UMLS:C0085580 - FACTA Search

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Query: UMLS:C0085580 (essential hypertension)
14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension in spontaneously hypertensive rats (SHR) develops initially without any obvious organic lesions, and mainly with hemodynamic alteration due to increased peripheral vascular resistance. It is then followed later by various cardiovascular complications such as stroke. These facts indicate that this spontaneous hypertension is very similar to essential hypertension in man. Studies on the pathogenic mechanisms of spontaneous hypertension up to the present have revealed the following points. (1) This hypertension is genetically transmitted to the offspring in an additive mode by a relatively small number of major genes; (2) Environmental factors such as stress and salt-loading accelerate the hypertension; (3) Parabiosis between SHR and normotensive rats offered no positive evidence indicating the involvement of any strong humoral factors; (4) Assays on adrenal and thyroid hormones have suggested that this hypertension is not a simple endocrine hypertension; (5) The destruction of the central nervous system or sympathectomy on blood pressure or peripheral vascular resistance, as well as the recording of spontaneous sympathetic discharge, etc. have indicated the positive involvement of the autonomic nervous system in the development of this hypertension; (6) Changes in the enzyme activities of the central nervous system and in the central responses to various candidates of central neurotransmitters suggested that 'noradrenergic inhibitory mechanisms for blood pressure regulation in the brainstem' (Yamori, Lovenberg and Sjoerdsma, 1970) might be insufficient and result in the initial enhancement of peripheral vasomotor tone causing labile hypertension; (7) Noradrenalin turnover study of the heart and hindlimb perfusion experiments indicated that the neural factor was mainly involved in the development or the early stage of hypertension; this finding was further supported by the increased noradrenalin level or dopamine-beta-hydroxylase activity in the blood; (8) Histometrical studies indicated that the structural component of the peripheral vascular resistance stabilized the hypertension; (9) The initial neurogenic factors and successive involvement of nonneurogenic factors are relayed by the acceleration of protein metabolism of the vascular wall ('adaptive metabolic change', Yamori, 1974). This acceleration is commonly detected by amino acid incorporation study in both spontaneous and other experimental hypertension; (10) Increased lysine incorporation into the noncollagenous protein of the mesenteric arteries detected in the prehypertensive SHR was experimentally confirmed to be influenced by neural innervation. This confirmation indicated the importance of such a trophic effect of the nervous system on the structural alteration of blood vessels in the development of hypertension (neurovascular linkage, Yamori, 1975)...
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PMID:Pathogenesis of spontaneous hypertension as a model for essential hypertension. 87 Jul 22

L-2H-Leu, L-2H-Val, L-2H-Ile, L-2H-Phe, 14N-Lys were chosen for comparing their metabolic kinetic variables among those with prominent genetic predisposition of essential hypertension (FH*, 10 subjects), of stroke (FS*, 12 subjects) and those without (F-, 12 subjects) groups by gas chromatography-mass spectrometry. Results showed that only the metabolic kinetics of phenylalanine was dearranged: (1) The plasma pools of FH* and FS* groups were enlarged; (2) The turnover rate constant between plasma pool and cell pool of FH* was constricted; (3) The cell pool of FH* was larger, while the turnover rate constant was smaller than that of FS* group. The aberration of phenylalanine metabolism in essential hypertension and stroke might relate with hyperfunction of sympathetic nervous activity genetically. These diseases possibly belong to the category related to the inherited amino-acid metabolic aberration.
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PMID:[Inherited metabolic aberration of phenylalanine in the family members of patients with essential hypertension and stroke]. 165 82

