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)

The influence of reserpine on the nasal mucous membrane in the various conditions of its autonomic denervation was investigated in the rabbits. Histochemical analysis of a acetylcholine esterase and quantitative measurements of acetylcholine were performed. The results point out that reserpine influence is found only on the vascular elements in the mucous membrane and not on the subepithelial glands. Analogically it was concluded that in some patients with arterial hypertension who were treated with reserpine, its side effect, nasal obstruction, was caused only by vasodilatation. In rhinitis vasomotorica, in the addition to the vasodilatation the abounding secretion of subepithelial mucous glands is present. The performed experiments also point out that resection of the vidian nerve in resistant cases of vasomotor rhinitis with aboundant secretion is reasonable.
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PMID:[Influence of reserpine on the nasal mucous membrane (author's transl)]. 13 41

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 effect of hypertension, which is known to enhance atherosclerosis, on acid esterase activity of rat aortic wall was studied histochemically. The purpose was to test our notion that atherogenesis depends on the balance between supply of lipids to the arterial smooth muscle cells and the lysosomal esterase activities. Hypertension was produced in rats by unilateral nephrectomy and administration of desoxycorticosterone acetate and sodium chloride. The animals reacted with varying degrees of hypertension. In rats with hypertension of a sufficiently high degree and of long duration, inhibition of aortic acid esterase activities occurred. No inhibition of these enzymes occurred in the other organs examined.
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PMID:Experimentally produced hypertension and aortic acid esterase. 98 72

Urinary and kidney kallikrein were studied in rats with renal clip hypertension. The effect of protease inhibitors on urinary and kidney BAEE esterase activity was similar. Both hypertensive and not hypertensive operated rats excrete significantly less kallikrein than controls; in the ischaemic kidney kallikrein is diminished whereas is not increased in contralateral. Kallikrein is therefore related to renal functional mass but does not seem responsible for a natriuretic effect.
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PMID:Urinary and kidney kallikrein in hypertensive rats. 99 Mar 80

The state of the kinin system of blood was studied in terms of its content of kininogen, prekallikrein, kallikrein inhibitor and the spontaneous esterase activity. The examination was conducted in 10 normal individuals and in 81 hypertensive patients with labile and stable arterial pressure and an uncomplicated course. The studies were conducted at rest, during the transfer into an orthostatic position, and after 15 or 60 minutes of walking. The normals demonstrated an activation of the kinin system that ensued in orthostasis, but was more distinct at walking. A significant correlation was noted between the content of prekallikrein and kininogen in all the states under examination. In cases of labile arterial hypertension an increased activation of the blood kinin system was observed at rest, a lack of its activation at walking, and disorders in the correlation between the content of prekallikrein and kininogen. The observed changes in the kinin system may affect the central haemodynamics and the formation of the hyperkinetic type of circulation.
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PMID:[Characteristics of changes in the kinin system of blood in hypertensive disease]. 108 40

Esterase and Acid phosphatase isozymes were examined in a number of organs, glands and tissues from Spontaneously Hypertensive Rats (SHR) and kidney and liver from DOCA hypertensive rats at various stages in comparison with those of normotensive rats (CR). In SHR, the abnormalities in the patterns of esterase isozyme were demonstrated in endocrine glands and respiratory tracts as well as in the kidney, liver and digestive tracts throughout the whole life span, and abnormalities in the patterns of acid phosphatase isozyme was also demonstrated in the liver after seven days of age. Moreover, in DOCA hypertensive Rats, minute alterations in esterase isozyme were demonstrated in the kidney and liver after seventh month of the duration of hypertension.
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PMID:Zymogram analyses of various organs, glands and tissues from spontaneously hypertensive rats (SHR) and DOCA hypertensive rats. 116 4

Carbonic anhydrase (CA) is a well characterized pH regulatory enzyme in most of the tissues in the body. Changes in activities of CA have been associated with altered metabolism, especially in diabetes mellitus. Insulin resistance and hyperinsulinemia are common in hypertension. To investigate the possible role of CA, we measured the CA activity spectrophotometrically using p-nitrophenyl acetate as a substrate and acetazolamide, the specific inhibitor, in erythrocytes from normotensive and essential hypertensive subjects. Further, to evaluate the insulin action on CA, we used two different hemolysates; (i) insulin applied into hemolysate and (ii) hemolysate from insulin treated erythrocytes in vitro before the determination of CA activity. Two different levels of CA activities were obtained in these patients. CA activities were much lower (mean +/- SD, 0.88 +/- 0.19 U/min/mL) and higher (mean +/- SD, 1.77 +/- 0.23 U/min/mL) in patients than the normotensive controls (mean +/- 1 SD, 1.41 +/- 0.1 U/min/mL). These differences in both the groups were statistically significant (p less than 0.001). Similarly, total esterase activities in patients were (1.41 +/- 0.27 U/min/mL) that was 30% less in low activity group and (2.47 +/- 0.25 U/min/mL) that was 22% more in higher activity group in comparison with those from normotensives (2.02 +/- 0.17 U/min/mL). The relative percent of CA activities of insulin treated erythrocytes from normotensives and hypertensives were 11% and 18% higher than without insulin (p less than 0.05). No difference was observed when insulin was applied in the hemolysate. We conclude that essential hypertensive patients are associated with altered CA activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in carbonic anhydrase may be the initial step of altered metabolism in hypertension. 190 43

