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)

This study was designed to evaluate the role of aldosterone, glomerular filtration and blood pressure on sodium excretion in renal disease. Sodium clearance (CNa), plasma aldosterone (PA), plasma renin activity (PRA), glomerular filtration rate (GF), paraaminohippurate clearance (CPAH) and blood pressure were measured simultaneously in 19 normal subjects, 38 patients with benign essential hypertension, 3 with renal artery stenosis, 48 with chronic glomerulonephritis, 20 with the nephrotic syndrome, 24 with tubulo-interstitial disease and 21 with a renal homograft. CNa was significantly depressed in patients with the nephrotic syndrome. Mean PA and PRA were increased in renal artery stenosis but within the normal range in other groups. CNa correlated inversely with PA in all groups but one (tubulo-interstitial disease). CNa correlated directly with GF in the nephrotic syndrome and with the mean blood pressure (mBP) in chronic glomerulonephritis and tubulo-interstitial disease. PA correlated directly with PRA and inversely with GF or CPAH in most groups. It is concluded that PA is an important determinant of the basal natriuresis in renal disease with the exception of tubulo-interstitial nephropathies. In the nephrotic syndrome sodium retention is largely determined by the interaction of PA and GF. In chronic nephropathies, but not in benign essential hypertension, the fractional sodium excretion is partly blood pressure-dependent. Impairment of renal function is often accompanied by a rise in PA.
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PMID:Interrelationships between sodium clearance, plasma aldosterone, plasma renin activity, renal hemodynamics and blood pressure in renal disease. 39 72

Estimation of urinary kininogenase activity by radioimmunoassay of generated kinin was studied. Bovine serum low molecular weight kininogen was proved not to cross-react with kallidin antibody and also bradykinin antibody. This kininogen was used as substrate measuring urinary kininogenase activity. Separation of released kinin from the kininogen was not required in the present method. Urinary kallikrein activity was found to be significantly decreased in essential hypertension, in chronic glomerulonephritis and in patients who had received renal transplantation. On the contrary, an increase in urinary kallikrein was found in primary aldosteronism and in Bartter's syndrome. The present method was very useful for measuring kininogenase activity.
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PMID:Estimation of urinary kininogenase activity using bovine serum low molecular weight kininogen. 49 4

Eighteen patients with advanced or malignant hypertension due to essential hypertension, systemic lupus erythematosus or chronic glomerulonephritis were infused intravenously with 1-Sar-8-Ile-Angiotensin II, a competitive antagonist of aniotensin II. The spectrum of responses was broad from a mild elevation to a marked fall in blood pressure. The changes in mean blood pressure caused by this peptide showed a significant correlation with the level of peripheral plasma renin activity immediately before the infusion (r=0.5652, p less than 0.02). This peptide infusion reduced blood pressre in 12 patients (responders), but not in 6 (non-respnders). There were no differences with age, sex and severity of hypertension except for the level of peripheral plasma renin activity between the two groups. Our retrospective study showed that in 12 responders propranolol reduced blood pressure to near the normal level, while in 6 non-responders furosemide induced similar depressor response. It is concluded that the vasodepressor effect of this peptide correlates with the levels of peripheral plasma renin activity and that the responses to this drug can be used as a guide for the selection of effective antihypertensive drugs.
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PMID:Clinical evaluation of angiotensin II antagonist in advanced hypertension. 88 41