Responses of renin release and blood pressure to aspirin DL-lysine (ASP) were examined to find out if the responses could help in the differentiation between unilateral renovascular hypertension (RVH) and hyperreninemic essential hypertension (EHT). The two studies involved ten patients with unilateral RVH, eight with hyperreninemic EHT, and five with hyporeninemic EHT. In a radiological study, before and 30 min after an intravenous injection of ASP (18 mg/kg), renal venous and abdominal aortic plasma was sampled and assayed for prostaglandin (PG) E2 and plasma renin activity (PRA). Systemic blood pressure was measured serially. The reproducibility of the responses to ASP was confirmed in a bedside study. In unilateral RVH, ASP suppressed renin release from the stenotic kidney and reduced the renal vein PRA ratio to less than 1.5 via the inhibition of PG synthesis, which is accelerated in that kidney. The mean suppression of aortic PRA at this dose of ASP was 35% in these patients, and their blood pressure decreased in proportion to the suppression of PRA. However, in the two EHT groups, ASP elevated the mean blood pressure. The renal synthesis of PGE2 was inhibited by ASP in all patients, but the suppression of PRA, while small, was significant (19% in the aorta) in the patients with hyperreninemic EHT, and not significant in patients with hyporeninemic EHT. The different responses of blood pressure and PRA to ASP between RVH and EHT were reproducible in the bedside study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aspirin test for differentiation of unilateral renovascular hypertension from hyperreninemic essential hypertension. 193 Aug 60

Thirty-one Japanese with essential hypertension were divided into training (n = 21) and non-training (n = 10) groups. Physical training of 10 weeks was instituted after 4 or more weeks of observation, and changes in blood pressure and serum concentrations of taurine and other amino acids were investigated. The workload in physical training was predetermined by the submaximal multistage graded exercise test on a bicycle ergometer, and the blood lactate threshold which reflects approximately 40-60% of maximal oxygen uptake was chosen. The hypertensive patients underwent bicycle ergometer training for 60 minutes, three times a week for 10 weeks. Blood pressures were significantly decreased by 14.8/6.6 mmHg in systole/diastole in the training group, but not in the non-training group. Serum concentrations of taurine and cystine were increased significantly by 26% and 287%, in the training group. Increase in serum asparagine (11%), histidine (6%) and lysine (7%) concentrations was also significant, only in the training group. Plasma norepinephrine level and whole blood and plasma volumes were significantly reduced. The change in serum taurine level was significantly negatively correlated with the change in plasma norepinephrine. In addition there was a significant positive correlation between the change in plasma norepinephrine and the change in diastolic blood pressure in the training group. Based on these results, the increase in serum taurine which is known for its antihypertensive activity could contribute, at least in part through the reduction in plasma norepinephrine level, to the antihypertensive effect of exercise.
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PMID:Changes in serum concentrations of taurine and other amino acids in clinical antihypertensive exercise therapy. 256 73

To clarify the role of renal prostanoid in hyperreninemia and high blood pressure in human renovascular hypertension, we measured prostaglandin E2 and renin activity in renal venous and abdominal aortic plasma before and after the intravenous administration of the cyclooxygenase inhibitor, aspirin DL-lysine. Subjects were six patients with unilateral renovascular hypertension and six with essential hypertension. In patients with renovascular hypertension, prostaglandin E2 concentration in renal venous plasma from the stenotic kidney was 9.25 +/- 1.48 pg/ml, which was significantly higher (p less than 0.01) than the concentration in the renal venous plasma from the normal kidney (4.97 +/- 1.02 pg/ml) or in the aortic plasma (2.59 +/- 0.15 pg/ml). Plasma renin activity was also higher in the renal vein of the stenotic kidney than in the other two sites. The stenotic side/normal side ratio of the renal venous prostaglandin E2 correlated significantly with a renin ratio greater than 1.5 (r = 0.8211, p less than 0.05). Intravenous injection of aspirin DL-lysine (18 mg/kg) 30 minutes later markedly suppressed prostaglandin E2 and renin levels at all sites and clearly lowered arterial blood pressure (mean: from 120 +/- 6 to 110 +/- 5 mm Hg, p less than 0.01). The reduction in blood pressure correlated significantly with the suppression of plasma renin activity in the aorta (p less than 0.05) and in the renal vein of the stenotic kidney (p less than 0.01). Conversely, in patients with essential hypertension, aspirin had little effect on renin levels and increased mean blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aspirin lowers blood pressure in patients with renovascular hypertension. 268 Sep 59

