Increased plasma vasopressin in low renin essential hypertension.

Baseline plasma vasopressin concentrations were measured in 48 men (all 50 years old) with decreased plasma renin concentration and untreated, sustained essential hypertension and in 29 healthy normotensive men. Mean hypertensive plasma vasopressin concentration was more than twice as high as the corresponding normotensive level (15.7 +/- 2.2 [SE] vs 7.5 +/- 1.0 pg/ml; p less than 0.001). Plasma renin concentration in the hypertensive group was reduced compared with that in the normotensive group (0.28 +/- 0.04 vs 0.46 +/- 0.06 Goldblatt units X 10(-4)/ml). These differences appeared despite virtually identical serum osmolality, creatinine clearance, and urinary sodium excretion in the two groups. In the first 38 hypertensive subjects, arterial plasma epinephrine concentrations were significantly increased over those of the first 28 control subjects (99 +/- 12 vs 68 +/- 6 pg/ml; p less than 0.025). In contrast to those with low renin essential hypertension, 35 men with normal renin essential hypertension (all 40 years old) had normal plasma vasopressin levels that were not significantly different from those in a comparable normotensive control group (3.7 +/- 0.8 vs 3.5 +/- 0.4 pg/ml). Arterial epinephrine concentrations were not significantly different between normal renin subjects and the control group. After 6 weeks of treatment with the nonselective beta-adrenergic receptor blocker oxprenolol in 11 subjects with low renin hypertension, blood pressure was reduced and the plasma vasopressin concentration fell from 27.6 +/- 6.4 to 13.5 +/- 4.2 pg/ml (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Increased plasma noradrenaline during severe sodium restriction does not stimulate platelet release in essential hypertension.

Seventeen 50-year old hypertensive men, previously untreated with blood pressure 157 +/- 4/110 +/- 2 mmHg (means +/- SE) were given a low sodium diet for 2 weeks. During the second week, the diet was supplemented with potassium. The urinary Na+/K+ excretion ratio changed from 2:1 to 1:4 and 1:11, respectively. Sympathetic noradrenergic tone increased considerably during the first week. Thus, venous plasma noradrenaline increased from 254 +/- 22 to 347 +/- 28 pg/ml (p less than 0.001) and arterial concentration from 253 +/- 36 to 317 +/- 42 pg/ml (n = 10, p less than 0.001). No significant change was observed in sympathetic adrenal tone as reflected by normal plasma adrenaline in venous (42 +/- 5 vs 43 +/- 6 pg/ml, ns) or arterial blood (71 +/- 10 vs 82 +/- 15 pg/ml, n = 10, ns) or in venous plasma concentration of the blood platelet release product beta-thromboglobulin (BTG) (50 +/- 8 vs 43 +/- 5 ng/ml, ns). During the second week sympathetic noradrenergic tone remained highly significantly elevated compared to baseline but still no change in plasma adrenaline or plasma BTG was found. Thus, whereas sodium depletion did increase plasma noradrenaline concentration markedly in these hypertensive men, no change in adrenaline concentration was observed, and blood platelet release reaction was unchanged. Plasma noradrenaline within the physiological concentration range does not seem to serve as a regulator of in vivo platelet function.

Decreased serum phosphate in essential hypertension. Related to increased sympathetic tone.

Forty-year old men with untreated mild essential hypertension (n = 35) had decreased serum phosphate (P less than 0.001) concomitant with elevated resting plasma epinephrine (P less than 0.05) and heart rate (P less than 0.001) compared with age-matched, normotensive control men (n = 44). Blood pressure correlated negatively with serum phosphate (P less than 0.001) and positively with plasma epinephrine (P less than 0.01) and heart rate (P less than 0.01). Serum phosphate was significantly lowered during infusion of epinephrine, increasing arterial plasma epinephrine within the lower pathophysiological range corresponding to arousal reactions. Serum concentrations of immunoreactive parathyroid hormone were unchanged. Thus, hypophosphatemia in patients with mild essential hypertension appears to be inversely related to sympathetic adrenal tone and may be caused by increased plasma epinephrine within pathophysiologic arterial concentrations.