Serial, clinical, clinicopathologic and histologic studies performed simultaneously following onset of PS-AGN in children for a period of up to 144 months revealed no evidence of progression to chronic glomerulonephritis. Although acute morphologic changes were more severe in renal tissue obtained from patients with AGN following streptococcal upper respiratory infection than following pyoderma, the acute manifestations in both groups subsided 6 to 12 weeks after onset. Cumulative morphologic healing occurred in 20% of patients at 24 months, in 43% at 48 months after onset of PS-AGN; 1 patient who was unhealed at 49 months was lost to follow-up. In 2 patients (6%), acute histologic exacerbations without clinical signs occurred within 24 months after onset. Subsequent healing was documented histologically. Addis counts remained abnormal in a high percentage of patients throughout the 12 years of observation and did not correlate with the histologic findings of renal biopsy tissue. The occasional demonstration of renal vascular disease and/or hypertension may merely reflect the early development of spontaneous essential hypertension although the possibility of a relationship to the previous attack of PS-AGN is intriguing. This question cannot be answered at this time. Renal biopsy studies are more dependable than Addis counts in assessing the course of PS-AGN. The significance of persistence of immunofluorescent and/or electron microscopic changes (subepithelial dense deposits) many years after onset in 58% of 12 patients studied, at a time when a majority of patients (84%) revealed healing by light microscopy, remains to be assessed.
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PMID:Prognosis of acute poststreptococcal glomerulonephritis in childhood: prospective study and review of the literature. 100 3

Basic haemodynamic parameters were measured in 58 men in various stages of essential hypertension, 18 patients with hypertensive form of chronic glomerulonephritis, and 23 practically healthy persons during graded exercise in the supine position on a bicycle ergometer for 30 minutes. During exercise, the systolic pressure rose in all persons investigated, whereas the diastolic pressure markedly increased only in patients with arterial hypertension. The cardiac index increased, according to the intensity of the exercise equally in the healthy persons and in patients in early stages of essential hypertension; a lesser increase in the cardiac index was observed in patients in late stages of hypertension and in those with chronic glomerulonephritis. The increase in the cardiac index during exercise is essentially due to an increase in the heart rate; the stroke index increases only slightly, and in later stages of essential hypertension even decreases. The total peripheral resistance diminishes during exercise, but less so in patients with arterial hypertension in whom it is distinctly higher than in healthy persons. The circulating blood volume decreases during exercise in consequence of a decrease in plasma volume, whereas the haematocrit value increases. Renal blood flow and glomerular filtration decrease during exercise, both in healthy untrained persons and in patients with arterial hypertension. In patients in late stages of essential hypertension and in those with glomerulonephritis, the above parameters decrease more markedly and at lower exercise intensity than in healthy persons.
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PMID:Changes in general haemodynamics and renal function during exercise in patients with arterial hypertension. 114 56

Plasma aldosterone, plasma renin activity, sodium and potassium in the plasma and the urine were determinated under acute stimulation with saline-depletion (furosemide) and under acute suppression with saline infusion in 40 patients with primary hypertension stage I, 19 patients with primary hypertension stages II and III, and 11 patients with renal hypertension (chronic glomerulonephritis and chronic pyelonephritis). The majority of the patients with primary hypertension stage I showed a good stimulation of the plasma aldosterone and the plasma renin activity under acute salt depletion. Three out of the 40 patients with primary hypertension stage I, and 13 of the 19 patients with primary hypertension stages II and III did not show any stimulation of the renin secretion ("low renin hypertension"). In all these patients the plasma aldosterone stimulation remained intact. With infusion of saline all the groups showed suppression of the plasma aldosterone and the plasma renin activity. A good stimulation of the plasma renin activity, demonstrates that in our experiments the renin-angiotensin system cannot be responsible for the increase in aldosterone secretion under salt depletion. Most likely the increase of the plasma aldosterone, in spite of the fixed renin activity, is stimulated by the sodium depletion due to diuretics. In all patients with primary hypertension we did not find an inadequate reaction of the aldosterone secretion under saline infusion. The patients with renal hypertension showed a minimal stimulation and suppression of the plasma renin activity. The plasma aldosterone secretion increased only slightly under sodium depletion and the decrease under saline infusion was statistically not significant. Thus we conclude that these patients show an inadequate reaction of the plasma aldosterone and renin secretion under salt infusion and depletion.
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PMID:[Plasma aldosterone and plasma renin activity in patients with essential and renal hypertension under acute stimulation with saline depletion and acute suppression with saline infusion]. 115 49

