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

The use of plasma renin assays in clinical practice is reviewed and experience with an assay for plasma renin activity (PRA) is reported. In normal subjects, 10am ambulant PRA was significantly related to plasma angiotensin II levels but not related to daily urine sodium exretion in these subjects consuming normal diets. PRA was suppressed in patients with mineralocorticoid hypertension and in a small proportion of patients with essential hypertension. Very high values were observed in patients with untreated primary adrenal insufficiency, treatment of which resulted in a prompt fall of PRA to normal. PRA was usually normal in adrenalectomised patients and those with chronic adrenal insufficiency receiving satisfactory steroid replacement therapy. It is concluded that provided standardised conditions are used for the collection and assay, PRA is helpful in the assessment of hypokalaemic hypertension as well as in the early detection and management of patients with primary adrenal insufficiency or related conditions of salt wasting.
 ...
PMID:Clinical use of plasma renin assays. 27 2

Studies on the Kyoto (SHR) and the New Zealand (GHR) strains of genetically predisposed hypertensive rats have shown that in the SHR neurogenic influences, primarily of higher central origin, play an important role in the initiation of hypertension. Studies on human essential hypertension indicate that this may also be true for man, although it is far from being the sole explanation. Brookhaven hypertension-prone rats illustrate the interaction between genetic and exogenous factors since they require an overload of salt for the development of high blood pressure. The Milan hypertensive rats (MHS), on the other hand, illustrate a genetic deviation of renal function with imbalance between glomerular filtration and tubular resorption of sodium and water, which may simulate at least some variants of the relatively mild forms of low renin hypertension in man. Structural adaptive vascular changes have been demonstrated in SHR and GHR and in nongenetic renal hypertension in rats, and there are several indications of their presence in MHS. Thus, regardless of the nature of the initiating factors, these secondary but rapidly established changes occur and greatly contribute to the maintenance and acceleration of the hypertensive state. The vascular changes can even be regarded as a common denominator for chronic hypertension and serve as an element which, in fact, reinforces the initiating mechanisms. The progress of the vascular changes can be interfered with by reducing the pressure load. Lowering the blood pressure by pharmacologic treatment is most effective when the treatment is initiated as such an early age when the cardiovascular structural adaptation is still minimal. Treatment in later phases is less successful since the adaptive increases in cardiac and vessel wall thickness can then no longer be fully normalized by pressure reduction because of increased amounts of collagen and other connective tissue elements in the vessel wall, which regress poorly. An increased wall thickness of the resistance vessels implies a vascular hyperreactivity to constricting influences which, in turn, rapidly brings the blood pressure back to supranormal levels as soon as therapy is stopped.
 ...
PMID:Mechanisms of spontaneous hypertension in rats. 32

Saralasin, a specific competitive inhibitor of angiotensin II, was administered in a controlled, prospective study designed to test the hypothesis that this agent is a useful tool for the detection of renovascular hypertension. 13 patients, 11 with renovascular hypertension and 2 with high-renin essential hypertension, showed a gross, readily apparent decrease in blood pressure after receiving saralasin. 8 patients with essential hypertension and normal or low renin levels exhibited no depressor response to the drug. In the patients with renovascular hypertension, blood pressure response during angiotensin blockade compared favourably with renal vein renin determinations as a predictor of operative results. Because saralasin testing has resulted in few if any falsely positive or negative results when considered as a diagnostic procedure for renin-mediated hypertension, and because it is safe, it may become an ideal initial screening procedure. The saralasin test (either bolus injection or sustained infusion) is completely valid only if the patient is mildly salt-depleted, is not taking other antihypertensive medication, and is genuinely hypertensive at the time of the test.
 ...
PMID:Angiotensin blockade in renovascular hypertension: a controlled, prospective study. 33 16

Approximately 1% of pregnancies are complicated by essential hypertension. During pregnancy the blood pressure often stabilizes or improves. In patients with sustained hypertension, prospective controlled studies have demonstrated enhanced fetal survival when the blood pressure was controlled with antihypertensive medication. Such medication must be chosen carefully to avoid fetal and mateerial toxicity, and diuretics and salt restriction during pregnancy should be avoided. Among patients with essential hypertension the problem accelerates late in pregnancy in 2% to 11%; the acceleration may be predicted by determination of maternal mean arterial pressures and intravascular volumes early in pregnancy. The treatment of accelerated hypertension is identical to that of severe pre-eclampsia. Fetal loss is considerable but can be lessened by careful fetal and maternal monitoring and early controlled delivery. The risks of pregnancy in most patients with essential hypertension are small, and essential hypertension is not a uniform contraindication to pregnancy.
 ...
PMID:Essential hypertension and pregnancy. 34 89

Evidence is presented demonstrating the role of prostaglandins in salt metabolism and on peripheral vasodilation. A number of animal studies and observations in human hypertensive subjects suggest that the prostaglandin system plays a role in the pathogenesis of hypertension. The most striking and consistent finding over many decades of investigation is the relationship between dietary salt intake and the development of hypertension. Only a small percentage of any population develops hypertension. It is suggested that those people whose kidneys have an abnormal salt-handling capacity develop hypertension when challenged by a chronic high-salt intake. The salutary effects of diuretics or low-salt diet support this concept. Hypertension then is an expression of a renal abnormality. Prostaglandins, one of the renal salt regulating factors of the kidney, amy be involved in this abnormality. Whether there is a defect in the matabolic pathways or an unresponsiveness to normal stimuli of prostaglandins has not been determined. The use of prostaglandins in the treatment of hypertension is being explored. The demonstration that PGA1 can effectively lower blood pressure and reverse hypertensive emergencies indicates that prostaglandins probably have a broader, still unidentified role in the overall management of essential hypertension.
 ...
PMID:Prostaglandins and hypertension. 35 95