We detected a novel vasoconstrictor in an arginine esterase fraction separated from fractions containing tonin and other esterases that were obtained from a rat submandibular gland extract. When tested on isolated rabbit aorta rings, the substance caused dose-related contractions that were slow in onset, long-lasting, and difficult to reverse by rinsing. The substance acts directly on vascular smooth muscle, since preincubation with plasma or intact endothelium is not required. The fact that the constrictor was destroyed by heat and incubation with pronase suggests that it is a protein. Molecular sieving indicates an estimated molecular weight of 24,000 Da. It has a neutral isoelectric point that is higher than the pI of tonin, from which it can be separated by anion exchange chromatography. A small amount of the vasoconstrictor was obtained by gel filtration and eluted from isoelectric focusing polyacrylamide gels. The purified substance showed a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. It was a potent vasoconstrictor; an estimated concentration of 2.5 nM induced contraction of isolated rabbit aorta rings ranging from 15% to 40% of the maximum contraction obtained by 60 mM KCl. Contraction was completely blocked by 1 mM (p-amidinophenyl)methanesulfonyl fluoride, a serine protease inhibitor. Contractile activity was not affected by hirudin, a thrombin inhibitor, but was completely inhibited by soybean trypsin inhibitor and blunted by aprotinin; thus it may be a trypsin-like serine protease. Purified vasoconstrictor preparation showed hydrolyzing activity on Pro-Phe-Arg-methyl-coumarin amide, a kallikrein substrate. We conclude that a novel vasoconstrictor serine protease is present in the rat submandibular gland.
Hypertension 1991 Jan
PMID:A potent vasoconstrictor in the rat submandibular gland. 198 78

The inhibition of angiotensin converting enzyme by ramipril, ramiprilat, enalapril, enalaprilat, and captopril was studied in the plasma and various tissues (lung, heart, renal cortex, renal medulla) of normotensive rats and spontaneously hypertensive rats. Displacement curves for [3H]ramiprilat were established on each tissue with the converting enzyme inhibitors, and their potencies were expressed as the concentration that inhibited 50% of the specific [3H]ramiprilat binding. In the plasma, lung, and heart, the order of activities was: ramiprilat greater than enalaprilat greater than captopril greater than ramipril greater than enalapril. This order was different in the kidney (cortex and medulla): ramiprilat greater than enalaprilat greater than ramipril greater than captopril greater than enalapril. For ramiprilat, enalaprilat, and captopril, there were no differences in their respective potencies between tissues or between rat strains. However, the two prodrugs ramipril and enalapril were 10-30 times more active in the kidney than in the other tissues in both groups of rats. This was due to the deesterification of the prodrugs: in the presence of an esterase inhibitor (diethyl nitrophenyl phosphate, 10 microM), the potencies of ramipril in the kidney were not different from that obtained in the lung, which was not affected by the presence of the esterase inhibitor. These results suggest that the variations in the tissue activities of an angiotensin converting enzyme inhibitor are probably not due to differences in tissue affinities of the angiotensin converting enzyme inhibitor but depend on the concentration of this angiotensin converting enzyme inhibitor in each tissue.
Hypertension 1991 Apr
PMID:In vitro tissue potencies of converting enzyme inhibitors. Prodrug activation by kidney esterase. 201 76

A study was made of the effects of heparin and sodium fepromaron on prekallikrein (PK); kallikrein inhibitors (KI), initial esterase activity (IEA) of rat blood in health and pituitrin hypertension. Pituitrin hypertension was associated with IEA increase and KI decrease. A single administration of heparin raised IEA; if administered for 3 days, heparin reduced IEA. After pituitrin administration heparin decreased IEA if administered once or for 3 days. Administration of fepromaron in courses following pituitrin also reduced. IEA, with that reduction being preserved for not less than 4 days after drug discontinuation. Similarity of the effects of heparin and fepromaron on hemocoagulation and the tone of blood vessels suggests the common mechanisms of their action on the blood kinin system.
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PMID:[Effect of heparin and fepromaron on the kallikrein-kinin system in pituitrin-induced hypertension]. 241 94


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