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

The relationship of arginine vasopressin (AVP) in plasma to cyclic adenosine 3' 5'-monophosphate (cAMP), sodium excretion in urine, and arterial blood pressure were determined during intravenous infusion of hypertonic sodium chloride solution (500 ml of 50 g/l) in 10 normotensive control subjects and in 11 normotensive and 10 hypertensive patients with chronic glomerulonephritis and relatively well preserved kidney function. The concentration of AVP in plasma increased 2-4 fold, osmolality in serum increased 12-16 mosmol/kg, and urinary excretion of cAMP increased 20-40% during sodium loading to the same extent in all three groups. Sodium and water excretion were higher during the sodium loading in the hypertensive patients, but not in the normotensive patients when compared to the control subjects. Neither AVP nor changes in AVP correlated significantly with changes in cAMP excretion, sodium excretion or blood pressure. In the control subjects the level of parathyroid hormone in serum was unchanged during the sodium chloride infusion. Water loading without sodium loading in eight of the control subjects caused a decrease in the excretion of cAMP. In conclusion, the increase in cAMP excretion in urine during the sodium loading might be explained by an AVP-induced stimulation of renal cAMP production. The study does not suggest that AVP plays a role in the increased sodium excretion during sodium loading or in the development of hypertension or chronic glomerulonephritis.
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PMID:Arginine vasopressin and cyclic adenosine monophosphate during acute sodium loading in chronic glomerulonephritis. 298 6

A study of the clinical presentation and conceivable causes of chronic renal failure (CRF) in 61 Sudanese patients in Khartoum is presented. The clinical features involved almost all the systems, however, gastrointestinal and cardiovascular signs and symptoms predominated. The causes of chronic renal failure in Sudan and Sweden are also studied for comparison. The causes of CRF in Sudan are chronic glomerulonephritis, obstructive nephropathy (stone disease), hypertension and diabetes mellitus in that order. The main causes of CRF in Sweden are chronic glomerulonephritis, diabetes mellitus and chronic pyelonephritis. Of the 61 Sudanese patients 16 have kidney transplants, only one in Sudan, three patients are on regular hemodialysis, nine patients are on intermittent peritoneal dialysis, 16 are on conservative treatment and 17 died during the course of treatment.
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PMID:Chronic renal failure in Khartoum, Sudan. 303 72

In 24 patients with chronic glomerulonephritis the echographic findings were compared with some basic parameters established by histomorphologic examinations. In the echographic examinations 4 degrees of echogenicity were used (Rosenfield, Hrisak). The conclusion is that there is no typical echographic image for the different morphologically defined renal diseases. The cortical echogenicity depends on the degree of interstitial infiltration, the fibrous and sclerotic changes. The echographic image of the kidney is a mixed reflection of the histomorphologic changes of the glomeruli, tubules and interstice. A long-standing hypertension affects the echographic image by increasing the cortical echogenicity. A careful and thorough echographic examination of patients with chronic glomerulonephritis is obligatory but the basic diagnostic method is the needle renal biopsy.
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PMID:[Echographic diagnosis of diffuse kidney diseases]. 306 92

Blood volume, extracellular volume, blood pressure and the plasma levels of angiotensin II, aldosterone, adrenaline, noradrenaline and arginine vasopressin were determined in sixteen normotensive (group 1) and thirteen hypertensive patients (group 2) with chronic glomerulonephritis and in eleven normotensive control subjects (group 3). Blood volume and extracellular volume did not differ between the groups and no significant differences were found in any of the hormones measured when comparing group 1 or group 2 with group 3. In the hypertensives but not in the normotensives or control subjects, a highly significant positive correlation was found between diastolic blood pressure and blood volume (rho = 0.75, P less than 0.01) and between diastolic blood pressure and extracellular volume (rho = 0.74, P less than 0.01). Blood volume and extracellular volume correlated (P less than 0.05) in each of the groups. In conclusion, although no expansion of either blood or extracellular volume was found in chronic glomerulonephritis, a positive volume-pressure relationship could be demonstrated in hypertensive patients suggesting a role of volume factors in the pathogenesis in early stage chronic glomerulonephritis. The study does not give support to a major role of either angiotensin II, arginine vasopressin or catecholamines in the maintenance of nonmalignant hypertension in early stage chronic glomerulonephritis.
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PMID:Relationship of angiotensin II, aldosterone, arginine vasopressin, adrenaline and noradrenaline in plasma, blood and extracellular volumes to blood pressure in chronic glomerulonephritis. 308 77

We present two patients with proved chronic glomerulonephritis who had severe refractory hypertension and chronic renal failure. In both patients normal-sized kidneys were demonstrated in addition to vascular bruits and Grade III hypertensive retinopathy. These findings raised the suspicion of an etiological condition other than chronic glomerulonephritis underlying the hypertension and renal failure. Renal angiography revealed bilateral severe renal artery stenosis. In both cases renal revascularization was followed by a drop in blood pressure to normal or near normal levels. In selected cases with severe hypertension and chronic renal failure, renal artery stenosis should be considered, despite the coexistence of chronic glomerulonephritis.
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PMID:Symptomatic renal artery stenosis superimposed on chronic glomerulonephritis. 315 24