The subject of sodium toxicity has been controversial for a long time. There is no question that the element can be noxious when consumed acutely in large quantities and there is little doubt as to cause and effect Conversely the consequences of mederate chronic sodium consumption are much harder to document. The effects are insidious and are subject to modification by a variety of environmental influences such as dietary potassium. In addition most studies of chronic sodium excess have dealt with elusive subject of "essential" hypertension. Interpretations of data have been very difficult, and conflicting reports have occurred. Nevertheless epidemiological, clinical, and animal studies show that chronic excess sodium ingestion acting upon a substrate of genetic susceptibility, is an important etiologic factor in essential hypertension and the expression of its sequelae. Positive correlations have also have been obtained between dietary salt and the incidence of stroke and gastric cancer. Dietary potassium appears to confer some degree of protection from the toxic properties of sodium through some unknown mechanism. Available evidence indicates that a suitable intake of salt for man might be approximately 3.5 g/day and probably less. Salt consumption in most developed countries ranges between 8 to 40 g/day, and modern methods of food processing and preparation deplete the protective potassium. The incidences of hypertension in these countries range between 15 to 40% of their populations, and it exacts a dreadful toll. Recognition of the toxic properties of sodium and knowledge of the mechanisms involved in its toxicity offer great possibilities in the area of preventive medicine It may be possible by the sorting out of hypertension-prone subjects and dietary intervention to prevent or minimize the development of hypertension in susceptible individuals. This says nothing of other aspects of sodium toxicity, of which we are largely ignorant.
 ...
PMID:The toxicity of salt. 35 85

The safety and efficacy of tienilic acid have been evaluated in studies of patients with mild to moderate essential hypertension, salt and water retention states and hyperuricaemia associated with gout. During the course of these studies 675 patients were treated with tienilic acid, 310 were treated with hydrochlorothiazide, 43 were treated with probenecid and 34 were treated with placebo. Overall, adverse reactions characterized as probably drug-related or questinably drug-related were reported in 28% of patients treated with tienilic acid, 24% treated with hydrochlorothiazide, 25% of patients treated with probenecid and 33% treated with placebo. The side effects encountered were mild in severity, reversible and represented extensions of the pharmacological activity of tienilic acid, hydrochlorothiazide and probenecid. These initial studies demonstrate that tienilic acid is safe and effective in the treatment of mild to moderate essential hypertension, salt and water retention states, including oedema associated with congestive cardiac failure or mild to moderate renal dysfunction, and in the management of elevated serum uric acid levels associated with gout.
 ...
PMID:Safety of tienilic acid. 38 98

Kallikrein excreted with the urine appears to be formed in the kidney. The kallikrein-kinin system in the kidney is localized in the distal nephron from the juxtaglomerular apparatus to the collecting duct. It has been shown that intrarenal infusion of kinins produces an increase in renal blood flow as well as diuresis and natriuresis. Part of the effect of kinins appears to be mediated by the release of prostaglandins. However, the precise role of the renal kallikrein-kinin system in sodium and volume homeostasis and in blood pressure regulation still remains to be determined. Mineralocorticoids as well as the diuretics furosemide, bumetanide and bendroflumethiazide increase, spironolactone decreases kallikrein excretion. Urinary kallikrein has been shown to increase acid-as well as cryoactivation of prorenin in vitro. It is unclear as yet, however, whether the renal kallikrein-kinin system takes part in converting inactive prorenin into active renin in vivo. There are reports on subnormal, normal as well as increased kallikrein excretion in spontaneously hypertensive rats. In rats susceptible to the hypertensive effect of salt a substantially decreased excretion of kallikrein has been observed. Kallikrein excretion has been described to be increased in primary aldosteronism and to be reduced in a proportion of patients with established essential hypertension. In patients with labile hypertension, however, kallikrein excretion appears to be normal suggesting that decreased urinary kallikrein in essential hypertension is a consequence rather than a cause of hypertension. The renal kallikrein-kinin system does not appear to play a primary role in the pathogenesis of hypertension.
 ...
PMID:[Renal kallikrein-kinin system and control of blood pressure (author's transl)]. 39 77

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.
 ...
PMID:Salivary kallikrein excretion in hypertension. 39 78

Observations relating to hypertension in humans and rat experiments have been reviewed from several viewpoints including clinical medicine, pathophysiology, epidemiology, and genetics. It seems likely that much of essential hypertension results from excessive salt intake by individuals with an inherited inability to excrete sodium efficiently which is compensated by blood pressure elevation. A few major genes are likely responsible for a few basic mechanisms involving renal membranes and hormones controlling sodium transport. Excess hypertension in blacks, diabetics, the elderly, and oral contraceptive users can be explained by this theory. If hypertension and other genetically predisposed CHD risk factors are to be fully understood, future studies are needed with detailed data on both genetic and environmental factors, and analytic tools that allow an adequate examination of their interactions.
 ...
PMID:Salt, hypertension, and genetic-environmental interactions. 39 27


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>