A non-ACTH aldosterone-stimulating factor(s) has been implicated in the pathogenesis of idiopathic hyperaldosteronism (IHA). Although this factor has not been fully characterized, some evidence suggests that it may be related to a pro-gamma-melanotropin (pro-gamma-MSH), derived from the NH2-terminal region of pro-opiomelanocortin. In the present study, plasma immunoreactive (IR-) gamma-MSH levels at 0800 h in patients with IHA were evaluated (90 +/- 17 fmol/ml; range: 13-173 fmol/ml) and found to be significantly higher (P less than 0.05) than those in subjects with aldosterone-producing adenomas (33 +/- 8 fmol/ml), essential hypertension (33 +/- 6 fmol/ml), and normotensive controls (19 +/- 2 fmol/ml). Seven of nine IHA subjects had circulating IR-gamma-MSH levels above the normal range (greater than 35 fmol/ml). In plasmas sampled at 1200 h, IR-gamma-MSH was significantly higher in patients with IHA (95 +/- 26 fmol/ml) and adenomas (63 +/- 23 fmol/ml), as compared with essential hypertensives (31 +/- 6 fmol/ml) and normotensives (19 +/- 3 fmol/ml). Mean plasma IR-ACTH, plasma cortisol, and urinary cortisol levels did not differ significantly between any of these groups. In order to evaluate the effect of a pro-gamma-MSH in vitro, adrenal adenoma tissue was obtained from two patients, one with elevated IR-gamma-MSH (61 fmol/ml) and a second with low IR-gamma-MSH (12 fmol/ml). Aldosterone secretion by dispersed adenoma cells from the former, but not the latter, underwent a fourfold dose-dependent (10(-14)-10(-9) M) increase in response to human Lys-gamma 3-MSH. These data suggest that a pro-gamma-MSH may be implicated as a pathogenic factor in a subset of patients with primary aldosteronism, particularly among those differentially diagnosed as having IHA.
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PMID:Plasma immunoreactive gamma melanotropin in patients with idiopathic hyperaldosteronism, aldosterone-producing adenomas, and essential hypertension. 401 76

Low renin hypertension (LRH), which accounts for 10-20% of patients with idiopathic "essential" hypertension, bears hormonal similarities to mineralocorticoid-induced hypertension, but elevated mineralocorticoid concentrations have not been found. Some patients with LRH have normal, rather than suppressed, plasma aldosterone concentrations, so that the ratio of aldosterone concentration to PRA (Aldo/PRA) is high, suggesting inappropriately increased aldosterone biosynthesis. We characterized the CYP11B2 gene that encodes the aldosterone synthase, P450c11AS, in hypertensive and control populations in a single clinic in Santiago, Chile. We directly sequenced the entire CYP11B2 gene in 12 patients with LRH, 2 high renin hypertensive controls, and 2 normotensive controls. All sequences were identical, except that 8 of 24 LRH alleles encoded arginine rather than lysine at position 173. The Arg173 and Lys173 variants were expressed in transfected MA-10 cells, and their ability to convert deoxycorticosterone to aldosterone was measured; the apparent Michaelis constant (Km) for Lys173 was 2.73 mumol/L; the Km for Arg173 was 2.53 mumol/L. The apparent maximal velocity (Vmax) for Lys173 was 6.5 x 10(-3) micrograms/mL.24 h; the Vmax for Arg173 was 7.8 x 10(-3) micrograms/mL.24 h. The first order rate constant, Vmax/Km was 2.38 for Lys173 and 3.08 for Arg173. As these values were not significantly different, we sought to determine whether Arg173 is a polymorphism linked to LRH. We examined position 173 in 52 unselected patients with idiopathic hypertension and 55 normotensive controls by PCR amplification of CYP11B2 exons 3-5 followed by digestion with Bsu361, which digests the Arg173 sequence, but not the Lys173 sequence. More of the hypertensive alleles (39 of 104, 37.5%) than normotensive alleles (25 of 110, 22.5%) carried Arg173 (chi 2 = 5.57; P < 0.02). Most of the Arg173 alleles (31 of 72, 43.1%) were from hypertensive patients with Aldo/PRA below 30, whereas only 5 of 24 (20.8%) Arg173 alleles were found in patients with Aldo/PRA greater than 30 (chi 2 = 3.79; P = 0.05) Thus, the ARg173 variant of CYP11B2 may be linked to LRH in Chilean patients.
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PMID:Genetic variation in P450c11AS in Chilean patients with low renin hypertension. 895 40

