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

Environmental factors, genetic polymorphisms, and different experimental designs have been the main impediments to evaluating a genetic association between cell membrane cation transport abnormalities and human essential or genetic hypertension. We review the results obtained in the Milan hypertensive strain of rats (MHS) and in its appropriate control normotensive strain (MNS) to illustrate our approach to defining the role of cation transport abnormality in a type of genetic hypertension. Before the development of a difference in blood pressure between the two strains, the comparison of kidney and erythrocyte functions showed that MHS had an increased glomerular filtration rate and urinary output, and lower plasma renin and urine osmolality. Kidney cross-transplantation between the strains showed that hypertension is transplanted with the kidney. Proximal tubular cell volume and sodium content were lower in MHS while sodium transport across the brush border membrane vesicles of MHS was faster. Erythrocytes in MHS were smaller and had lower sodium concentration, and Na+-K+ cotransport and passive permeability were faster. The differences in volume, sodium content, and Na+-K+ cotransport between erythrocytes of the two strains persisted after transplantation of bone marrow to irradiated F1 (MHS X MNS) hybrids. Moreover, in normal segregating F2 hybrid populations there was a positive correlation between blood pressure and Na+-K+ cotransport. These results suggest a genetic and functional link in MHS between cell membrane cation transport abnormalities and hypertension. Thus erythrocyte cell membrane may be used for approaching the problem of defining the genetically determined molecular mechanism underlying the development of a type of essential hypertension.
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PMID:The Milan hypertensive rat as a model for studying cation transport abnormality in genetic hypertension. 331 5

Epidemiologic and experimental studies disclosed that the sympathetic nervous system might play a pivotal role in the pathogenesis of essential hypertension. Although systolic pressure exhibits a weak endogenous rhythm, diurnal fluctuations of arterial pressure are provoked primarily by physical or emotional stress factors. The magnitude of the cardiovascular response, however, varies widely from individual to individual. Subjects at high risk of future hypertension,--such as those with a positive history of familial hypertension, high resting heart rate, or transient increase in arterial hypertension--revealed blood pressure hyperresponsiveness to stress stimuli mediated by an overreactivity of the sympathetic nervous system. Furthermore, cardiovascular reactivity to mental arithmetic tasks and to traffic noise put a patient at high risk of developing arterial hypertension. In women, exaggerated cardiovascular response to stress stimuli appeared to be mitigated by estrogens, whereas oral contraceptives overrode this 'protective' effect of estrogens. At a certain point, repeated episodes of high stress blood pressure could produce structural vascular changes finally inducing sustained hypertension.
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PMID:Psychophysiologic aspects in essential hypertension. 333 31

Abnormalities in Ca metabolism in genetic hypertension have been suggested by studies of the spontaneously hypertensive rat and of humans with essential hypertension. A state of relative Ca deficiency in genetic hypertension was previously hypothesized to explain the reduced serum ionized Ca, increased serum parathyroid hormone levels, and the association between oral Ca loading and mild reduction in blood pressure. Renal Ca leak, reduced intestinal Ca absorption, and diminished Ca intake were further postulated to account for the Ca deficient state. This hypothesis, however, is not supported by the following lines of evidence in genetic hypertension: the absence of fasting hypercalciuria owing to intrinsic tubular defects, increased net Ca absorption in vivo despite greater Ca retention before and during established hypertension, increased intracellular free Ca concentrations, the failure to aggravate the hypertension by 50% reduction in dietary Ca intake, and the failure to ameliorate the hypertension by maneuvers that augment Ca balance (parenteral Ca administration, a high Mg diet, and 1,25-dihydroxyvitamin D3 injections). The available literature may be explained by the alternative hypothesis that genetic hypertension is characterized by generalized membrane defects in Ca regulation, resulting in a relative increase in cytosolic free Ca. The mechanism (or mechanisms) and physiological consequences of the disturbances in Ca homeostasis, however, remain to be defined.
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PMID:The nature and role of disturbances in calcium metabolism in genetic hypertension. 353 40

Dopaminergic mechanisms in genetic hypertension were explored via the measurement of catecholamine (CA) turnover, tissue concentration and urinary excretion of dopamine (DA) and its metabolites. In salt-sensitive (S) Dahl rats, the tissue concentration and urinary excretion of DA and its metabolites were decreased in response to salt loading, while adrenal dopamine-beta-hydroxylase (D beta H) activity and aldosterone responsiveness to angiotensin II (A II) were increased. In contrast, spontaneously-hypertensive rats (SHR) showed elevated tissue levels and urinary excretion of DA and its metabolites, adrenal DA turnover and ganglionic DA generation following cholinergic stimulation, but D beta H activity and aldosterone responsiveness to A II were diminished. These two patterns, the hypodopaminergic state in Dahl S rats and the hyperdopaminergic state in SHR, account for two distinct mechanisms of hypertension and precede its development. We detected striking dopaminergic activity-related similarities between Dahl S rats and low-renin essential hypertension (EH) on the one hand, and SHR and non-modulator EH patients on the other.
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PMID:Contrasting dopaminergic patterns in two forms of genetic hypertension. 362 31

An exaggerated blood pressure response to mental stress is believed to characterize young adults with genetic risk of essential hypertension, suggesting that stress-induced changes might provide a useful index of pathogenetic processes. We explored this by studying pressor responsivity to competitive tasks in adolescents drawn from a large urban population. Individuals with systolic or diastolic pressures persistently between the 85th and 95th percentiles were evaluated on basal blood pressure, parental history of hypertension, and pressor and heart rate response to a challenging video game. Basal pressure was measured again at 6, 10, and 14 months. A persistently diminished pulse pressure was the cardiovascular characteristic that most reliably typified normotensive subjects with familial hypertension. Response to the video game was the best indicator of risk status. Contrary to expectations derived from research with convenience samples, epidemiologic investigation points to an increased peripheral resistance and lower cardiac output as the cardiovascular pattern more prominently associated with genetic risk in the normotensive adolescent.
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PMID:Diminished pulse pressure under mental stress characterizes normotensive adolescents with parental high blood pressure. 376 88

