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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To define the role of the renin-angiotensin system in post-transplantation hypertension we studied 12 hypertensive recipients of renal transplants. The patients received saralasin acetate, an angiotensin II antagonist, while on a normal sodium diet and again after seven days of sodium restriction. In six patients with only one kidney, saralasin did not lower blood pressure on either diet; salt depletion did not lower systolic or diastolic blood pressures. In six patients with more than one kidney, salt depletion also did not lower blood pressure; however, salt depletion plus saralasin lowered their systolic pressures from a mean (+/- S.E.M.) of 146 +/- 9 to 128 +/- 8 mm Hg, and mean diastolic pressures fell from 103 +/- 5 to 89 +/- 5 (P less than 0.001). In four of five patients renal-vein renin activity was greater in one or more host kidneys than in the transplant kidney (or kidneys). Although pre-transplant blood pressure was the same in both groups, post-transplantation hypertension is more likely to be angiotensin II-dependent in patients with more than one kidney.
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PMID:Role of the renin-angiotensin system in post-transplantation hypertension in patients with multiple kidneys. 34 89

The seeds of premature coronary heart disease are often sown in childhood and it is the developing arteries of children which are the most susceptible. Paediatricians and all who work with them have the earliest and most promising opportunities for prevention. Coronary protection can be added to the potential advantages of breast feeding and to ensure appropriate fatty acid balance throughout weaning. It is reasonable to accept the strong consensus of opinion on diet reflected in the reports of the eighteen national committees. They are: to reduce total fat intake to 30-35% of the energy, to restrict consumption of saturated fat, cholesterol, sugar, and salt, to increase unrefined carbohydrate and polyunsaturated fat, and to maintain a P/S balance of 1.0-1.5:1. Food is the fundamental coronary risk factor, but others may add insult to injury. Smoking, hypertension, obesity, lack of exercise, and stress, each of which is related to behaviour, may start in childhood. Smoking doubles the overall risk CHD and increases it ten times in males under 45 years old. Good habits, including food preferences and eating patterns learned early, are those most likely to be continued. School meals require and should match revised nutritional education. The co-operation of the food industry is essential and can be anticipated, but it requires a clear lead by paediatricians. The nutritional advice should come from the medical profession. Every contact with children and their parents provides an opportunity for enquiry and giving advice.
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PMID:Perspectives in coronary prevention. 34 32

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.
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PMID:Prostaglandins and hypertension. 35 95

Sodium appetite reflects the importance of sodium homeostasis and the relative scarcity of sodium for many terrestrial animals. Man, for various reasons, also seems to have a specific preference for salt which he consumes in excess of need, and this has been characterized as an important contributor to hypertension. Gustatory sensibility is necessary for the development of sodium appetite. Thus, research on the possible role salt taste sensitivity plays in controlling NaCl consumption in the sodium deficient rat was reviewed as a potential model for the study of salt taste and hypertension in man. Taste acuity experiments began first by examining salt taste thresholds. These studies found that thresholds were not altered by sodium deficiency in rat and the results in hypertensive humans were inconclusive. Threshold determinations may not reveal true sensitivity differences because they varied significantly across experiments and because they are restricted to a small portion of the intensity domain. When research was directed to suprathreshold stimuli, concentrations a rat or man might normally experience, the evidence suggested that hypertensive humans, like sodium-deficient rats, were less sensitive to the taste of salt. This reduced sensitivity may account, in part, for the fact that these two groups consume more salt.
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PMID:Salt taste and disease. 35 28

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.
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PMID:The toxicity of salt. 35 85

Twenty-one insulin-dependent diabetics with azotemic nephropathy were evaluated for renal transplantation by selective coronary angiography and cine left ventriculography. All had hypertension, retinopathy, neuropathy, and required salt restriction plus diuretics for volume overload. There was no clinical or electrocardiographic evidence of ischemic coronary artery disease in twenty. Ten patients (five males, five females, mean age 29.3 years; mean duration of diabetes 21.9 years; mean serum cholesterol 239 mg%) had significant coronary artery disease, seven demonstrating focal abnormalities in left ventricular wall motion. Two patients (one male, one female; mean age 36.5 years; mean duration of diabetes 28.5 years; mean serum cholesterol 250 mg%) had no significant coronary artery disease, but demonstrated diffusely abnormal left ventricular wall motion with diminished ejection fraction. Thirty-eight percent had significant coronary artery disease unpredictable by electrocardiographic or clinical data. The finding of no significant coronary artery disease in 52% of a group with severe renal-hypertensive complications of diabetes is surprising. Two patients may have a demonstrated cardiomyopathy.
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PMID:Asymptomatic coronary artery disease: angiographic assessment of diabetics evaluated for renal transplantation. 36 Dec 77

The kallikrein-kinin system in the kidney is localized in the distal nephron, where it appears to be linked to processes that control water and electrolyte excretion. Some evidence exists that the effect of the renal kallikrein-kinin system is partially mediated by the release of prostaglandins. It has not yet been determined whether endogenous kinins affect the function of the nephron directly or indirectly by changes in renal blood flow distribution. Further, a number of studies in animals and humans indicates that kallikrein excretion is decreased in most types of hypertension, with the exception of hypertension caused by an excess of mineralocorticoids (where kallikrein is increased). In rats susceptible to the hypertensive effect of salt, kallikrein is conspicuously decreased. In renal diseases, urinary kallikrein excretion is also decreased. Finally, it still needs to be determined whether or not low kallikrein excretion is a pathogenetic factor in hypertension and renal diseases.
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PMID:The renal kallikrein-kinin system in human and in experimental hypertension. 36 76

In the system of long-term maintenance of the arterial pressure level by means of the renal excretion mechanism described by Guyton et al., the renal medulla with its counterflow-concentrating multiplier and powerful source of natural natriuretics, the prostaglandins, plays the role of a "control device", a regulator setting the level of arterial pressure required for fulfilling the complete volume of renal excretion of salts and water. Increase in systemic arterial pressure causes the development of a complex of structural-functional changes in the kidney, the common purpose of which consists in preventing the loss of salts and water by the organism by shifting parameters of the excretory renal function in such a manner that the normal (balanced with the supply of salts and water to the organism) volume of excretion may occur with higher values (kidney "resetting"). The central role in accomplishing this "resetting" is played by the medullary excretory mechanism which is closely connected, due to the absence of autoregulated blood flow in the medulla, with systemic arterial pressure. When the kidney reaches the "resetting" this mechanism provides for a sufficiently full volume of excretion only when the arterial pressure increases, maintaining its fixed (higher) level by means of the feedback mechanism. In hypertension caused by overdosage of corticosteroid hormones or excess of salt in the diet the increase of pressure develops as a compensation for the occurring deficiency of the medullary excretory mechanism.
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PMID:[Kidney in chronic arterial hypertension: "resetting" and the role of the renal medulla in its development]. 39 Feb 6

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


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