Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

According to immunohistochemical investigations kallikrein in the majors salivary glands is located predominantly at the apical border of the striated duct cells and as a luminal rim in the main excretory ducts. Comparatively the highest concentrations are observed in the submandibular gland of rats and cats in the cytoplasmic granules of the granular tubules. In normal humans and rats the kallikrein activity of parotid saliva is inversely related to flow rate and sodium concentration. An increased salivary kallikrein concentration is found in human essential hypertension and renoparenchymal hypertension associated with impaired kidney function. Furthermore in rats with various forms of hypertension (genetic hypertension, DOCTMA salt and renovascular hypertension) the salivary kallikrein secretion - as determined by the BAEE-esterase activity - is enhanced. In contrast to the kallikrein secretion the flow dependent sodium concentration of parotid saliva is reduced in human essential and renoparenchymal hypertension as well as in rats with various forms of experimental and genetic hypertension, which indicates an enhanced sodium reabsorption in the glandular duct system. Furthermore in most forms of hypertension, there is a tendency of higher potassium levels in the saliva. The pathogenesis of the enhanced glandular kallikrein secretion in hypertension is discussed with regard to a counterregulatory mechanism in hypertension as well as to a sympathicoadrenergic activation. The enhanced sodium reabsorption in the duct system in the various forms of hypertension could be the cause as well as a consequence of the enhanced kallikrein secretion.
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PMID:Salivary kallikrein excretion in hypertension. 39 78

The relationship between urinary kallikrein, urinary aldosterone, and plasma renin activity (PRA) was studied in hypertensive patients and normal subjects. Kallikrein was measured by a radiochemical esterolytic assay. Nine white males with normal renin, mild essential hypertension (25 +/- 5 [SD] yr; blood pressure [BP] 143 +/- 7 / 95 +/- 5 mm Hg) and six white normal males (23 +/- 3 yr; BP 115 +/- 15 / 70 +/- 6 mm Hg) were placed on a one-week diet consisting of 400 mEq Na+, 80 mEq K+ diet and a one week diet of a 10 mEq Na+, 80 mEq K+ diet. During salt restriction, PRA, urinary aldosterone, and urinary kallikrein progressively rose. (Urinary kallikrein on day 7: normals 18.3 +/- 13.7 esterase units [EU] per 24 hr; hypertensives 22.7 +/- 12.5 EU/24 hrs). There were no significant differences between the normals and hypertensives in PRA, aldosterone, or kallikrein excretion. After sodium balance was achieved, during salt loading, the PRA, aldosterone and kallikrein values were similar in both normals and hypertensives. (Urinary kallikrein on day 7: normals 5.0 +/- 5.2; hypertensives 7.9 +/- 4.4 EU/24 hrs.) Abnormalities in urinary kallikrein in hypertensives were not found when young white males with normal renin essential hypertension were compared to age-matched white male normal subjects. PRA appears related to urinary kallikrein excretion in this type of patient.
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PMID:Urinary kallikrein in normal renin essential hypertension. 91 48

The spontaneously hypertensive rat (SHR)--animal model for human essential hypertension--develops a generalized arteriopathy. The present paper discusses the atherogenic influence of hypertensive arterial lesions. The following changes in the intima might influence its permeability and barrier function, increase the trapping effect and stimulate the smooth muscle cell proliferation: the hyper-reactivity of endothelial cells; the decreased thickness of endothelial cell periphery; the reduced intercellular junction pathways; the increase in basal lamina and glycosaminoglycan sub-endothelial material; the mononuclear cell infiltrations; the widened fenestrae in the internal elastic lamina. Some hypertensive changes of the tunica media may also interact with atherogenic process through reduced smooth muscle cell lipolytic capabilities, slowed transmural diffusion, perturbed efflux, aggravated media hypoxia, namely: the decrease in esterase and cholinesterase activities, the activations of some lysosomal enzymes, the increase in collagen, glycosaminoglycan and elastin content; the increased media thickness and transmural passage; the modified smooth muscle cell behavior.
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PMID:[Hypertensive arteriopathy and atherogenesis: cellular and molecular interactions]. 310 95

Decreased urinary kallikrein (UK) output has been suggested as a preclinical indicator of essential hypertension. In preparation for UK studies in hypertension prone Utah kindreds, we assessed selected UK assay parameters and physiological variability. Precision for the colorimetric kallikrein assay was quite acceptable, coefficient of variation (CV) less than 5% within run and 14% day-to-day at a concentration of 9.5 TU/l. The mean recovery was 105% and assay results were correlated with results from the 3H-TAME esterase method, r = 0.990. Urine specimens were stable at room temperature for up to 4 days, frozen at -20 degrees C for 6 weeks, or frozen at -80 degrees C after Sephadex treatment for a year. UK output varied significantly throughout the day with excretion highest in the morning. Urine collections at 10.00, 12.00 and 14.00 had significantly (p less than 0.05) more UK than the overnight collection. Intra- and inter-individual variations were of the same magnitude, mean 20%. In children UK output increased with age until the adult levels were reached at age 15. Male and female values were similar. Smoking; consumption of alcohol, coffee, tea, cola of chocolate; and female hormone medications did not significantly influence the 12-hour UK output in the 1110 caucasian subjects.
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PMID:Urinary kallikrein: assay validation and physiological variability. 385 8

