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

Several models of experimental hypertension are described (neurogenic, mineralocorticoid, renovascular and genetic hypertension). An activation of the sympathetic nervous system is seen in these situations (increases in sympathetic nervous discharge, in the synthesis of noradrenaline and in the level of plasma catecholamines). This activation may be connected with biochemical abnormalities within the medulla which have been noticed for catecholamines and serotonin. These medullary abnormalities could themselves depend on abnormalities situated at higher levels (hypothalamus). The factors which determine the central problem and their mechanism of action are still hypothetical (e.g. the direct effect of sodium on the brain, the effect of stress and the environment as well as genetically determined biochemical abnormalities of the central nervous system). In the case of essential hypertension in man, available data are limited to the levels of plasma catecholamines which suggest an increased sympathetic activity of central origin when these levels are elevated.
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PMID:[Arterial hypertension: the role of the central nervous system. II. Experimental and clinical study (author's transl)]. 64 71

1. Increased erythrocyte sodium-lithium countertransport activity has been reported to be associated with nephropathy in type 1 diabetes and linked to a family history of essential hypertension. 2. This study aimed to determine the mechanism of increased sodium-lithium countertransport activity. Sodium-lithium countertransport kinetics were measured in uncomplicated and hyperlipidaemic type 1 diabetic patients. 3. In the nine out of 31 uncomplicated type 1 diabetic patients who had high sodium-lithium countertransport activity, the sodium affinity (Km) was normal but the maximum velocity (Vmax) was increased. 4. Hyperlipidaemia, when present in diabetic patients, was associated with increased sodium-lithium countertransport activity, but could not explain the high activity in uncomplicated type 1 diabetic patients in whom plasma lipid concentrations were normal. 5. Sodium-lithium countertransport activity is increased in type 1 diabetes by a mechanism different to that in essential hypertension, where the mechanism is a low Km (increased sodium affinity). Hence familial hypertension cannot explain the raised sodium-lithium countertransport activity in type 1 diabetes.
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PMID:Kinetics of sodium-lithium countertransport activity in patients with uncomplicated type 1 diabetes. 131 14

The hereditary nature of familial hypertension has been clearly established by a number of clinical studies. About 30% of the blood pressure variance can be attributed to genetic factors. As a consequence, the relative risk for developing coronary artery disease or cardiovascular death is increased in patients with a family history of hypertension and cardiovascular disease. Patients with such familial history should be considered at the same risk as those who have independent epidemiologic risk factors. The development of molecular genetics allows establishment of a link between high blood pressure, intermediate phenotypes, and the genes involved in blood pressure regulation. Gene markers should be available in the near future that will help to identify patients predisposed to hypertension. The genes of the renin-angiotensin-aldosterone system are good examples of candidate genes whose products are known to participate in blood pressure regulation. The possible involvement of these genes in essential hypertension is critically analyzed.
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PMID:Can the genetic factors influence the treatment of systemic hypertension? The case of the renin-angiotensin-aldosterone system. 141 20

1. The purpose of the present study was to examine changes in membrane fluidity in hypertension by means of an electron spin resonance (ESR) and a spin labelling methods. 2. Erythrocytes from spontaneously hypertensive rats (SHR) and from patients with essential hypertension were examined and compared with those from age-matched normotensive controls. ESR spectra were obtained for a fatty acid spin label agent (5-nitroxide stearate) in the membranes. The values of outer hyperfine splitting (2T' parallel) and of order parameter (S) of the ESR spectra were significantly higher in erythrocytes from SHR and patients with essential hypertension than in those from normotensive controls. Similar results were obtained in cultured vascular smooth muscle cells of SHR. This finding shows that the membrane fluidity might be lower in SHR and in essential hypertension. 3. When Ca was loaded to erythrocytes with a Ca-ionophore (A23187), the parameters of the ESR spectra showed a greater increase (membrane fluidity was decreased) in SHR and in patients with essential hypertension than that in the normotensive controls. The Ca-induced alterations in membrane fluidity were not definitely observed in secondary hypertension. 4. These results suggest that the lower membrane fluidity might be a genetically determined abnormality of hypertension. The marked reduction of the membrane fluidity by Ca-loading in SHR and in essential hypertension might support the hypothesis that an abnormality of the Ca-handling at cellular levels could affect physical properties of the biomembranes in genetic hypertension.
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PMID:Membrane fluidity as a genetic marker of hypertension. 144 3

As is well known, genetic factors play a decisive role in the pathogenesis of essential hypertension (EH), even if they are closely related to environmental factors; it is therefore not possible to quantify with any degree of certainty the role and importance of each in the onset of hypertensive disease. The aim of the present study was to ascertain the presence of hypertensive 1st and 2nd degree ascendant, collaterals and descendants in a group of 355 out-patients with EH (167 males, 188 females; mean age: 52.9 +/- 0.7 years) using an anamnestic analysis. The results of this study confirmed the high prevalence of the hereditary component in EH: familial hypertension was found in 60.6% of the group. From a detailed analysis of the group, with regard to hypertensive ascendant, the hereditary transmission of EH by the mother was significantly higher than that by the father, both the parents and the forefathers, even if it is worth pointing out that the penetration of the genetic character was not always sex-related and was equally distributed between male and female descendents. In addition, it was observed that patients with a familial pattern of hypertension in common with collateral relatives showed significantly enhanced levels of systolic and diastolic pressure in relation to those with another hereditary component. These findings serve to underline the importance of evaluating the effective incidence of EH with regard to an entire family nucleus and not only in individual terms, in order to identify the various means of genetic transmission and possible interactions with environmental factors.
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PMID:[Evaluation of the hereditary component in patients with essential arterial hypertension]. 152 3