In 366 patients with bioptical verified and functional compensated chronic glomerulonephritis the relations between the clinical course types of glomerulonephritis according to Ratner, the histological changes and the tubular homoeostatic parameters of renal function, respectively, were investigated. A reliable connection was found between the clinical course type and special tubular functional parameters. With reference to histological changes the occurrence of a tubulo-interstitial lesion (tiK) is the cause of an excessive disturbance of the renal tubular function. Independently of this, however, the clinical course type of chronic glomerulonephritis may be responsible for the pathological reactive failure of tubular functional parameters. In the case of renal tubular dysfunction in the active nephritic type (ANT) and the nephrotic type with hypertension (NHT), respectively, the occurrence of a tik is much likely. By the lack of reno-tubular dysfunction in ANT and NHT a tik be cannot excluded. In contrast to this, in the inactive nephrotic type (INT) and the nephrotic type without hypertension (NHT), respectively, a tik be can excluded by lack of tubular dysfunction. On the other side, a tubular dysfunction in these groups is not a certain proof of a tik.
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PMID:[Correlations of homeostatic disorders of tubule function, type of clinical course of chronic glomerulonephritis and histologic changes in the diagnosis of tubulo-interstitial lesions]. 321 83

Effects of guanfacine, a centrally acting antihypertensive, on blood pressure, heart rate, plasma renin activity, serum aldosterone, plasma norepinephrine, and renal function were evaluated in 16 patients with hypertension with biopsy-proved chronic glomerulonephritis. Guanfacine monotherapy with a daily dose of 1 to 2.5 mg at bedtime for 6 months brought about a significant reduction in blood pressure (171 +/- 2/110 +/- 2 to 144 +/- 2/89 +/- 1 mm Hg; P less than 0.01), with concurrent decreases in heart rate (78 +/- 2 to 70 +/- 2 bpm; P less than 0.01), plasma renin activity (1.96 +/- 0.12 to 1.21 +/- 0.19 ng/ml/hr; P less than 0.05), aldosterone (14.6 +/- 1.5 to 9.7 +/- 0.9 ng/dl; P less than 0.05), plasma norepinephrine (220.5 +/- 24.2 to 132.8 +/- 27.7 pg/ml; P less than 0.05). There was no change in serum creatinine, beta 2-microglobulin, or endogenous creatinine clearance during guanfacine monotherapy. Our data suggest that guanfacine exerts its antihypertensive effect via the inhibition of sympathetic outflow and in part the suppression of the reninangiotensin-aldosterone system and that guanfacine is suitable for the effective treatment of hypertension associated with chronic glomerulonephritis.
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PMID:Effects of guanfacine monotherapy on blood pressure, heart rate, plasma renin activity, aldosterone, and catecholamines in hypertensive patients with chronic glomerulonephritis. 327 21

In 35 initially normotensive patients with chronic glomerulonephritis and lupus nephritis (including 27 patients with nephrotic syndrome; NS), blood pressure (BP), urinary sodium excretion, plasma renin activity (PRA), plasma aldosterone level (PA), urinary aldosterone excretion (Au and blood volume were measured before and during prednisolone treatment. In 7 patients (all with NS) steroid-induced hypertension has developed. The patients prone to develop hypertension were hypervolemic nephrotics with initial depression of PRA, PA, Au, and severe sodium retention. In these patients prednisolone did not produce diuresis of natriuresis nor did it decrease proteinuria. In normo- and hypovolemic patients prednisolone produced significant diuresis and natriuresis and failed to induce hypertension. Thus, two types of response to prednisolone could be observed in patients with NS.
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PMID:Steroid-induced hypertension in patients with nephrotic syndrome. 328 84

The circadian blood pressure rhythm was compared in patients with Cushing's syndrome, essential hypertension, and primary aldosteronism. In patients with essential hypertension or primary aldosteronism, a clear nocturnal fall in systolic and diastolic blood pressure and heart rate was observed. This fall was seen in untreated subjects as well as in patients receiving combined treatment with a calcium antagonist, diuretic, converting enzyme inhibitor, alpha-blocker and beta-blocker, or sympatholytic drug. In these groups, there was a positive correlation between heart rate and systolic or diastolic blood pressure. On the other hand, in patients with Cushing's syndrome, there was no nocturnal fall in blood pressure but in some patients a rise was observed. In all patients there was a nocturnal fall in heart rate. Thus, there was no significant correlation between heart rate and blood pressure in these patients. Exogenous glucocorticoid eliminated the normal nocturnal fall of blood pressure in patients with chronic glomerulonephritis or systemic lupus erythematosus. These results suggest that the changed circadian blood pressure pattern in patients with Cushing's syndrome is not due to antihypertensive treatment or to the mineralocorticoid excess accompanying this disease, but it is attributable to excess glucocorticoid or the associated disturbance in the adrenocorticotropic hormone-glucocorticoid system (or both). This conclusion also implies that the normal circadian rhythm of blood pressure may be regulated at least in part by the adrenocorticotropic hormone-glucocorticoid system.
Hypertension 1988 Jul
PMID:Altered circadian blood pressure rhythm in patients with Cushing's syndrome. 339 72

Forty-five patients with high arterial hypertension (AH) refractory to hypotensive therapy were treated with 3 or 4 prostaglandin E2 (PGE2) infusions (Prostenon). Twenty-two of those had the malignant AH syndrome. The hypotensive effect of prostenon was most pronounced in patients with essential hypertension, less marked in those with chronic glomerulonephritis and pyelonephritis and virtually nonexistent in cases of renovascular hypertension. It persisted until the discharge in most patients, and for several months in some. In severe AH, prostenon improved blood supply to the brain, kidneys and, less notably, the limbs, normalized venous dilatability and the cardiac index, brought down total peripheral resistance, particularly in cases where pretreatment values had been high, reduced platelet aggregation 1.8-fold, and contributed to reverse development of eyeground changes in some patients with malignant AH syndrome.
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PMID:[Use of prostenon in the treatment of severe and malignant forms of hypertension]. 347 May 53


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