Urinary kallikrein excretion (UKal), determined by the esterase method, was measured in 10 normotensive volunteers, 10 patients with essential hypertension and in 7 patients with primary aldosteronism before and after operative removal of the adenoma. UKal values were low in 5 of the patients with essential hypertension. Preoperative UKal values in the patients with aldosteronism did not differ significantly from those of the normal subjects, but decreased in all after operation in parallel with changes in urinary excretion of tetrahydroaldosterone and plasma aldosterone concentration. The study supports the assumption of an association between the renal kallikrein-kinin system and the mineralocorticoid state in man.
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PMID:Urinary excretion of kallikrein before and after operation for aldosterone-producing adenoma. 389 26

Twelve white men with essential hypertension were treated for 1 month in randomized order with either placebo or low-dose furosemide (40 mg/day) and compared to 22 race-, age-, and diet-matched normal controls. Furosemide therapy significantly reduced mean arterial pressure (108.6 +/- 2.4 vs. 101.0 +/- 2.7 mm Hg, p < 0.02) in association with a significant increase in 24 hr urinary kallikrein activity (7.9 +/- 1.8 vs. 13.4 +/- 2.8 esterase units/24 hr, p < 0.02). Normal controls on no therapy excreted 19.4 +/- 2.6 esterase units/24 hr of urinary kallikrein activity, significantly greater than hypertensives on placebo (p < 0.01) but not hypertensives on furosemide (p > 0.1). A significant (p < 0.05) inverse correlation between mean arterial pressure and urinary kallikrein activity suggests a possible role for the kallikrein-kinin system in the antihypertensive mechanism of furosemide.
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PMID:Involvement of kallikrein in the antihypertensive response to furosemide in essential hypertension. 616 Mar 45

Recently, we established a very sensitive, specific and simple direct radioimmunoassay method for human urinary kallikrein. In this study, in order to clarify whether or not the low or high excretion rate of urinary kallikrein activity in patients with essential hypertension, primary aldosteronism, pheochromocytoma and Bartter's syndrome is caused by changes in enzyme quantity, urinary kallikrein excretion was measured with this direct radioimmunoassay method in normal subjects and in patients with these diseases. Urinary kallikrein excretion measured as enzyme quantity was significantly lower in patients with essential hypertension, and higher in patients with primary aldosteronism and Bartter's syndrome. These results are consistent with other previously reported data and our data measured by means of esterase assay or kininogenase assay. The results also suggest that lowered or elevated excretion of urinary kallikrein activity in these diseases is caused, in part at least, by the lowered or elevated excretion of enzyme quantity.
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PMID:Excretion of human urinary kallikrein quantity measured by a direct radioimmunoassay of human urinary kallikrein in patients with essential hypertension and secondary hypertensive diseases. 691 9

Urinary kallikrein excretion has been reported to be decreased in patients with essential hypertension and elevated in patients with primary aldosteronism as a reflection of mineralocorticoid activity. Low renin essential hypertension (LREH) has been postulated to result from excess production of an unknown mineralocorticoid(s). Urinary kallikrein excretion was compared in outpatients with essential hypertension, mineralocorticoid hypertension (primary aldosteronism and 17alpha-hydroxylase deficiency), and in normal subjects of the same race. No significant difference in urinary kallikrein excretion of patients with LREH vs. normal renin essential hypertension (NREH) was found for either black (4.1+/-0.4 vs. 4.8+/-0.5 esterase units (EU)/24 h, mean+/-SE, for 27 LREH and 38 NREH, respectively) or white patients (12.2+/-2.3 vs. 11.7+/-1.4 EU/24 h for 13 LREH and 25 NREH, respectively). Urinary kallikrein was decreased in black vs. white hypertensive patients and normal subjects. However, in patients with normal renal function (creatinine clearance >/=80 ml/min) urinary kallikrein was not significantly decreased in either black hypertensive vs. black normal subjects (4.3+/-0.3 vs. 5.4+/-0.6 EU/24 h) or in white hypertensive vs. white normal subjects (11.9+/-1.2 vs. 8.4+/-0.9 EU/24 h). In contrast, hypertensive patients with mild renal insufficiency (creatinine clearance of 41.8+/-78.5 ml/min) had reduced (P < 0.05) urinary kallikrein (3.3 EU/24 h with creatinine clearance of 63.6+/-2.0 for 24 black patients and 4.2+/-0.7 EU/24 h with creatinine clearance of 67.0+/-3.5 for 6 white patients). These results suggest that a reduction in urinary kallikrein excretion rate is an early accompaniment of hypertensive renal injury. Urinary kallikrein excretion in response to a 6-d 10-meq sodium diet and a 3-d Florinef (0.5 mg b.i.d.) administration was compared in hypertensive patients with normal renal function vs. race and age-matched normal subjects. Stimulation of urinary kallikrein excretion by Florinef was equal in black and white normal subjects vs. hypertensive patients (black normals = 12.3+/-2.7 [n = 9], NREH = 11.7+/-1.8 [n = 10], LREH = 10.9+/-1.5 [n = 12]; white normals = 21.2+/-2.9 [n = 11], essential hypertension = 20.9+/-3.2 [10 NREH, 5 LREH]). Stimulation of urinary kallikrein excretion with low sodium diet was decreased (P < 0.05) only in black LREH (black normals = 11.2+/-2.4 [n = 10], NREH = 10.1+/-2.7 [n = 10], LREH = 7.4+/-1.1 [n = 13]; white normals = 19.1+/-2.7 [n = 13], essential hypertension = 17.5+/-2.3 [nine NREH, four LREH]). However, during low sodium diet, black patients with LREH had evidence for less sodium depletion as manifested by a decreased rise in urinary aldosterone excretion (16.3+/-2.7 vs. 33.3+/-6.4 mug/24 h for black normals) and a failure to achieve metabolic balance in 11/13 patients. Thus, the lesser kallikrein stimulation appeared to result from these two factors. Black and white hypertensives with creatinine clearance <80 ml/min had little increase in urinary kallikrein excretion with Florinef or low sodium diet.5 of 12 patients with primary aldosteronism or 17alpha-hydroxylase deficiency did not have an elevated urinary kallikrein excretion rate. Mild renal insufficiency may have contributed to this finding in two of these five patients. Nevertheless, this finding illustrates a limitation to the use of urinary kallikrein excretion rate as an index of mineralocorticoid activity. However, it appears that the majority of patients with LREH have no evidence for excess production of an unknown mineralocorticoid. The failure to find a decrease in urinary kallikrein excretion in racially matched patients with essentil hypertension and normal renal function questions the postulate of a role of the kallikrein-kinin system in the initiation of essential hypertension.
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PMID:Urinary kallikrein excretion in essential and mineralocorticoid hypertension. 735 84

