Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe two patients with unusual neuro-ophthalmologic complications during long-term therapy with lithium carbonate given for bipolar affective disorder, "benign" intracranial hypertension in one, and downbeat nystagmus, with oscillopsia in the other. A review of the literature is proposed. Though rare, such neuro-ophthalmologic manifestations are worth being recognised since they usually disappear with cessation--when possible--of lithium therapy.
 ...
PMID:[2 rare neuro-ophthalmologic complications of long-term treatment with lithium salts]. 250 94

A 23 years old woman, diagnosed as having manic-depressive psychosis, in treatment with lithium carbonate for eight months, developed a benign cranial hypertension secondary to the lithium. Suppression of the lithium gave place to the normalization of the pressure of the cerebrospinal liquid which increased again with the reintroduction of the drug. This rare complication of the lithium salts, has only been described in five other cases, all women, with a relative short time of treatment, non-toxic lithium serum levels and without precipitating factors.
 ...
PMID:[Benign cranial hypertension secondary to treatment with lithium]. 257 50

Besides anemia, coagulopathies, and hypertension, electrolyte disturbances are among the most significant features of end-stage renal disease. Although plasma potassium represents only 1.5%-2% of the whole-body content, hyperkalemia has definite effects on cardiac pacemaker cells and myocardial conduction. The typical ECG findings and therapeutic management will be discussed. Case report. A 64-year-old man with chronic renal failure due to phenacetin abuse was scheduled for transplantation of a 41-h-old cadaver kidney. The preoperative laboratory check revealed BUN 51 mg% and creatinine 11.5 mg%; serum sodium and potassium were within normal limits (sodium 141 mmol/l, potassium 5.11 mmol/l). A central-venous blood gas sample after induction of anesthesia and intubation revealed pH of 7.32, pCO2 43 mmHg, HCO3 22.1 mmol/l, base excess - 3.4 mmol/l, and venous oxygen saturation 84%. Plasma potassium (5.22 mmol/l) was within the normal range. As an endarterectomy of the left common and external iliac arteries had to be performed, the arterial cross-clamping time was longer than normal (73 min). After declamping an ECG pattern (modified V5 lead) typical of hyperkalemia (atrial arrest, idioventricular rhythm, right bundle-branch block-like QRS, AV dissociation, AV block I) was observed. Plasma potassium had increased to 6.77 mmol/l (+1.55 mmol/l). Immediate treatment was started with a bolus injection of 20 ml 10% calcium gluconate, rapid infusion of 200 ml 8.4% sodium bicarbonate, and glucose-insulin infusion (glucose 33 1/3%, 15 U regular insulin). After 25 min sinus rhythm was restored and potassium levels decreased to normal. Despite the observed ECG changes the cardiovascular status remained stable.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Atrial arrest and intraventricular conduction disorders due to accidental hyperkalemia during kidney transplantation]. 267 72

Twenty-five samples of amniotic fluid obtained by amniocentesis from 25 pregnant women with hypertension in the 35 to 40 weeks of pregnancy were studied. The following biochemical determinations were done in the samples: acid-base equilibrium (pH, pO2, pCO2, base deficit, standard HCO3- and total CO2), concentrations of potassium and sodium ions, total and ionised calcium and inorganic phosphorus. The results were analysed depending on the presence of the respiratory distress syndrome in the newborn, and were subjected to statistical analysis. It was found that determination of acid-base equilibrium and concentrations of K+, Na+, total and ionised Ca++ and inorganic phosphorus in the amniotic fluid of hypertensive women are probably without prognostic significance with respect to the development of the respiratory distress syndrome in newborns.
 ...
PMID:[Respiratory distress in newborns born to hypertensive mothers and acid-base equilibrium and the ion composition of the amniotic fluid]. 270 90

Forty-seven patients with mild hypertension and 48 normotensive patients entered a blinded, parallel study in which they received a placebo, 10 mmol/day calcium carbonate (CaCO3), or 20 mmol/day CaCO3. There were no significant differences in blood pressure changes among the groups. In the hypertensive group and in patients with the highest blood pressure there were individual falls in systolic pressure, particularly in the group receiving 10 mmol daily CaCO3. In the hypertensive group the changes were: with placebo, -3 +/- 2/-2 +/- 2 mm Hg; with CaCO3 (10 mmol), -7 +/- 3/-2 +/- 2 mm Hg; and with CaCO3 (20 mmol), -2 +/- 3/1 +/- 2 mm Hg. No change was significant, and no pressure changes of patients taking CaCO3 differed significantly from changes of patients taking placebo. Ten of 33 patients taking placebo, 11 of 31 taking 10 mmol/day CaCO3, and nine of 31 taking 20 mmol/day CaCO3 were classified as responders from their systolic blood pressure fall. These response rates did not differ. Eight patients had falls of systolic blood pressure greater than 15 mm Hg. Five were on 10 mmol/day CaCO3 and three on 20 mmol/day CaCO3. This response was significantly different from that with placebo. Univariate analyses failed to reveal any predictive dietary or biochemical parameter. After 3 months of not taking CaCO3, 12 patients classified as responders, including six of the eight with a fall of 15 mm Hg or more, were rerandomized to placebo or to 20 mmol/day CaCO3. In the rechallenge, responses to CaCO3 and placebo were similar, neither causing a significant pressure fall. Calcium carbonate did not reduce blood pressure. The apparent response in a few patients was not verified by rechallenge. The present study does not support calcium supplementation as a useful nonpharmacological measure for reducing elevated blood pressure.
Hypertension 1989 Jun
PMID:Effect of calcium carbonate on blood pressure in normotensive and hypertensive people. 273 11

