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

Several special problems were noted regarding the vascular reconstruction for renovascular hypertension of the patient with a solitary kidney. It is difficult to use the value of plasma renin activity for decisive diagnosis or determination of surgical indications because most of the one-kidney patients with renovascular hypertension showed a normal plasma renin activity preoperatively and it is theoretically impossible to obtain a ratio of the affected to the opposite renal vein renin level. Most patients presented moderate to severe degree of renal dysfunction so that vascular reconstruction should be the treatment of choice because the conservative therapy with anti-hypertensive drugs such as captopril may further worsen the renal function by decreasing the renal perfusion pressure. Patients showed extensive polyuria immediately after surgery which was attributed to sudden increases in glomerular filtration rate and urinary sodium excretion. There was no correlation between the preoperative serum osmolarity and the postoperative polyuria. Correlation was not obtained between the intraoperative clamping time of the renal artery and the aggravation of the previously existing renal dysfunction. A comparative pathohistological study of primarily vs secondarily nephrectomized kidneys revealed no evidence of parenchymal damage of the kidney after arterial reconstruction. Both acute and chronic animal experiments in which autologous whole blood was forcibly injected into the canine renal artery via extracorporeal shunt under the high pressure of 200 or 300 mmHg showed no light microscopic evidence of acute histological damage of the kidney. It is concluded that the intensive care with an aid of a Swan Ganz catheter during the postoperative polyuric period and the swift starting of hemodialysis when necessary can solve the postoperative problems of one-kidney renovascular hypertension although the sudden rise in renal perfusion pressure after reconstruction may cause an acute hypertensive damage in the level of electron microscopic findings.
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PMID:[Clinical and experimental study on vascular reconstruction for one-kidney renovascular hypertension]. 332 Jul 40

The use of nisoldipine (10-20 mg b.i.d.) was evaluated as a replacement therapy for long-acting nifedipine (40-120 mg/day) in 21 patients with severe hypertension, who were resistant to or intolerant of nifedipine. Except for one patient with specific contraindications, all participants received an individually determined constant dose of beta blocker throughout the 8-month study. Results indicated a significant decrease in blood pressure after four weeks of treatment with nisoldipine (173 +/- 5/98 +/- 4 to 156 +/- 3/91 +/- 2 mmHg, p less than 0.05) without an associated change in pulse rate in 19 patients; only 5 of the 21 patients showed no further benefit from nisoldipine. No significant biochemical changes were noted in any of the patients during the study. In three patients, leg edema that had developed as a consequence of previous nifedipine therapy resolved completely following nisoldipine administration. Two patients withdrew from the study before term because of headaches and palpitations. An additional two patients suffered headaches, but tolerated the drug and continued the study. One patient suffered from polyuria. Nisoldipine appears to be an effective substitute treatment for nifedipine in severely hypertensive patients sensitive or resistant to nifedipine.
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PMID:Nisoldipine: a replacement therapy for nifedipine in the treatment of severe hypertension. 338 70

Sixty patients with idiopathic retroperitoneal fibrosis presenting between 1965 and 1984 are reviewed. Their mean age at presentation was 56 years and the male:female ratio was 3:1. The commonest presenting symptoms were flank and abdominal pain, weight loss, nausea and polyuria. Physical examination was usually normal, expect for the presence of hypertension. Anaemia and elevation of erythrocyte sedimentation rate were usually present. Proteinuria was found in less than a third of patients at presentation and significant bacteriuria was uncommon. The correct diagnosis was made or suspected in very few patients before referral. The cumulative actuarial survival rate was 86% at 1 year and 78% at 2 years. Seventeen patients died; they were significantly older and more uraemic at the time of referral than those who survived. A few patients did well with either corticosteroid therapy or ureterolysis alone. In the majority, both operation and steroid treatment were necessary. In bilateral obstruction with residual function in both kidneys, bilateral ureterolysis proved superior to unilateral operation (each followed by steroid therapy) in conserving renal function. Operation alone or steroid therapy alone should be considered in cases where steroids or surgery respectively present particular hazards. The less traumatic unilateral operation should be considered in poor risk patients and in those whose renal function is absent on one side. In many survivors, disease activity has persisted for many years. Life-long follow-up is recommended.
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PMID:Idiopathic retroperitoneal fibrosis. A retrospective analysis of 60 cases. 275 67