Increased erythrocyte magnesium in never treated essential hypertension.

In the present study we aimed at evaluating the intracellular concentrations of magnesium, potassium and sodium in 50-year-old, otherwise healthy white men with never treated, essential hypertension (n = 12) and in normotensive control subjects (n = 12) matched for age, sex, race, height, weight and smoking habits. Intraerythrocyte magnesium was significantly increased in the hypertensive group (P less than .001) and correlated positively and significantly to blood pressure in the total group (P less than .01). The intracellular potassium to sodium ratio tended to be lower in the hypertensive group (P less than .05). Thus, the present study supports increased intracellular magnesium probably unrelated to intracellular potassium-sodium imbalance in never treated, essential hypertension.

Increased erythrocyte magnesium in untreated essential hypertension.

In the present study we tested the hypothesis of magnesium deficiency and intracellular magnesium depletion in essential hypertension. Atomic absorption was used to determine the erythrocyte content of magnesium in 50-year-old otherwise healthy white men with never-treated, essential hypertension (n = 12, supine blood pressure 155 +/- 4/109 +/- 2 mmHg) and in a group of particularly well-matched normotensive control subjects. The erythrocyte magnesium content was higher in the hypertensive group (P less than 0.001). No significant difference between the groups was detected for serum concentration or the 24-h urinary excretion of the magnesium. In conclusion, magnesium deficiency is unlikely in white middle-aged hypertensive men.

Dietary sodium intake and vasopressin excretion in man.

The present study was undertaken to examine the possible relationship between dietary sodium intake and arginine vasopressin (AVP). In 12 normotensive men (aged 23-26 years) urinary AVP excretion decreased from 6.7 +/- 1.0 to 3.9 +/- 0.3 ng/h (P less than 0.01) when sodium excretion by dietary intervention for one week was reduced from 188 +/- 18 to 16 +/- 2 mmol/24 h. At a high sodium intake (300 mmol/day), AVP excretion increased to 10.0 +/- 1.2 ng/h during the first day (P less than 0.01) and remained high throughout one week of sodium load. These results are compatible with a major physiological role of sodium in AVP secretion in man. A sodium-AVP relationship may play a role in the pathogenesis of essential hypertension since recent reports suggest elevated plasma AVP in essential hypertensive states.

Influence of antibiotics on microbial intestinal transformation of cholesterol to coprostanol in man.

Fecal excretion of coprostanol was followed in groups of healthy volunteers receiving various antibiotics per os. No effect upon excretion was found in the groups receiving phenoximethylpenicillin or doxicycline, whereas a prolonged reduction was found in the groups receiving clindamycin, ampicillin, oxitetracycline or a fixed combination of bacitracin and neomycin.

Lithium intoxication: pharmacokinetics during and after terminated hemodialysis in acute intoxications.

Pharmacokinetics of lithium were studied in 4 females acutely intoxicated with lithium with maximal plasma concentrations of 8.7, 4.0, 3.4 and 1.3 mmol/l. Mean plasma dialysance values were 103, 105, 102 and 89 ml/min compared to mean renal clearance values of 13, 16, 20 and 30 ml/min, respectively. A rebound effect in plasma concentration suggested that the sum of the dialysance and renal clearance overestimated the total body clearance of lithium during hemodialysis. During hemodialysis the measured half-lives of the plasma lithium levels in three cases were 4.8, 3.4 and 2.3 hours compared to the corrected values of 12.0, 7.3 and 6.2 hours respectively, when this rebound effect was taken into consideration. These corrected half-lives were 30-66% of the control half-lives recorded later when each patient served as her own control, thus illustrating the effectiveness of hemodialysis in removing lithium. Forced diuresis with sodium chloride did not significantly increase renal lithium elimination.

[Hyponatremia. A retrospective study of occurrence, etiology and mortality]. / Hyponatremi. En retrospektiv studie med henblikk på forekomst, årsak og mortalitet.

