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

A 12-year-old boy with a norepinephrine-secreting pheochromocytoma that caused hypertension resistant to oral alpha adrenergic blockade is reported. Resistance to alpha adrenergic blocking agents developed when the patient's daily propranolol dosage was lowered from 10 to 1 mg/kg. Subsequently, alpha methyl tyrosine, an inhibitor of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis, controlled the patient's blood pressure and was associated with reduction in total urinary catecholamine excretion. Norepinephrine content of the tumor and uninvolved adrenal gland removal at surgery was reduced. These findings confirm that alpha methyl tyrosine inhibited in vivo synthesis of catecholamines.
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PMID:Childhood pheochromocytoma: treatment with alpha methyl tyrosine for resistant hypertension. 1 59

Noradrenaline (NA), 100 microgram intraventricularly (ivtr), produces an evident hypertension, lasting for up to 15 min. A previous ivtr administration of propranolol (100 and 500 microgram), alprenolol (100 microgram), sotalol (100 microgram), (-)INPEA (100 microgram), (+)INPEA (100 microgram), Ko 1366 (100 and 200 microgram), or practolol (20 microgram) abolishes the hypertensive action of NA. The results indicate that the central nervous system of the rat contains structures similar to the peripheral beta-adrenoceptor, and that they are involved in the central regulation of circulation.
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PMID:The effect of beta-adrenergic receptor blocking agents on hypertensive action of noradrenaline injected into the lateral ventricle of rat brain. 2 Jun 10

1. Noradrenaline content of several rat brain stem and hypothalamic nuclei falls transiently at 72 h after initiation of renovascular hypertension (one-kidney Goldblatt model). 2. Tyrosine hydroxylase activity is significantly reduced in posterior, paraventricular and periventricular nuclei of hypothalamus at this time but returns to control value by 7 days. 3. Treatment with hydrallazine, 5 mg/kg intraperitoneally, twice daily or methaoxamine, 5 mg/kg, three times daily for 3 days respectively raises and lowers the noradrenaline content of brain nuclei, suggesting that short-term changes in noradrenaline may be secondary to afferent baroreceptor input. 4. At later times after the development of renovascular hypertension (7 and 28 days) activity of phenylethanolamine-N-methyl transferase is increased in the nucleus of the solitary tract and the locus coeruleus. 5. Brain catecholamines may participate both early in the development and later in the maintenance of renovascular hypertension.
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PMID:Brain catecholamines and catecholamine-synthesizing enzymes in renovascular hypertension in the rat. 3 99

1. Noradrenaline and adrenaline in the adrenal vein of essential hypertensive patients are almost exclusively (99%) unconjugated or free. However only 17% of dopamine is free, the rest is conjugated. The further the site of sampling from the adrenal vein the closer come the free catecholamines to their normal peripheral venous proportion (noradrenaline + adrenaline 20%, dopamine less than 1% of total catecholamines). Deviations from these patterns help to detect the site and type of secretion of phaeochromocytoma. 2. Essential hypertensive patients have, compared with control subjects, higher conjugated plasma dopamine, less urinary free and conjugated dopamine with blunted urinary free dopamine and sodium responsiveness to frusemide. Conjugated noradrenaline + adrenaline, mean arterial pressure and age are positively interrelated. 3. Patients with primary aldosteronism have elevated plasma and urinary total dopamine. After removal of the adenoma urinary dopamine excretion decreases to normal. 4. Elevated conjugated dopamine appears to reflect a compensatory activation of the dopaminergic vasodilator pathway in hypertension, the total urinary dopamine excretion an intrinsic deficiency or compensatory increase of a dopamine-modulated natriuretic mechanism.
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PMID:Free and conjugated catecholamines in human hypertension. 28 3

Angiographic and histological studies of the intrarenal circulation have been undertaken in 20 patients following complicated pregnancies: 12 patients had had hypertension of pregnancy (group 1); 7 acute renal failure due to either ante- or post-partum haemorrhage and 1 patient post-partum renal failure (group 2). 3 months after delivery all patients had angiographic evidence of structural and functional abnormalities involving intrarenal blood vessels and cortical blood flow. The severity of the structural changes was related to the degree of microangiopathic haemolytic anaemia noted in the acute obstetric complication but not to the height of the blood pressure at this stage. Histological abnormalities of the cortical blood vessels were minimal. At the time of the renal angiogram and biopsy, 3 of the 12 group 1 patients were hypertensive and 3 had impaired renal function, compared with 5 and 1, respectively, in the 8 group 2 patients. Although during the follow-up period (mean 5 years) no further deterioration in renal function in either group has been observed, hypertension developed in 50% of the group 1 patients compared with only 1 of the patients in group 2. The relationship between the late onset of hypertension and the intrarenal vascular and haemodynamic abnormalities is discussed.
Nephron 1979
PMID:Structural and functional changes in the renal circulation after complicated pregnancy. 31 35