Genetic factors are clearly involved in the pathogenesis of essential hypertension in man. In at least three rat models of genetic hypertension it is possible to transplant the hypertension with the kidney. To see whether or not the same is true for humans, we carried out a 2-year retrospective study of 50 selected recipients of a cadaver kidney. We correlated the following factors by multivariate statistical analyses: presence or absence of hypertension in the family of donor and recipients; donor's and recipient's age; mean blood pressure (MBP) and antihypertensive therapy (AHT) score during dialysis; months of dialysis and body surface before transplantation; body weight, plasma creatinine, prednisone dosage and cumulative rejections with MBP and AHT score at various time intervals after transplantation. The results obtained showed that, considering the recipients coming from normotensive families, the AHT score after transplantation was significantly greater (p less than 0.05 1st and p less than 0.01 2nd year) in the patients receiving a kidney removed from donors with hypertensive families than in patients receiving a kidney removed from donors with normotensive families. This difference was not present when the recipients coming from hypertensive parents were considered. AHT score after transplantation is also correlated with AHT score on dialysis (p less than 0.01 1st and 2nd year), body weight (p less than 0.02 1st and p less than 0.01 2nd year), cumulative rejections (p less than 0.025 1st and 2nd year) and inverse MBP after dialysis (p less than 0.025 2nd year).
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PMID:Hypertension in man with a kidney transplant: role of familial versus other factors. 389 86

Cytosolic free Ca2+ concentrations were measured in platelets from hypertensive and normotensive humans and rats with the use of the fluorescent indicator Quin-2/AM. Without external Ca2+ added, no difference was observed between platelets of hypertensive patients and those normotensive subjects or between platelets of spontaneously hypertensive rats and those of the normotensive Wistar Kyoto and regular Wistar rats. In the presence of 0.5-1 mM external Ca2+, the cytosolic free Ca2+ concentrations were higher both in patients with essential hypertension and rats with genetic hypertension than in their respective normotensive controls. These results suggest that primary hypertension is accompanied by a disequilibrium between cellular Ca2+ influx, storage and extrusion. Such a characteristic if present in other excitable cells and in particular in vascular smooth muscle cells may play a major role in the rise of peripheral resistances.
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PMID:[Elevation of intraplatelet free Ca2+ in primary hypertension in man and the rat]. 393 48

An immunogenetic study of 71 patients with essential hypertension associated with no signs of heart or renal failure, and 276 normal Russian male residents of Moscow demonstrated a significantly increased frequency of antigens HLA-B13 (p less than 0.01) and HLA-B22 (p less than 0.05), as well as HLA-A11 (p less than 0.05), in the hypertensive sample. Aggravated heredity (familial hypertension) was established in 64% of hypertensive carriers of antigens HLA-B13 and HLA-B22.
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PMID:[Distribution of HLA antigens in patients with hypertension]. 406 58

In this review, postulated passive and active fluxes of sodium, potassium, and calcium across the sarcolemma of the normal vascular smooth muscle cell are first summarized. Some practical problems encountered in their measurement are also mentioned. The review then considers how these fluxes appear to be altered in various forms of hypertension in animals and humans. Emphasis is given to abnormal fluxes of sodium and potassium due to altered sodium pump activity and permeability. Increasing evidence indicates that sodium retention due to increased sodium intake or decreased sodium excretion causes hypertension by releasing a humoral pressor substance from brain. This substance, which may be the putative natriuretic hormone, inhibits Na+, K+-ATPase and sodium pump activities in blood vessels and heart, thereby increasing contractile activity. In the genetic models of hypertension, the primary defect appears to be increased permeability of the vascular smooth muscle cell wall to sodium; pump activity increases to compensate for the increased inward leak of sodium. This may also be the case in patients with heritable essential hypertension. The possible consequences of super-imposing the sodium pump inhibitor on the primary defect are also considered. This may occur when animals with genetic hypertension or patients with heritable essential hypertension retain sodium subsequent to increased sodium intake and/or decreased ability to excrete sodium. Such superimposition should raise intracellular sodium concentration to high levels since now the pump would not fully compensate for the increased inward leak of sodium.
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PMID:Abnormalities of membrane transport in hypertension. 636 Aug 83

Studies with school aged children of several communities of the United States have indicated that between one and two percent of them should be considered hypertensive. These findings contradict previous statements of a very rare incidence of hypertension in childhood. Some studies show that children of Black and Hispanic American ancestry, especially females, have a higher incidence of hypertension. The highest incidence of hypertensive children was related to a history of familial hypertension and obesity. In children less than three years of age and in infants, hypertension is less frequent. A disease of the urinary apparatus (nephropathy) or of the cardiovascular system (aorta coarctation) can often be identified as the primary cause of the hypertension. Less frequent is hypertension sustained by adrenal cortical dysfunction or a neoplasm of the adrenal medulla. Hypertensive crisis also frequently develops in children after thermal injury or renal transplant. In children, the use of antihypertensive drugs should be reserved for cases where the disease is very severe. Effective regulation of dietary and hygienic habits should be recommended, particularly for those cases of "mild" or "borderline" essential hypertension.
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PMID:Considerations of the renin-angiotensin aldosterone system in the pathogenesis of hypertension in infancy. 675 76


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