alpha(2A)-Adrenergic receptors (alpha(2A)AR) are presynaptic autoinhibitory receptors of noradrenergic neurons in the central and peripheral sympathetic nervous systems, which act to dynamically regulate neurotransmitter release. Signaling through the G(i)/G(o) family of G-proteins, the receptor subserves numerous homeostatic and central nervous system functions. A single nucleotide polymorphism of this receptor, which results in an Asn to Lys substitution at amino acid 251 of the third intracellular loop, was identified in the human population. The frequency of Lys-251 was 10-fold greater in African-Americans than in Caucasians, but was not associated with essential hypertension. To determine the consequences of this substitution, wild-type and Lys-251 receptors were expressed in CHO and COS-7 cells. Expression, ligand binding, and basal receptor function were unaffected by the substitution. However, agonist-promoted [(35)S]GTPgammaS binding was approximately 40% greater with the Lys-251 receptor. This enhanced agonist function was observed with catecholamines, azepines, and imidazolines albeit to different degrees. In studies of agonist-promoted functional coupling to G(i), the polymorphic receptor displayed enhanced inhibition of adenylyl cyclase (60 +/- 4. 4 versus 46 +/- 4.1% inhibition) and markedly enhanced stimulation of MAP kinase (57 +/- 9 versus 15- +/- 2-fold increase over basal) compared with wild-type alpha(2A)AR. The potency of epinephrine in stimulating inositol phosphate accumulation was increased approximately 4 fold with the Lys-251 receptor. Unlike previously described variants of G-protein-coupled receptors, where the minor species causes either a loss of function or increased non-agonist function, Lys-251 alpha(2A)AR represents a new class of polymorphism whose phenotype is a gain of agonist-promoted function.
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PMID:An asn to lys polymorphism in the third intracellular loop of the human alpha 2A-adrenergic receptor imparts enhanced agonist-promoted Gi coupling. 1094 91

EHT and CNDO/2 types of calculations permit the interpretation of the course of hydroxylation of collagenous proline and lysine. Calculations were performed for the models of proline (I), zwitterion of proline (II), proline-containing peptide (III), and lysine (IV). The theoretical results are consistent with an electrophilic mechanism.
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PMID:Molecular-orbital study of hydroxylation of collagenous proline and lysine. 1145 71

Adipocyte-derived leucine aminopeptidase (ALAP) inactivates angiotensin II and/or generates bradykinin in the kidney, suggesting a possible role for ALAP in the regulation of blood pressure. We considered the hypothesis that genomic variants of the ALAP gene are associated with hypertension or individual variations in blood pressure. We screened for mutations in the ALAP gene in 48 unrelated Japanese individuals and identified 33 polymorphisms including 15 novel polymorphisms. We then performed a two-stage analysis. In the first stage, the eight missense polymorphisms were evaluated for associations with blood pressure in 96 apparently healthy individuals. In the second stage, only the most promising polymorphisms were evaluated for association with essential hypertension in 143 hypertensive and 348 normotensive subjects. Among the eight missense polymorphisms, the Ile276Met and Lys528Arg polymorphisms showed significant association with blood pressure. Subsequent analysis confirmed association between the Lys528Arg polymorphism and essential hypertension. The estimated odds ratio for essential hypertension was 2.3 for presence of the Arg allele at codon 528, in comparison with presence of the Lys/Lys genotype (P = 0.004). These findings support involvement of ALAP in the regulation of blood pressure.
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PMID:Identification of 33 polymorphisms in the adipocyte-derived leucine aminopeptidase (ALAP) gene and possible association with hypertension. 1185 41

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