The influence of intravenous injection of Prostacyclin (PGI2) on systemic blood pressure was investigated in conscious and anaesthetized hypertensive rats. PGI2 in doses of 1.0, 5.0 and 10.0 micrograms/kg showed a dose dependent antihypertensive effect in conscious rats with spontaneous and chronic renal hypertension. A similar response could be demonstrated in conscious rats with normal blood pressure with doses of 1.0, 10.0 and 100.0 micrograms/kg. In anaesthetized rats with acute renal hypertension or blood pressure increase, induced by continous infusion of Angiotensin II or Norepinephrine, PGI2 caused a marked decrease of blood pressure. PGI2 induced an increase of plasma renin activity in anaesthetized rats with doses of 0.1, 1.0 and 10.0 micrograms/kg. These findings support the suggestion of an antihypertensive role for PGI2 in experimental hypertension.
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PMID:Antihypertensive effect of prostacyclin (PGI2) in experimental hypertension and its influence on plasma renin activity in rats. 36 7

End-stage kidneys in patients who are receiving long-term intermittent treatment with hemodialysis are metabolic structures that participate in many body processes and that themselves develop and change despite severe excretory deficiencies. Nephron loss is severe. Other lesions in such kidneys include the following: smooth muscle nodules that arise in necrotic arteries and arterioles; embryonal hyperplasia of Bowman's capsular epithelium; remodeling of the arteries and veins; tubular atrophy; dilation and cyst formation (acquired cystic disease); arteriolar granular cell hyperplasia and hypertension; deposits of oxalate, calcium, and immune complexes; interstitial fibrosis with collagen and smooth muscle; mucoid change; and cellular infiltration. This list does not include all pathologic conditions found in the end-stage--dialysis kidney. The necessity of and the criteria for an experimental model of human long-term intermittent hemodialysis for end-stage renal disease, presently lacking, are indicated.
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PMID:New therapies and new pathologies: end-stage--dialysis kidneys. 36 73

The authors investigated post-renal transplantation hypertension behaviour in 20 patients with primary malignant hypertension (PMH), in 42 patients with secondary malignant hypertension (SMH) and in 62 controls (without malignant hypertension). All cases of malignant hypertension required removal of primary kidneys, either before or after transplantation. Hypertension was noticed at different periods of the post-renal transplantation phase, in 93% of PMH cases, 90% of SMH cases and in only 31% of the controls. After a period of time following transplantation, a decrease of hypertension incidence in the SMH and control groups was noticed, and persistence of hypertension was observed in the PMH group. The long-term development of PMH patients was worse than that of the other two groups.
Nephron 1978
PMID:Blood pressure behaviour in patients with malignant hypertension submitted to kidney transplantation. 37 Jun 28

18 patients undergoing renal transplantation were studied prospectively to determine the incidence and mechanism of blood pressure elevations which sometimes occur after release of vascular clamps from the grafts. No patients became as severely hypertensive as noted in previous reports. A weak, but statistically significant (r=0.56, p less than 0.05) positive correlation was found between changes in plasma renin activity and small incremental changes in blood pressure. 2 patients in whom the greatest change in renin occurred showed little or no increase in blood pressure. In view of the small blood pressure changes seen in the face of significant changes in plasma renin activity, it appears unlikely that acute hyperreninemia alone is sufficient explanation for postdeclamping hypertension which is sometimes observed during renal transplantation.
Nephron 1978
PMID:Hyperreninemia during renal transplantation. 37 Jun 29

The pattern of renal disease and its basic principles of management are essentially the same in the tropics as in the temperate environment. Glomerulonephritis and pyelonephritis with concomitant hypertension account for most cases of renal failure. Malaria is now well recognised as a cause of the nephrotic syndrome. Economic and manpower factors dictate a conservative approach to therapy. Maintenance haemodialysis and renal transplantation are not realistic in the present context, having regard to the order of priorities in health care delivery.
Nephron 1978
PMID:Nephrology in the tropical setting. 37 Jun 31


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