Familial juvenile nephronophthisis (FJN) is a frequent cause of chronic renal failure in children and adolescents. Typically it presents after 6 years of age through adolescence, but may become apparent in early childhood. The clinical presentation is insidious, and the early symptoms of polyuria and polydipsia are often overlooked in the presence of a relatively normal urinalysis and in the absence of proteinuria, azotemia, and hypertension. Thus most patients are not diagnosed until after the onset of renal failure. These children are excellent candidates for properly selected transplantation.
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PMID:Familial juvenile nephronophthisis. A review and differential diagnosis. 351 Jul 94

A 2 1/2 year old dystrophic girl with polyuria and polydipsia was found to have an arterial hypertension, increased catecholamines in serum and urine, and a suprarenal tumour was diagnosed by ultrasonic scan. By means of histology and staging a neuroblastoma grade 3 was revealed. The sonography and Iodine-benzyl-guadinin-scintigraphy gave the clearest information about the tumour. Before operating it is necessary to stabilize the blood pressure at a normal level with alpha and beta blocking substances, in order to reduce the risk of an intraoperative hypertonic crisis and a vasodilative shock after tumour extirpation.
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PMID:[Differential diagnostic and therapeutic problems in a neuroblastoma patient with hypertension]. 352 13

A woman with triplet gestation had polydipsia and polyuria during pregnancy. She subsequently had preeclampsia for which she was delivered. The presumed diabetes insipidus was transient, resolving by postpartum day 5. The association of preeclampsia and diabetes insipidus may be confusing to the practitioner. Careful attention to fluid status and consideration of this abnormality will lead to the best outcome when hypertension is accompanied by polydipsia and polyuria.
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PMID:Transient diabetes insipidus and preeclampsia. 356 89

Hypertension developed within 3 to 5 weeks in uninephrectomized rats administered deoxycorticosterone acetate (DOCA) at a dose of 850 micrograms X kg-1 X day-1 via Silastic tubes and given isotonic saline to drink. Chronic dietary administration of tryptophan (25 and 50 g/kg of food) to DOCA-treated rats reduced their exaggerated intake of NaCl solution and attenuated the elevation of blood pressure induced by treatment with DOCA alone. Treatment with tryptophan also protected against the reduction in urinary concentrating ability during a 24-h dehydration that is characteristic of DOCA-treated rats. Other tests assessed the responsiveness to the beta-adrenergic agonist, isoproterenol. These included measurement of drinking and heart rate following acute administration of isoproterenol. The characteristically depressed drinking and chronotropic responses of DOCA-treated rats to acute administration of isoproterenol were unaffected by tryptophan. Responsiveness to angiotensin II (AII) was also tested by assessment of dipsogenic and metabolic responses to acute administration of AII. The increased drinking and tail skin temperature responses to administration of AII, characteristic of DOCA-treated rats, were reduced in a graded fashion by treatment with graded doses of tryptophan. The specific binding of AII to its receptors in membranes form the diencephalon of the brain was increased by treatment with DOCA but was returned to control level by concomitant treatment with tryptophan. The content of serotonin in the mesencephalon of the brain was not changed significantly by treatment with tryptophan, but the content of 5-hydroxyindole acetic acid in the same region increased significantly, suggesting that turnover of serotonin was increased by chronic treatment with tryptophan. The cardiac hypertrophy characteristic of treatment with DOCA was attenuated significantly by chronic treatment with tryptophan, while the low, resting plasma renin activity of the DOCA-treated group was unchanged. These results suggest that tryptophan provides significant protection against the development of DOCA-induced hypertension, polydipsia, polyuria, and cardiac hypertrophy in rats. It also reduces the hyperresponsiveness to treatment with AII, possibly by decreasing the specific binding of AII to its receptors. It also appears to increase the turnover of serotonin in the brain. Whether either one or all of these is responsible for the antihypertensive effect of tryptophan remains for further study.
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PMID:Chronic dietary administration of tryptophan prevents the development of deoxycorticosterone acetate salt induced hypertension in rats. 362 Oct 37

