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

In order to investigate a role of sympathetic nervous system in the mechanism of blood-pressure elevation in essential hypertension, urinary catecholamines, serum dopamine-beta-hydroxylase (DBH) activity and a pressor response to infused noradrenaline (noradrenaline response) were measured, in the patients with essential hypertension, before and 2 weeks-rest after hospitalization or following salt restriction. In addition, plasma renin activity (PRA) and water-sodium contents were determined and a correlation between these variables and noradrenaline excretion, serum DBH or noradrenaline response was observed. A blood pressure fall after hospitalization was associated with a decrease of urinary noradrenaline and serum DBH, and there was a significantly positive correlation between the changes in blood pressure and those in urinary noradrenaline or in serum DBH. A significantly adverse correlation was found between plasma volume and the amounts of urinary noradrenaline excretion. The changes in noradrenaline response was negatively correlated with those in urinary noradrenaline excretion. In addition, noradrenaline response was correlated positively with plasma volume, extracellular fluid volume and total exchangeable sodium and negatively with PRA. Following salt restriction, a fall of the blood pressure was associated with an elevation of urinary noradrenaline excretion. The patients with more marked blood pressure fall showed a higher increase of urinary noradrenaline, and a significant correlation was found between the changes in these two variables. Noradrenaline response was significantly reduced, although it was not correlated significantly with noradrenaline excretion. In these experiments, adrenaline, unlike noradrenaline, did not show any obvious changes. These findings suggested that an excessive sympathetic nerve activity caused an elevation of blood pressure in the labile type of essential hypertension. It was demonstrated that a sympathetic nervous function was dependent on sodium intake and that there exisited a close relationship between noradrenaline response and water-sodium contents or PRA.
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PMID:Studies on the role of sympathetic nervous system in the mechanism of essential hypertension. 87 Jul 20

Body fluid volumes, cardiac output, PRA and pressor responses to angiotensin II (AT) and norepinephrine (NE) were compared between untreated patients with essential hypertension aged younger than 35 (EH-I) and those aged older than 36 years (EH-II). Men blood volume, total body water and extracellular volume were not significantly different between the patients with essential hypertension and normotensive subjects. There were no difinite differences in each volume between the EH-I and EH-II patients either. However, the distribution of blood volume was significantly larger in the essential hypertensive patients than in the normotensive subjects, suggesting that the changes in blood volume might not be homogenous in essential hypertension. In addition, blood volume was noted to have a significant inverse correlation with PRA. Cardiac output at rest was slightly but not significantly less in the EH-I and EH-II groups than in the normotensive group. A decline in blood pressure following 'bed-rest' was accompanied by a decrease in total peripheral resistance index (TPRI). Thus, elevated peripheral vascular resistance seems to be responsible for the mild to moderate hypertension even in the younger patients. PRA and its increases in response to standing or furosemide were normal in the EH-I patients, while they were markedly suppressed in the EH-II patients as compared to the age-matched normotensive subjects. In addition, PRA had a significant inverse correlation with the blood pressure and the scores of the severity of hypertension in the patients with essential hypertension. Thus, it seems likely that low renin in essential hypertension is secondary to long-lasting hypertension. Pressor response to AT significantly correlated with mean blood pressure and that to NE did so with 24 hours' urinary sodium excretion in essential hypertensive patients. The influence of aging on the pressor responses were obscure: the relationships of the pressore responses to blood pressure or to urinary sodium excretion were not different between the EH-I and EH-II groups. The examinations were repeated in 16 patients with essential hypertension (16 to 48 year-old) in 11 to 30 days after the initial study. Twelve of the 16 patients had declines in blood pressure and TPRI at the second study. In 7 of the patients whose blood pressure declined following 'bed-rest', there were significant decreases in pressor response to AT and in blood volume and a significant increase in PRA (group A). The other 5 patients showed a significant decrease in PRA and an enhanced pressor response to NE (group B). The blood volume in the group A was significantly larger than that in the group B at the initial study. It is suggested that the cause of essential hypertension is not homogeneous in that the increased vascular resistance may have been attributed to sodium excess in some patients and to an increased sympathetic activity in others. Some additional factors remain to be taken into account to clarify the complicated aspects of essential hypertension.
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PMID:Comparisons of body fluid volumes, plasma renin activity, hemodynamics and pressor responsiveness between juvenile and aged patients with essential hypertension. 87 Jul 21