In patients admitted to a general medical ward, the incidence of hyponatremia on admission was 3.6%. Mortality was more than three times higher among patients with hyponatremia than among the patients as a whole. The triad hyponatremia, hypoalbuminemia and hypervolemia indicated a poor prognosis. A diversity of medical illnesses was associated with hyponatremia, and the use of diuretics was a major contributor to the electrolyte disturbance. Treatment of asymptomatic hyponatremia is discussed, with special emphasis on restriction of fluids.

[Diagnoses and increased levels of troponin T among discharged patients]. / Utskrivningsdiagnoser ved forhøyede troponin T-verdier.

BACKGROUND: New criteria for diagnosing acute myocardial infarction, in which the cardiac troponin T or I plays a central role, have recently been proposed. We wanted to estimate what an application of these criteria would have meant for the diagnoses given patients discharged from our hospital in 2000. MATERIAL AND METHODS: From the hospital data bases, 3,461 in-hospital patients were identified in whom troponin T levels in blood had been determined. Maximal troponin T levels and diagnoses on discharge were recorded. Only one diagnosis was used for each patient. The diagnoses were selected in a priority order favouring those diseases that are known most often to cause increased troponin T levels, starting with the codes for acute myocardial infarction. RESULTS: By applying the new criteria, the number of patients with myocardial infarction was estimated to increase 17%, 33% and 61% depending on the decision level for troponin T used, 0.20, 0.10 or 0.03 microgram/l, respectively. Congestive heart failure and atrial fibrillation were the most frequent cardiac diagnoses in patients with increased troponin T level without evidence of acute coronary syndromes. Other, non-cardiac diagnoses included renal diseases, sepsis, and acute lung diseases. INTERPRETATION: Application of the new diagnostic criteria will markedly increase the recorded incidence of acute myocardial infarction. The number of positive troponin T values in patients without acute coronary syndromes will increase progressively by lowering the diagnostic decision level of troponin T.

Increased erythrocyte magnesium content in essential hypertension.

The present study aimed at testing the hypothesis of decreased erythrocyte magnesium content and magnesium deficiency in essential hypertension. Atomic absorption was used to measure the erythrocyte content of total magnesium in 50-year-old otherwise healthy white males with essential hypertension (n = 12, blood pressure (mean +/- SE) 155 +/- 4/109 +/- 2 mmHg) that had never been treated and in normotensive control subjects (n = 12, blood pressure 128 +/- 2/88 +/- 1 mmHg) matched for age, sex, race, height, weight and smoking habits. The erythrocyte magnesium content was significantly increased in the hypertensive group (2.266 +/- 0.063 vs 1.903 +/- 0.069 mmol/l erythrocytes, p less than 0.001). No significant difference between the groups was detected for serum concentration or the 24-h urinary excretion of magnesium. In conclusion, the present study indicates increased rather than decreased erythrocyte content of magnesium in 50-year-old white males with 'never-treated', essential hypertension. Magnesium deficiency is, therefore, unlikely in this subset of critically selected and matched hypertensive patients.

Diagnostic efficiency of biological markers in blood serum on prostate cancer: a comparison of four different markers and 12 different methods.

Serum-acid phosphatase as measured by nine different methods, serum prostate-specific antigen, cancer antigen CA-50, and creatine kinase BB isoenzyme have been evaluated and compared with respect to efficiency in differentiating between prostate cancer and benign hyperplasia. The patient material consisted of 92 prostate cancer patients (59 untreated, and 33 previously treated), 106 patients with benign hyperplasia and 66 patients with non-prostatic urological diseases. The cancer group was classified according to the TNM-system, and also graded according to histopathological findings. The following main conclusions were drawn. Acid phosphatase activity, when measured with continuous monitoring procedure (substrate: alpha-naphthyl phosphate), showed on the average slightly, but statistically not significant higher diagnostic efficiency than when measured with conventional two-point discontinuous monitoring method (substrate: p-nitrophenyl phosphate). There was no or only marginal differences in diagnostic efficiency between activity measurements of the total acid phosphatase and the tartrate-labile fraction, and also between activity measurements and immunological measurements (PAP-RIA and PAP-IEA). Prostate-specific antigen was found to have statistically significant higher diagnostic efficiency than acid phosphatase, the former being positive in 17 of 25 patients with prostate cancer without distant metastases, and in six of 11 patients classified as T0-2 M0. Cancer antigen CA-50 and creatine kinase BB isoenzyme appeared to be of little diagnostic value. From a cost-effective point of view, total or tartrate-labile prostatic acid phosphatase activity, as measured by continuous monitoring technique with alpha-naphthyl phosphate as substrate, is suggested suitable as a first-choice parameter both for diagnostic and monitoring purposes with respect to prostate disease. Prostate-specific antigen may give additional information, and should be considered analysed on special request.