Insulin resistance has been described in nonobese subjects with essential hypertension. At present it is unknown whether hypertension per se may lead to the onset of insulin resistance. To examine this question we studied in vivo insulin action in two rat models of genetic hypertension. Four groups of conscious rats were studied: Milan hypertensive (MHS), Milan normotensive (MNS), spontaneously hypertensive (SHR), and Wistar-Kyoto (WKY). Mean arterial pressure was increased in SHR vs. WKY in both the fed (184 +/- 5 vs. 126 +/- 6 mmHg; P less than 0.001) and fasting (160 +/- 5 vs. 129 +/- 5; P less than 0.001) states. During high-dose insulin clamps, total body glucose uptake (mg.kg-1.min-1) was similar in MNS (28.7 +/- 1.4) vs. MHS (33.6 +/- 3.0) and in WKY (34.6 +/- 1.8) vs. SHR (35.7 +/- 2.4). During low-dose insulin clamps, suppression of hepatic glucose production (3.5 +/- 0.6 vs. 3.0 +/- 0.5 mg.kg-1.min-1) and stimulation of glycolysis (12.9 +/- 0.8 vs. 14.4 +/- 1.5 mg.kg-1.min-1) were similar in WKY vs. SHR, whereas glucose uptake (24.6 +/- 1.9 vs. 18.3 +/- 1.2 mg.kg-1.min-1; P less than 0.01) and muscle glycogenic rate (10.2 +/- 1.1 vs. 6.5 +/- 1.1 mg.kg-1.min-1; P less than 0.05) were increased in SHR vs. WKY. In conclusion, 1) feeding markedly augments blood pressure in hypertensive but not in normotensive rats, and 2) hepatic and muscle insulin sensitivity are normal or increased in two different rat models of genetic hypertension. These results provide evidence that high blood pressure per se does not invariably lead to the development of insulin resistance.
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PMID:In vivo insulin action in genetic models of hypertension. 153 44

Essential hypertension is a highly hereditable disorder in which genetic influences predominate over environmental factors. The molecular genetic profiles which predispose to essential hypertension are not known. In rats with genetic hypertension, there is some recent evidence pointing to linkage of renin gene alleles with blood pressure. The genes for renin and antithrombin III belong to a conserved synteny group which, in humans, spans the q21.3-32.3 region of chromosome I and, in rats, is linkage group X on chromosome 13. The present study examined the association of particular human renin gene (REN) and antithrombin III gene (AT3) polymorphisms with essential hypertension by comparing the frequency of specific alleles for each of these genes in 50 hypertensive offspring of hypertensive parents and 91 normotensive offspring of normotensive parents. In addition, linkage relationships were examined in hypertensive pedigrees with multiple affected individuals. Alleles of a REN HindIII restriction fragment length polymorphism (RFLP) were detected using a genomic clone, lambda HR5, to probe Southern blots of HindIII-cut leucocyte DNA, and those for an AT3 PstI RFLP were detected by phATIII 113 complementary DNA probe. The frequencies of each REN allele in the hypertensive group were 0.76 and 0.24 compared with 0.74 and 0.26 in the normotensive group. For AT3, hypertensive allele frequencies were 0.49 and 0.51 compared with normotensive values of 0.54 and 0.46. These differences were not significant by chi 2 analysis (P greater than 0.2).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association and linkage analyses of restriction fragment length polymorphisms for the human renin and antithrombin III genes in essential hypertension. 168 42

Metabolic acidosis has recently been observed in rat models of salt-sensitive genetic hypertension. Studies in normotensive salt-sensitive men have likewise demonstrated slightly but significantly lower arterial pH and bicarbonate levels, relating salt-sensitivity to the presence of a relative acidosis in man. The administration of alkalinizing sodium salts such as sodium bicarbonate or citrate have been shown to have no effect on or to even lower blood pressure in patients with essential hypertension. Possible factors contributing to the perturbation in acid-base status include an enhanced Na+/H(+)-antiport activity, lower intracellular pH levels and altered renal electrolyte handling as found in rat models of hypertension and in patients with essential hypertension.
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PMID:Abnormal acid-base regulation in salt-sensitive normotensive man. 192 Dec 51

It has been proposed that increased Na-H exchange activity is involved in the pathophysiology of genetic hypertension. We studied platelets of spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto (WKY), and domestic Wistar rats (DWR), since platelets have similarities to smooth muscle cells and have been shown to have potentially related ion metabolism abnormalities, such as increased intracellular calcium activity. We determined the exchange rate by the intracellular acidification-dependent, extracellular sodium-dependent volume increase. The rate of increase during the first 3 min is linear and is shown to be higher in SHR (0.475 X min-1) than in WKY (0.410 X min-1) or DWR (0.389 X min-1). We conclude that the Na-H activity is increased in platelets of SHR. Similar findings in lymphocytes and neutrophils of SHR, and analogous findings in platelets of humans with essential hypertension, suggest that this abnormality is expressed by several cell types, some of which may be involved in the pathophysiology of genetic hypertension in both rats and humans.
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PMID:Increased platelet membrane sodium-proton exchange rate in spontaneously hypertensive rats. 196 85


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