Inexpensive and rapid radioimmunoassay techniques for the measurement of aldosterone in unprocessed plasma and simple plasma extracts are described. The use of low pH (pH 5.0) and merthiolate to minimise plasma protein binding and the use of aldosterone-free plasma in the standards allows the measurement of aldosterone in 50 microliter of unprocessed plasma, which has been found useful in the diagnostic screening and classification of hyperaldosteronism. Despite quantitative recovery of added (+)-aldosterone and high specificity, the aldosterone content of unprocessed plasma is overestimated, probably by the presence of a water-soluble compound which closely resembles aldosterone. The use of a simple preliminary dichloromethane extraction procedure gives an excellent correlation with values obtained after chromatography. Values are given for chosen normal people and people with benign essential hypertension, using both assay procedures in three different physiological contexts.
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PMID:Development of radioimmunoassays for the measurement of aldosterone in unprocessed plasma and simple plasma extracts. 91 14

Muscle content of water and electrolytes (needle biopsy), intraarterial BP and cardiac output (dye dilution technique) were measured in 12 patients with essential hypertension before and after 4 months of mefruside therapy (25 mg/day). Before therapy there were no significant differences in muscle tissue electrolyte and water content compared with normotensive subjects. No correlation was found between central hemodynamic variables and the electrolyte and water content of muscle tissue either before or after therapy. After 4 months of mefruside therapy, muscle tissue water showed a mean decrease which was not significant. Serum potassium and muscle potassium content decreased significantly but there was no significant change in intracellular potassium concentration. Intracellular sodium concentration increased significantly, while muscle sodium content showed a mean increase which was not statistically significant. The change in intracellular sodium concentration showed a significant negative correlation with the decrease in mean arterial BP. The change in total cellular water content showed a significant negative correlation to the changes in total peripheral vascular resistance. Saluretic therapy seems to induce counterregulatory mechanisms that interfere with the hypotensive effect.
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PMID:Effect of saluretic therapy on muscle content of water and electrolytes in relation to hemodynamic variables. 92 Feb 62

Urinary kallikrein was measured in normal pregnant women stages of gestation and in women who developed hypertension in late pregnancy. Mean urinary kallikrein was highest in the first trimester and fell significantly in the third trimester to nonpregnosterone system. A negative correlation was observed between urinary kallikrein and the length of gestation in normal pregnancy. Urinary kallikrein fell significantly below nonpregnant levels in patients with hypertension while the renal excretion of sodium and water was not different from that in normal pregnancy of the same dy is discussed in the light of factors known to increase kallikrein excretion. It is considered unlikely that this elevation is due to the escape from the sodium-retaining effect of the high aldosterone of pregnancy. It may be due in part to the stimulating effect of raised angiotensin II levels but it is considered most likely to be the effect of a circulating renal vasodilator. The reduced kallikrein in hypertension of pregnancy may play a part in the development of the hypertension and resembles the reduced kallikrein excretion in essential hypertension.
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PMID:Urinary kallikrein in normal and hypertensive pregnancies. 100 45

The renal prostaglandins PGS2 and PGE2 possess potent antihypertensive and vasodepressor activity. The mechanism of blood pressure lowering effect is through peripheral arteriolar dilation with a fall in total peripheral resistance. PGA unlike PGE escape degradation by the lung and thus could circulate as antihypertensive hormones. Since plasma PGA levels rise in humans on a low sodium intake, it has been postulated that the beneficial effects of a low sodium diet in some hypertensives may be the result of an increase in peripheral vasodilating PGA. Support that plasma PGA may be a regulator of systemic blood pressure is also derived from the fact a PGA-secreting renal tumor was associated with a fall in blood pressure and a rise in plasma PGA in a previously hypertensive woman. The removal of the tumor resulted in a return of blood pressure to elevated levels and a concomitant fall in PGA. Recently, a number of human patients with essential hypertension have been infused with PGA1 and PGA2. It was observed that there was an initial increase in renal blood flow, sodium and water excretion which was associated with no change in the elevated blood pressure. When blood pressure ultimately fell, there was a return of renal blood flow, sodium and water excretion to preinfusion levels. It would appear that PGA compounds act as 'ideal' antihypertensive agents since they favorably effect renal resistance, sodium and water homeostasis, plasma volume, total peripheral resistance, blood pressure and indirectly cardiac output through baroreceptor stimulation, all factors known to be important in etiology in human hypertension.
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PMID:Renal prostaglandins. 110 Oct 92