Clinical course in acute self-poisonings: a prospective study of 1125 consecutively hospitalised adults.

The clinical course in an unselected group of 1125 consecutively hospitalised self-poisonings was studied during 1 year in Oslo. Mortality was 0.5%, but only 0.3% in those admitted without cardiac and respiratory arrest. Mortality among those in grade IV coma was 4.2%. The deepest comas (grade III or IV) occurred in 25.1% of the admissions with a mean duration of the coma of 5.8 h (range 1-80). Complications occurred in 21.7% of the admissions and 6.9% suffered more than one complication of which the most frequent were respiratory depression (13.5%), hypotension (5.3%), pneumonia (4.4%), and hypothermia (1.6%). The complication rate was highest in poisonings with opiates (60.7%), meprobamate (37.5%) and antihistamines (30.0%). Arrhythmias and respiratory depression were closely associated with poisonings with antidepressants and opiates, respectively. Owing to frequent polydrug overdoses it was difficult to associate other complications with other main toxic agents. Administration of antidotes (20.6%), cuffed intubation (4.4%) and forced alkaline diuresis (3.4%) were the most frequent special therapeutic measures taken. The change in pattern of self-poisonings in Oslo focuses on antidote therapy and intensive care, especially outside hospital, but limits the need for haemodialysis and haemoperfusion which were performed in only 1.0% of the admissions.

A prospective study of 1212 cases of acute poisoning: general epidemiology.

A prospective multicentre study of all acute poisonings among adults admitted to hospital (n = 1145) or dying outside hospital (n = 67) in Oslo was performed during 1980. Of the 1212 episodes, 98.3% were self-poisonings, giving an annual incidence of 2.8 per 1000 inhabitants (0/00), 3.1 0/00 in males and 2.6 0/00 in females. The main toxic agents among the self-poisoned patients were ethanol (19.7%), benzodiazepines (17.8%), opiates (14.9%), neuroleptics (10.4%) and antidepressants (9.3%). In 58.9% of the episodes more than one toxic agent was taken. Abuse among the self-poisoned patients was significantly (p less than 0.005) more common among males than females (64.2 v. 34.5%). The rate of suicide attempts was significantly (p less than 0.005) higher among females than males (20.2 v. 12.9%), females showing increasing rate with age. However, when excluding abusers the rate of suicide attempts was similar in both sexes (27.6 v. 25.0%). Compared to a reference population self-poisonings were most common in the lower middle and the lowest social classes. Patients in these social classes, however, showed a lower rate of suicide attempts than those in the two highest social classes. Overall mortality was 6.0% (n = 73), but 91.8% of all deaths occurred outside hospital indicating the importance of including these figures when self-poisonings are studied.

Hormonal responses to treatment of high blood pressure with low-salt diet alone and combined with added potassium.

One week strict sodium depletion in essential hypertensive men (n = 17) decreased blood pressure and body weight. Plasma renin concentration increased four-fold (p less than 0.001), plasma noradrenaline with 38% (p less than 0.001), plasma dopamine with 58% while plasma adrenaline remained unchanged. The urinary excretion of vasopressin was reduced with 50% (p less than 0.001). Extra potassium induced only small changes when already sodium depleted. Thus, vasopressin was the only pressor hormone which varied directly with sodium intake, blood pressure and body weight during sodium depletion.

The effect of sodium depletion and potassium supplementation on vasopressin, renin and catecholamines in hypertensive men.