Current information suggests that alpha 2-adrenoceptors do not directly influence vascular resistance or Na reabsorption in the rat kidney. To reexamine the effects of alpha 2-agonists we used isolated rat kidneys perfused at 37.5 degrees C with precise measurement of renal artery pressure and flow. The recirculating perfusate contained pyruvate as the sole metabolic substrate which enabled us to use gluconeogenesis as an index of proximal tubular alpha 1-responses. Clonidine and guanfacine in 100 nM concentrations decreased phosphate excretion without altering Na, Cl, or K reabsorption or gluconeogenesis; 500 nM concentrations increased vascular resistance and decreased glomerular filtration rate and Na, Cl, and K excretion with no significant effect on gluconeogenesis. Prior thyroparathyroidectomy prevented the antiphosphaturic but not the antinatriuretic or vascular responses. Clonidine, an alpha 2-agonist with some alpha 1-activity, was a more potent vasoconstrictor than methoxamine or guanfacine. In the presence of prazosin (1 microM), norepinephrine (60 nM) stimulated phosphate reabsorption; norepinephrine alone did not stimulate phosphate reabsorption which indicates alpha 1-antagonism of this alpha 2-response to NE. These results and a literature review suggest that increased renal alpha 2-adrenoceptors could raise renal vascular resistance, reduce renin secretion, and antagonize parathyroid hormone effects on Pi, Ca, HCO3, and Na reabsorption to produce a low renin type of hypertension with increased proximal Na reabsorption and abnormal Ca and Pi excretion.
 ...
PMID:Is there a role for renal alpha 2-adrenoceptors in the pathogenesis of hypertension? 289 22

Hyperreninemic hypoaldosteronism was diagnosed in a 34-year-old woman with hypertension who was receiving captopril therapy. Renal biopsy revealed an advanced stage of IgA nephropathy, and her creatinine clearance was 40 ml/min. Elevation of serum potassium from 4.7 to 5.8 mEq/l and development of hyperchloremic metabolic acidosis with laboratory findings of pH 7.285, HCO3- 13.5 mEq/l, Na 141, and Cl 114 mEq/l were observed after captopril therapy. When captopril was withdrawn, elevated serum potassium levels and metabolic acidosis returned to normal. Challenge with captopril resulted in a decrease in plasma aldosterone levels, an increase in plasma renin activity, and development of hyperkalemic, hyperchloremic metabolic acidosis which is corrected with mineralocorticoid replacement. This case study demonstrates that captopril can cause hyperreninemic hypoaldosteronism with the laboratory finding of hyperkalemic, hyperchloremic metabolic acidosis.
 ...
PMID:Captopril-induced metabolic acidosis with hyperkalemia. 307 Nov 39

The effects of 800 mg of elemental calcium per day (calcium carbonate or calcium citrate) on blood pressure were compared with a placebo in a controlled randomized, crossover, double-blinded trial involving 26 patients with uncomplicated primary hypertension. Each patient took two of the three forms of therapy orally for 8-week intervals with a 2-week washout period in between. Standing mean blood pressure rose an average of 5.7 mm Hg on placebo, rose an average of 0.5 mm Hg on calcium carbonate, and fell an average of 2.2 mm Hg on calcium citrate. Changes in sitting mean pressures averaged +1.9 mm Hg on placebo, -0.4 mm Hg on calcium carbonate, and -0.4 mm Hg on calcium citrate. Some patients had a fall, others had a rise in blood pressure on each form of calcium. Similarly, inconsistent responses were noted among the nine patients who took both forms of calcium. Neither initial nor post-treatment biochemical measures nor patient characteristics were predictive of the blood pressure response. Combinations of various measures and characteristics analyzed by the multiple regression technique explained only 30% of the overall variability in blood pressure. Therefore, until ways can be found to predict the response, calcium supplements should not be routinely prescribed for the treatment of hypertension and, if given for any indication, blood pressure should be monitored.
 ...
PMID:The inconsistent effects of calcium supplements upon blood pressure in primary hypertension. 331 Jun 39

To test the hypothesis that the supplementation of dietary calcium intake influences sodium homeostasis, the renin-angiotensin system, and sympathetic nervous system in a manner that might evoke a decrease in arterial blood pressure, we gave 16 participants (eight normal and eight with hypertension) placebo for 8 days, followed by 500 mg elemental calcium as the carbonate salt twice a day for 8 days. The same diet was prepared for each meal for the entire study. Sodium intake was fixed for each participant and averaged 150 mEq/day. All urine was collected every day. Blood was drawn at the end of the placebo and calcium periods for determinations of plasma renin, aldosterone, and norepinephrine values. Calcium supplementation increased urinary calcium excretion significantly in both groups. However, calcium supplementation failed to influence sodium or potassium excretion, serum electrolytes, total serum calcium, renin, aldosterone, or norepinephrine levels, or heart rate. Systolic and diastolic blood pressure were not influenced in normal subjects, but in patients with hypertension the supine systolic blood pressure decreased significantly. We conclude that blood pressure lowering effects of calcium, should they occur, are not likely the result of augmented urinary sodium excretion or of straight-forward influences on the renin-angiotensin system or sympathetic nervous system.
 ...
PMID:Short-term augmented calcium intake has no effect on sodium homeostasis. 351 53

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.
 ...
PMID:Subtotal nephrectomy in the rabbit: a model of chronic hypercalcemia, nephrolithiasis, and obstructive nephropathy. 371 20


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>