Our object was to evaluate the effects of regular mild exercise on blood pressure and on circulating level of ouabainlike factors (OLF) and of nitrate anion, an endproduct of nitric oxide (NO) in humans. We measured plasma ouabainlike immunoreactivity (OLI) and nitrate ions (NO3.) before and after mild exercise for 3 months' duration in 16 patients with essential hypertension, diabetes mellitus, obesity, or hyperlipidemia. Plasma OLI was measured using an amplified ELISA system with anti-ouabain antibody and biotinyl-tyramide. Serum NO3. was measured with high-performance liquid chromatography (HPLC) with an anion-exchange column. With the reverse phase HPLC system with an octa decylsilyl silicagel column, the elution volume of plasma OLI of a healthy volunteer matched that of authentic ouabain in a gradient elution system of acetonitrile/H2O. Plasma OLI levels decreased significantly by about 34% after mild exercise, and NO3. levels tended to be within the reference interval in normal volunteers. Body weight, diastolic and systolic blood pressure, serum triglyceride and acetylcholine esterase (a marker of the fatty liver) were significantly decreased (p < 0.01) after 3 months of regular mild exercise. The plasma OLI level was significantly correlated with plasma NO3., there was a trend toward a correlation with diastolic blood pressure (p = 0.06) before and after regular exercise. Regular mild exercise led to a decrease in plasma levels of OLI, and acetylcholine esterase activity and blood pressure in adult patients. Results suggest that changes in OLF production contribute to the blood pressure regulation seen in patients who exercise regularly.
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PMID:Vasodepressor effects of exercise are accompanied by reduced circulating ouabainlike immunoreactivity and normalization of nitric oxide synthesis. 910 42

The ethanol O-acyltransferase EHT1 is an important element of key signaling pathways and is widely expressed in yeast strains. In this study, we investigated the expression of EHT1 in the overexpression lines or knockout system of Pichia pastoris using qRT-PCR and western blotting. The amount of total protein was determined using the Bradford method; the esterase activity was determined using p-nitrophenyl acetate as a substrate, and the production of volatile fatty acids in wild-type, knockout, and over-expression systems was detected using SPME GC-MS. The esterase activity of EHT1-knockout P. pastoris was significantly lower than that in wild type (P<0.01), and the activities of esterase in three EHT1-overexpressing strains-OE-1, OE-2, and OE-3-were significantly higher than those in wild type (P<0.01). In the EHT1-knockout strain products, the contents of nine volatile fatty acids were significantly lower than those in wild type (P<0.01), and the relative percentages of three fatty acids, methyl nonanoate, methyl decanoate, and ethyl caprate, were significantly lower than those in the other six species in the wild-type and knockout groups (P<0.05). The nine volatile fatty acids in the fermentation products of the overexpressed EHT1 gene were significantly higher than those in the wild-type group (P<0.01). The relative percentages of the three fatty acid esters, methyl nonanoate, methyl caprate, and ethyl caprate, were significantly higher than those in the other six species (P<0.05). EHT1 plays an important regulatory role in esterase activity and the production of medium-chain volatile fatty acids.
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PMID:Ester-Producing Mechanism of Ethanol O-acyltransferase EHT1 Gene in Pichia pastoris from Shanxi Aged Vinegar. 3071 44


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