Seventeen 50-year-old hypertensive men (157 +/- 4/110 +/- 2 mmHg, mean +/- SE) were given low sodium diet for one week, which was supplemented with potassium the following week. The urinary Na+/K+ excretion ratio changed from 2:1 to 1:5 and 1:12, respectively, during dietary intervention. Arterial plasma vasopressin decreased by 3.4 +/- 1.7 ng/l (0.05 less than p less than 0.10) and urinary excretion of vasopressin was reduced by nearly 50% (p less than 0.001) during sodium depletion, while plasma noradrenaline increased by 38% (p less than 0.001) and plasma dopamine showed an increase by 58% (p less than 0.001). Plasma renin concentration increased four-fold during sodium depletion (p less than 0.001). With combined salt depletion and potassium supplementation, arterial plasma vasopressin decreased by 9.5 +/- 4.0 ng/l (p less than 0.05) compared to control. Urinary excretion of vasopressin together with plasma noradrenaline and dopamine were unchanged during the second week. The reduction of blood pressure was most marked during the first week (143 +/- 3/103 +/- 2 mmHg, p less than 0.05), but continued to fall also during the second week. Thus, during sodium restriction in middle-aged hypertensive men, blood pressure reduction occurs concomitantly with inhibited vasopressin release, despite enhanced renin and catecholamine release. Potassium supplementation during sodium restriction induces only minor changes in these variables.

Dietary sodium intake increases vasopressin secretion in man.

Plasma vasopressin concentration and urinary vasopressin excretion were measured in a control situation, during sodium depletion and on days 1, 2, and 7 during high sodium intake in twelve 23-26-year-old men on a free-water intake. Urinary vasopressin excretion decreased from 6.7 +/- 1.0 ng/hr (control) to 3.9 +/- 0.3 ng/hr (p less than 0.01) when sodium excretion decreased from 188 +/ 18 to 16 +/- 2 mmol/24 hr. During the first day of high sodium intake, the urinary vasopressin excretion increased to 10.0 +/- 1.2 ng/hr (p less than 0.01) compared with control and remained high throughout the sodium repletion. Through all collection periods at low, normal, and high sodium intake, vasopressin excretion increased concomitantly with serum sodium concentration and osmolality. After low sodium intake for 7 days, the serum vasopressin concentration averaged 2.7 +/- 0.6 ng/l, and this level was maintained throughout the sodium repletion period. These results are compatible with a stimulatory effect of dietary sodium intake on pituitary vasopressin secretion in man. Dietary sodium may stimulate vasopressin secretion through extracellular osmolality or even by a direct effect of extracellular sodium on periventricular receptors. Plasma renin concentrations or sympathetic nervous activity offered no further explanations. Urinary vasopressin excretion provides more useful information than do plasma concentrations, as the latter can fluctuate rapidly.

Self-poisoning and moon phases in Oslo.

During 1980 the relation between the moon phases and 1187 cases of self-poisonings in Oslo was studied. In contrast to a previous report from India no significant correlation was found between the full moon and self-poisoning. The aetiology of self-poisonings in western countries is rather more complex than to be explained by speculative 'human tidal waves'.

Serum phosphate and sympathetic tone in mild essential hypertension.

Forty-year old, normocalcaemic men with mild essential hypertension (n = 35) had decreased serum phosphate (p less than 0.001) concomitant with elevated plasma adrenaline (p less than 0.03) and heart rate (p less than 0.001). All had unchanged serum immunoreactive parathyroid hormone concentrations compared to age-matched normotensive control men (n = 44). Serum phosphate levels correlated negatively with plasma adrenaline (p less than 0.05), plasma noradrenaline (p less than 0.05), mean blood pressure (p less than 0.001) and heart rate (p less than 0.05). Serum phosphate was significantly lowered by infusion of small amounts of adrenaline at all four infusion rates in a hypertensive group (n = 12) while a similar effect was obtained only at the two highest infusion rates in a normotensive group (n = 10). No change in serum calcium was observed in either group. Thus, hypophosphataemia appears to be inversely related to sympathetic tone in essential hypertension.