It is apparent that the split function study and renal vein renin determination are complementary and afford valuable information for selecting patients with potentially curable renovascular hypertension. The split function study, when interpreted with the recently defined split function ratio, offers the clinician a highly accurate means of diagnosing significant renal ischemia. Because the split function ratio shows the disparity between the ischemic and contralateral kidney to a greater degree, the chance of misdiagnosis due to laboratory or physician error is minimized. The split function study, however, is of limited value in patients with pyelonephritis since the water- and salt-losing characteristics of the pyelonephritic kidney may mask significant renal ischemia. In these patients, as well as those with a nonfunctioning kidney or hydronephrosis, the renal vein renin determination is the test of choice. In addition, the added morbidity of the split function study is not warranted in a patient with an elevated peripheral renin which, for interpretation, requires an accurate 24 hour urine for sodium, a renal vein renin ratio outside the range of patients with essential hypertension (renal vein renin ratio greater than 1.7) and evidence of suppression of renin secretion from the contralateral kidney. If, however, the renin determination does not afford convincing evidence of significant renal ischemia in a patient with radiographic evidence of renal arterial stenosis, a split function ratio definitely should be determined to more completely define the pathology. The attendant morbidity of a carefully performed split renal function study does not approach the morbidity and mortality associated with unnecessary surgery or inadequately treated hypertension.
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PMID:Ureteral catheterization studies. 115 55

1. Many forms of human and experimental hypertension begin with compromised renal function. Essential hypertension may be another such case. 2. The kidneys of subjects with essential hypertension excrete normal amounts of salt and water at higher-than-normal renal perfusing pressures. Other overt signs of renal dysfunction are few; renal disease is excluded by definition. However, renal blood flow and glomerular filtration rate are usually less than normal in essential hypertension. 3. Renal afferent resistance can be calculated from arterial pressure, renal blood flow, and an estimate of glomerular capillary pressure. These calculations indicate that afferent resistance is increased to two or more times normal in essential hypertension. 4. It is not clear whether afferent constriction causes hypertension or results from it. The ability of high pressure to produce vascular damage points to the latter. But, most essential hypertensives show low-to-normal plasma renin levels and a marked afferent dilation after saline loading. These observations do not suggest nephrosclerosis: they are consistent with a causal role for afferent constriction. 5. We can speculate that, in essential hypertension, there is a defect in one of the mechanisms that sets afferent resistance. Afferent constriction could result from extrinsic influences (neural or humoral) or something totally within the kidney, such as abnormal handling of information from the macula densa. 6. The effect of afferent constriction on salt-and-water excretion would theoretically be offset by elevated arterial pressure so that the actual salt-and-water excretion would be normal, but only so long as the arterial pressure remained elevated.
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PMID:The role of the kidney in essential hypertension. 123 7

In groups of healthy volunteers (C), patients with essential hypertension (EH), and patients with renal arterial stenosis (S), the following indicators were followed during 12-hour daytime (d) and nighttime (n) intervals: mean BP, endogenous creatinine clearance Ccr (GF), excretion of sodium (UNaV) and potassium (UKV), and their excretion fractions (CNa/GF and CK/GF). The d/n ratios of both UNaV and CNa/GF were significantly lowered in both groups of hypertensive persons as against the controls (1.5): in the EH, to 1.1, and in the S, to 0.8 on the average. Positively correlated with the value of the d/n ratio of the sodium excretion are the changes in the d/n ratios of water and solute excretions. The daytime potassium excretion exceeded the nighttime values in both groups of hypertensive persons. The d/n ratios of UKV and CK/GF were, however, significantly lowered as compared to the control values. These signs of disturbances of the circadian excretion of Na and K in EH and S exhibited no correlations with the values, or rhythms, of the mean BP, GF, or dietary uptake of sodium. The results do not indicate that the antihypertensive drugs used (alpha-methyldopa, dihydralazine, reserpine) would influence the circadian rhythm of Na excretion. The factors responsible for the disturbances of the circadian rhythms of Na and K excretion in hypertensive subjects have not yet been revealed.
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PMID:Changes in circadian sodium excretion in patients with essential hypertension and with renal artery stenosis. 126 Dec 73

The lithium test was conducted to evaluate transport of water, sodium and osmotic active substances in 46 chronic glomerulonephritis (CG) patients. Sixteen CG patients entered group 1. All of them had secondary hypertension (SH). Twelve CG patients with SH symptoms of moderate reduction of endogenic creatinine clearance were assigned to group 2. Twelve patients of group 3 had CG and isolated urinary syndrome. Group 4 consisted of 6 patients with essential hypertension. As shown by the test, association of SH and CG is not an essential factor for renal transport of sodium, water and electrolytes. Some shifts in the transport in group 2 are attributed to reduced number of functioning nephrons. The tendency to enhanced lithium clearance was registered in group 4. This may reflect an increased supply of sodium, water and osmotic active substances to the uriniferous tubules.
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PMID:[The transport of sodium, water and active osmotic substances in different parts of the nephron of patients with chronic glomerulonephritis and hypertension]. 129 28


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