The difference of the prognosis between essential and renal hypertension (chronic glomerulonephritis) was examined by compairing the survival rate of the patients, and the effect of lability of blood pressure and the effect of the response to hypotensive drugs on the prognosis of the two types of hypertension was observed. The prognosis of renal hypertensives was remarkedly worse when it was compaired with the prognosis of essential hypertensives. More then 80% of the latter was still alive after ten years, while the mortality rate of the former after 5 years was only 20%. Each factor of severity (diastolic pressure, optic fundi, cardiac, cerebrovascular and renal complication) in non severe patients (group O-II) did not differently affect the survival rate of both hypertensives. Diverse prognosis was observed in severe patients (group III-IV), depending on each factor of severity. In renal hypertension the survival rate was extremely low when the patients had high diastolic pressure, severe cardiac and cerebrovascular complication. It was not so low in the patients with severe ophthalmoscopic change. The prognosis of essential hypertension was poor in the order of severe cerebrovascular complication, renal complication and cardiac complication. The survival rate of the patients with high diastolic pressure or severe ophthalmoscopic change was considerably high. The patients with both renal and essential hypertension showed greater survival rate when the blood pressure was much more reduced by bed rest or antihypertensive drugs during the first hospitalization.
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PMID:Comparison of the prognosis of hypertension associated with chronic glomerulonephritis with that of essential hypertension. 115 38

Results are presented on the treatment with Inderal of 57 patients with essential hypertension and symptomatic renal hypertension in whom the changes in central and renal haemodynamics were carefully traced. In all the patients with renal hypertension (chronic pyelonephritis, chronic glomerulonephritis) the function of the kidneys was adequate. Inderal when used in a daily dose of 120--160 mg produces a hypotensive effect in patients with stage IB and IIA essential hypertension with unstable symptomatic renal hypertension who have a predominantly hyperkinetic type of the circulation. In such cases the haemodynamic changes manifest themselves in a considerable reduction of the cardiac output at the expense of a slower pulse rate and decreased stroke volume; the total peripheral resistance was moderately elevated. In patients with stage IIB of essential hypertension and in those with persistent and severe symptomatic renal hypertension the hypotensive effect of Inderal given in a daily dose of 480 mg and sometimes even higher was accompanied by a statistically significant decrease in the total peripheral resistance and a moderate reduction of the cardiac output and cardiac index at the expense of a slower pulse rate.
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PMID:[Use of inderal for the treatment of different forms of arterial hypertension]. 119 58

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

The major target organs that become damaged as a consequence of long-standing arterial hypertension are the kidneys, heart, and brain. Left ventricular hypertrophy (LVH) cannot be considered only as an adaptive process to elevated blood pressure (BP), and the heart is also a major target organ in malignant arterial hypertension (MH). Magnetic resonance (MR) was used as a method for visualization of the heart in 68 patients with MH including 18 with essential hypertension, 16 with chronic glomerulonephritis, 13 with chronic pyelonephritis, 16 with renovascular hypertension, eight with adrenal tumors, and in 20 healthy volunteers (as a comparison group). Electrocardiogram-gated, double spin-echo magnetic resonance imaging was performed to image the right and left ventricles (RV and LV), interventricular septum, apex and LV posterior wall, left atrium, and aortic root. In all the patients, symmetric LV hypertrophy was registered and in the most severe cases LV wall thickness was more than 20 mm. There was no LV cavity enlargement or local contractility abnormalities. There was close correlation of LVH and diastolic BP. The degree of LVH and diastolic dimensions of the LV differed between etiologies of MH. These findings show that different pathophysiologic mechanisms of development of MH influence the processes of myocardial hypertrophy. The highly informative yield of MR tomography for evaluating structural and functional changes of the heart under MH must be underlined.
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PMID:Magnetic resonance imaging of cardiac hypertrophy in malignant arterial hypertension. 138 64


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