The association of a critical reduction in renal mass with the subsequent destruction of remaining nephrons has been observed in several species. We studied this process in experimental rabbits after 1 2/3 nephrectomy to define the course and its pathogenesis in this species. Control rabbits underwent sham operative procedures. After renal ablation, rabbits became increasingly cachectic and developed polyuria and hypertension. Despite food intake similar to that of controls (grams per kilogram per day), experimental rabbits developed severe hypercalcemia by 5 to 8 weeks after renal ablation, a change that persisted until death. During the study 17 experimental animals died of uremia 9 to 27 weeks after surgery, and the remaining seven experimental and 25 sham-operated rabbits were sacrificed at 5 to 7 months. At death, 19/24 experimental rabbits had severe obstruction of their collecting systems by concretions of gravel (n = 3) or large calcium carbonate stones (n = 16). Renal biopsy at 4 weeks revealed focal interstitial round cell infiltration progressing by 12 weeks to diffuse tubulointerstitial inflammation and fibrosis. Histologic evidence of obstruction was also evident at this time and became extensive on all subsequent examinations. By contrast, the glomeruli remained well preserved without evidence of sclerosis. We speculate that chronic hypercalcemia and, perhaps more significantly, urinary obstruction may have altered intrarenal hemodynamics and prevented the development of progressive sclerosis observed in the rat remnant kidney model. The present study describes an experimental model of chronic hypercalcemia and spontaneous calcium carbonate nephrolithiasis.
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PMID:Subtotal nephrectomy in the rabbit: a model of chronic hypercalcemia, nephrolithiasis, and obstructive nephropathy. 371 20

Weight loss, polydipsia, polyuria, hyponatremia are symptoms often seen in patients with severe renin-induced hypertension. To investigate the role of the maturing kidney in the development of high pressure diuresis hypertension was induced in infantile (18 days old) and adult (40 days old) Sprague-Dawley rats by clipping one renal artery. In infantile rats blood pressure increase was steeper than in adult rats (7.8 vs. 3.2 mmHg/day). High pressure diuresis resulting in body weight loss was observed at systolic blood pressure levels of about 140 to 150 mmHg in infantile animals compared to 180 mmHg in adult rats. At this time fluid intake was increased to 64 in infantile and 30 ml/100 g body weight/day in adult rats. Plasma renin concentration and aldosterone were two fold higher in infantile than in adult rats. The data show that infantile rats, due to a higher activation of the renin-angiotensin-aldosterone system, have a steeper blood pressure increase and, furthermore, that during maturation of the kidney high pressure diuresis starts at lower blood pressure levels and is much more pronounced.
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PMID:High pressure diuresis initiates malignant hypertension in the young. 375 87

To investigate mechanisms involved in the high incidence of hypertension in diabetes mellitus, the relationship between renin-angiotensin production and renal prostaglandin E2 synthesis was studied in rats 1 week after diabetes mellitus had been induced by streptozotocin injection. The diabetic rats became hypertensive, although plasma renin activity did not increase despite the plasma volume contraction resulting from polyuria and natriuresis. Subcutaneous insulin injection resulted in a marked increase in plasma renin activity, while more rigid control of diabetes mellitus achieved by constant insulin infusion decreased blood pressure. Cortical renin content and renin release as well as papillary prostaglandin E2 synthesis in vitro were significantly lower in diabetic rats than in nondiabetic controls. Isoproterenol and prostaglandin E2 stimulated renin release in controls, while diabetic rats responded only to isoproterenol. Insulin infusion by pump reversed these abnormalities. An additive effect of a maximum dose of isoproterenol (10(-5) M) and prostaglandin E2 (10(-4) M) on renin release was observed in nondiabetic controls and in diabetic rats treated with insulin pump, but not in untreated diabetic rats. The results suggest that 1) renal renin release and prostaglandin E2 synthesis in diabetes mellitus are insulin dependent, 2) inappropriately lower plasma renin activity in diabetes mellitus may be attributed to a diminished renal renin pool and a lack of renin release in response to renal prostaglandin E2, the synthesis of which is also impaired in diabetes, prostaglandin E2-induced renin release may operate independently from isoproterenol-induced renin release, and impaired renal prostaglandin E2 synthesis may contribute to the development of hypertension in the face of an unchanged prohypertensive renin-angiotensin II system.
Hypertension
PMID:Hypertension in experimental diabetes mellitus. Renin-prostaglandin interaction. 389 14


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