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)

Thoracic aortic histamine synthesis has been examined in rats rendered hypertensive for periods ranging from 1/4 to 8 days through ligation of abdominal aorta between origins of the renal arteries, in a preliminary attempt to establish whether activity of the aortic nonmast-cell histidine decarboxylase system is increased in experimental hypertension. Results indicate that aortic histamine synthesis is increased 66, 75, 96 and 55% at postsurgical intervals of 1/4, 1/2, 1 and 8 days. These data suggest at least one biochemical explanation for both increased arterial wall permeability and the arterial inflammation consistently associated with both clinical and experimental hypertension by resolving these into those associated with the prolonged inflammatory response.
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PMID:Rat aortic histamine synthesis during short-term hypertension. 124 95

Histaminergic neurons of the brain have been implicated in genetic hypertension. We investigated the effect of inhibition of histamine synthesis by alpha-fluoromethylhistidine (alpha-FMH), the irreversible inhibitor of histidine decarboxylase, on the development and maintenance of hypertension in spontaneously hypertensive rats. Young (3-week-old) and adult (7-week-old) rats were treated with alpha-fluoromethylhistidine for 29 and 13 days, respectively. Treatment of spontaneously hypertensive rats and normotensive Wistar-Kyoto rats with alpha-fluoromethylhistidine led to a pronounced decrease in the histidine decarboxylase activity and in the histamine concentration in the brain (hypothalamus, brainstem, cortex-midbrain). In adult spontaneously hypertensive rats, the development of hypertension was not influenced by alpha-fluoromethylhistidine. In young spontaneously hypertensive rats, alpha-fluoromethylhistidine led to a transient delay in the development of hypertension which was followed by a transient tendency to increased blood pressure. It is concluded that histaminergic neurons of the brain play only a subordinate role, if any at all, in the development of hypertension in spontaneously hypertensive rats.
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PMID:Does brain histamine contribute to the development of hypertension in spontaneously hypertensive rats? 186 29

Young (3-week old) and adult (7-week old) spontaneously hypertensive rats (SHR) and normotensive rats (WKY) were treated with alpha-fluoromethylhistidine (alpha-FMH) for 29 and 13 days, respectively. Treatment of SHR and WKY with alpha-FMH led to a pronounced decrease in the histidine decarboxylase activity and in the histamine concentration in all brain areas studied. In adult SHR, the development of hypertension was not influenced by alpha-FMH. In young SHR, alpha-FMH elicited a transient delay in the development of hypertension followed by a short-lasting tendency for increased blood pressure. It is concluded that histaminergic neurons of the brain play, if at all, only a secondary role in the development of hypertension in SHR.
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PMID:Inhibition of histamine synthesis influences the development of hypertension in spontaneously hypertensive rats. 189 29

Histamine levels, histidine decarboxylase and histamine-N-methyltransferase activities were determined in various brain areas of young (9-week old) and adult (18-week old) normotensive rats (WKY) and hypertensive rats (SHR). When compared with WKY, histamine levels were increased in the anterior and posterior hypothalamus of young and adult SHR, as well as in the brainstem of young SHR. Histidine decarboxylase activity was unchanged in the posterior hypothalamus and in the medulla oblongata of young and adult SHR as well as in the anterior hypothalamus of young SHR, but it was slightly decreased in the anterior hypothalamus of adult SHR. Histidine decarboxylase activity was enhanced in the cortex-midbrain of young, as well as adult SHR, histamine-N-methyltransferase in the cortex-midbrain of young SHR. The following differences were found between young and adult rats: histamine levels were elevated in the cortex-midbrain of adult WKY and SHR. In the cortex-midbrain and brainstem of adult WKY and SHR histidine decarboxylase activity was also increased, while histamine-N-methyltransferase activity was elevated in the cortex-midbrain of adult WKY. The findings show changes in histamine levels, histidine decarboxylase and histamine-N-methyltransferase activities in SHR and suggest involvement of histaminergic neurons in hypertension. The activity of histaminergic neurons of adult rats seems to be higher than that of young animals.
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PMID:Histamine, histidine decarboxylase and histamine-N-methyltransferase in brain areas of spontaneously hypertensive rats. 324 96

Centrally injected histamine (HA) affects heart rate (HR), arterial blood pressure (BP), and sympathetic activity in rats. The posterodorsal medial amygdala (MePD) has high levels of histidine decarboxylase, connections with brain areas involved with the modulation of cardiovascular responses, and is relevant for the pathogenesis of hypertension. However, there is no report demonstrating the role of the MePD histaminergic activity on the cardiovascular function in awake rats. The aims of the present work were: 1) to study the effects of two doses (10-100 nM) of HA microinjected in the MePD on basal cardiovascular recordings and on baroreflex- and chemoreflex-mediated responses; 2) to reveal whether cardiovascular reflex responses could be affected by MePD microinjections of (R)-alpha-methylhistamine (AH3), an agonist of the inhibitory autoreceptor H3; and, 3) to carry out a power spectral analysis to evaluate the contribution of the sympathetic and parasympathetic components in the variability of the HR and BP recordings. When compared with the control group (microinjected with saline, 0.3 microl), HA (10 nM) promoted an increase in the MAP50, i.e. the mean value of BP at half of the HR range evoked by the baroreflex response. Histamine (100 nM) did not affect the baroreflex activity, but significantly decreased the parasympathetic component of the HR variability, increased the sympathetic/parasympathetic balance at basal conditions (these two latter evaluated by the power spectral analysis), and promoted an impairment in the chemoreflex bradycardic response. Microinjection of AH3 (10 microM) led to mixed results, which resembled the effects of both doses of HA employed here. Present data suggest that cardiovascular changes induced by baroreceptors and chemoreceptors involve the histaminergic activity in the MePD. This neural regulation of reflex cardiovascular responses can have important implications for homeostatic and allostatic conditions and possibly for the behavioral displays modulated by the rat MePD.
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PMID:Histamine in the posterodorsal medial amygdala modulates cardiovascular reflex responses in awake rats. 1895 17

Kounis syndrome (KS) is a complex of cardiovascular symptoms and signs following either allergy or hypersensitivity and anaphylactic or anaphylactoid insults. We report the case of 57-year-old man, with hypertension and history of allergy, referred for facial rash and palpitations appeared after consumption of canned tuna fish. Suddenly, the patient collapsed: electrocardiogram showed ST-elevation in inferior leads. The patient was transferred from the spoke emergency room for coronary angio, which did not show any sign of coronary atherosclerosis. A transient coronary spasm was therefore hypothesized and the final diagnosis was KS. To the best of our knowledge, this is one of the first cases of KS following the ingestion of tuna fish. KS secondary to food allergy has also been reported, and shellfish ingestion has been considered as one of the most active KS inducer foods. Canned tuna fish too is well known as an allergy inducer. Tuna fish allergy should be considered, however, within the context of scombroid food poisoning, also called histamine fish poisoning. Fish with high levels of free histidine, the enzyme substrate converted to histamine by bacterial histidine decarboxylase, are those most often implicated in scombroid poisoning. Inflammatory mediators such as histamine constitute the pathophysiologic basis of Kounis hypersensitivity-associated acute coronary syndrome. Patients with coronary risk factors, allergic reaction after food ingestion, and suspected scombroid poisoning should be therefore carefully monitored for a prompt diagnosis of possible coronary complications.
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PMID:Kounis syndrome following canned tuna fish ingestion. 2801 91