy was also observed in the two nicotinic-acid-treated groups. Treatment with either dose of nicotinic acid did not, however, prevent either the renal hypertrophy characteristic of DOCA-salt-induced hypertension in rats or their reduced renal concentrating ability during a 24-hour dehydration; nor did treatment with nicotinic acid reduce the excessive ingestion of saline characteristic of chronic treatment with DOCA. In contrast, treatment with the higher dose of nicotinic acid prevented the excessive loss of sodium into urine characteristic of DOCA-salt-induced hypertension when the rats were loaded (3% of body weight, i.p.) with a hypotonic (0.075 M) saline solution. These results suggest that increased production of nicotinic acid resulting from dietary administration of tryptophan may play a role in the protective effect of tryptophan against the development of DOCA-salt-induced hypertension. These studies do not, however, provide a mechanism by which nicotinic acid may manifest its beneficial effects.
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PMID:Effect of chronic dietary treatment with nicotinic acid on the development and maintenance of deoxycorticosterone-acetate-salt-induced hypertension. 342 Jan 63

Hypertension developed within 3 to 5 weeks in uninephrectomized rats administered deoxycorticosterone acetate (DOCA) at a dose of 850 micrograms X kg-1 X day-1 via Silastic tubes and given isotonic saline to drink. Chronic dietary administration of tryptophan (25 and 50 g/kg of food) to DOCA-treated rats reduced their exaggerated intake of NaCl solution and attenuated the elevation of blood pressure induced by treatment with DOCA alone. Treatment with tryptophan also protected against the reduction in urinary concentrating ability during a 24-h dehydration that is characteristic of DOCA-treated rats. Other tests assessed the responsiveness to the beta-adrenergic agonist, isoproterenol. These included measurement of drinking and heart rate following acute administration of isoproterenol. The characteristically depressed drinking and chronotropic responses of DOCA-treated rats to acute administration of isoproterenol were unaffected by tryptophan. Responsiveness to angiotensin II (AII) was also tested by assessment of dipsogenic and metabolic responses to acute administration of AII. The increased drinking and tail skin temperature responses to administration of AII, characteristic of DOCA-treated rats, were reduced in a graded fashion by treatment with graded doses of tryptophan. The specific binding of AII to its receptors in membranes form the diencephalon of the brain was increased by treatment with DOCA but was returned to control level by concomitant treatment with tryptophan. The content of serotonin in the mesencephalon of the brain was not changed significantly by treatment with tryptophan, but the content of 5-hydroxyindole acetic acid in the same region increased significantly, suggesting that turnover of serotonin was increased by chronic treatment with tryptophan. The cardiac hypertrophy characteristic of treatment with DOCA was attenuated significantly by chronic treatment with tryptophan, while the low, resting plasma renin activity of the DOCA-treated group was unchanged. These results suggest that tryptophan provides significant protection against the development of DOCA-induced hypertension, polydipsia, polyuria, and cardiac hypertrophy in rats. It also reduces the hyperresponsiveness to treatment with AII, possibly by decreasing the specific binding of AII to its receptors. It also appears to increase the turnover of serotonin in the brain. Whether either one or all of these is responsible for the antihypertensive effect of tryptophan remains for further study.
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PMID:Chronic dietary administration of tryptophan prevents the development of deoxycorticosterone acetate salt induced hypertension in rats. 362 Oct 37

The total renin activity (TRP) and inactive renin levels (IR) in the blood plasma were examined with the help of cryo- and trypsin activation in 9 normal subjects, in 40 patients with essential hypertension and in 18 patients with primary aldosteronism (PA). The cryoactivation method was shown to detect 40-80% of IR determined by the method of trypsin activation. Both methods revealed analogous ratios of the two renin forms in its total production in the presence of essential hypertension (in different "renin" subgroups) and arterial hypertension secondary to PA and may be used as the methods of choice when examining essential hypertension patients with the normal and subnormal plasma renin activity. The method of trypsin activation is more preferable for a more accurate quantification of small amounts of IR found in essential hypertension patients with a high plasma renin activity. With a high level of the TRP (over 8 ng/ml/h) activation should be performed in diluted plasma.
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PMID:[Comparative evaluation of the efficacy of methods of cryo- and trypsin activation of inactive renin in vitro]. 388 76


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