Mean Plasma Potassium Concentration Research Articles

Phenotypic and genotypic characteristics of children with Bartter syndrome.

Bartter syndrome (BS) is a group of autosomal-recessive tubular disorders and it is classified into five genetic subtypes. BS can also be classified by phenotype (antenatal, classic). Patients with mutations in the same gene can present different phenotypes. In the present study, target gene sequencing was performed to evaluate the genotype-phenotype relationship. Biochemical, clinical and renal ultrasonography results were collected at presentation and the last clinic visit. Genetic analyses were performed. The findings of patients with classical BS (cBS) and antenatal BS (aBS) at presentation and the last visit were compared. Our study included 21 patients (12 female, 57.1%) from 20 families with BS. The median age at diagnosis was 8 months and the median follow-up period was 39 months. The most frequent complaint was growth failure. We have found 18 different types of mutations in four genes, including nine in the CLCNKB gene, seven in the SLCA12A1 gene, one in the KCNJ1 gene and one in the BSND gene. In ten patients, nine different types of CLCNKB gene mutations were detected, five of them were novel. Seven different mutations in the SLC12A1 gene were detected in eight patients, five of them were novel. Compared to patients with aBS and cBS, prematurity was significantly higher in the group with aBS. Nephrocalcinosis was present in only one patient with cBS, all the ten hypercalciuric patients with aBS had nephrocalcinosis at the time of diagnosis and the last visit. The mean height standard deviation score (SDS) of patients with aBS were significantly lower than the cBS group at the time of presentation. The mean weight SDS at the time of presentation was worse in patients with aBS than in patients with cBS. The mean plasma potassium and chloride concentrations were significantly lower in the patients with cBS at the time of diagnosis. This investigation revealed the mutation characteristics and phenotype-genotype relationship of our patients and provided valuable data for genetic counseling.

No change in plasma potassium concentration during 10minutes of apnoea: An observational study on potential organ donors.

Acute acidosis can increase the plasma potassium concentration. However, data on the effects of acute respiratory acidosis on plasma potassium concentration are conflicting. This study aimed to determine whether acute respiratory acidosis induces an immediate increase in plasma potassium concentration. This observational study was conducted on participants undergoing apnoea testing prior to final radiological examination, registered in an internal quality registry at Oslo University Hospital between 25 April 2013 and 1 May 2020. A total of 124 donors were assessed for inclusion. Sixteen donors with blood glucose concentrations exceeding 10mmolL-1 were excluded; finally, data from 108 donors were included in the study. The apnoea test, which is a standard neurological test performed in potential organ donors prior to radiological confirmation of ceased brain circulation, induces respiratory acidosis. The arterial plasma potassium concentration, pH and PaCO2 before and after the apnoea test were compared. Statistical analysis was conducted using the paired t test. The pre-apnoea and post-apnoea mean plasma potassium concentrations were 3.79 (95% confidence intervals [CI] 3.70-3.87) and 3.79mmolL-1 (95% CI 3.70-3.88), respectively. The mean difference was -0.002mmolL-1 (95% CI -0.04 to 0.04); the difference was not significant. The pre-apnoea and post-apnoea mean pH were 7.39 and 7.21, respectively, and the mean difference was 0.175 (P<.01). The pre-apnoea and post-apnoea mean PaCO2 were 5.66 and 9.48kPa, respectively, and the mean difference was -3.83 (P<.01). Acute respiratory acidosis does not lead to rapid changes in plasma potassium concentration during apnoea testing in potential organ donors.

THE EFFECT OF SPIRONOLACTONE VERSUS TORSEMIDE ON BLOOD PRESSURE TARGETS IN RESISTANT HYPERTENSION PATIENTS

Objective: to evaluate effects on blood pressure (BP) control in two treatment options spironolactone (SPIR) versus torsemide (TOR) as an add-on therapy in resistant hypertensive (RAH) patients. Design and method: We studied 78 patients with true RAH confirmed by the office and ambulatory BP monitoring (ABPM). Patients were randomized into 2 groups through 12 weeks of once daily treatment with of SPIR (25–50 mg) or TOR (5–10 mg) in addition to their baseline triple-combination and then rotated with drugs. BP was measured in the office and by ABPM. Changes in laboratory tests were also studied. The predictive values of plasma aldosterone, active renin concentration (ARC) and aldosterone-renin ratio (ARR), serum potassium, 24-h urinary excretion sodium of determining the antihypertensive response were analyzed. Results: There were no significant differences on the reduction of average office BP and average nighttime BP by SPIR and TOR. SPIR reduced average systolic 24-h BP by 11.7 mmHg and average systolic daytime BP by 12.2 mmHg compared with a reduction of 8.9 mmHg (P < 0.05) and 9.1 mmHg (P < 0.05) with TOR, respectively. Overall, 36.8 % RAH patients achieved targets of clinical BP and 24-h ABPM levels on SPIR and 30.9 % on TOR. After 12 weeks of treatment mean plasma potassium concentrations increased from 4.3 to 4.7 mmol/L (P < 0.0001) on SPIR but did not significant change on TOR. Serum potassium (β = −0.441, P < 0.05), 24-h urinary excretion sodium (β = 0.432, P < 0.05) and ARR (β = 0.543, P < 0.03) were predictors of BP-lowering effect of SPIR and plasma aldosterone (β = −0.680, P < 0.001), ARC (β = 0.463, P < 0.03) were predictors of reduction BP for TOR in multivariate modeling. Conclusions: Greater antihypertensive effect of SPIR is related to aldosterone status, urinary sodium excretion and serum potassium level in resistant hypertension. TOR may be suited for RAH patients that have high ARC and in people with lower sodium intake or high serum potassium level.

Neuromuscular blockade of atracurium in permissive hypercapnic versus normocapnic swine undergoing laparoscopy.

Neuromuscular blocking agents (NMBAs) are commonly used in experimental laparoscopy in swine undergoing carbon dioxide pneumoperitoneum. Hypercapnia may be present and may prolong NMBAs’ pharmacologic activity. The aim of this study is to evaluate the effect of permissive hypercapnia on the neuromuscular blockade of atracurium in swine. Six Large White swine weighing 30.5 ± 1.6 kg were sedated with intramuscular ketamine and medetomidine, after which anaesthesia was induced with propofol and maintained with sevoflurane. Atracurium 0.4 mg/kg was administered intravenously and the neuromuscular block monitored by acceleromyography during normocapnic and hypercapnic conditions (PaCO2 range 35–45 mmHg and 60–70 mmHg, respectively). Onset time and time to reach a train of four ratio (TOFR) of 0.7 and 0.9 were recorded. Cardiorespiratory parameters, electrolytes and acid-base status were measured under both conditions. Onset time was similar between the two conditions. Time to reach a TOFR of 0.7 and 0.9 (duration of the neuromuscular block) was longer in hypercapnic compared to normocapnic animals being 1325 ± 300 vs 855 ±111 (p = 0.002) and 1823 ± 434 vs 1218 ± 210 seconds (p = 0.005), respectively. Three hypercapnic swine had a TOF count of 2 and 1 instead of a count of 4 with fade. Permissive hypercapnia was associated with a decrease in pH from 7.444 ± 0.039 to 7.257 ± 0.025 (p < 0.001). No differences were observed for heart rate, end-tidal concentration of sevoflurane, body temperature and arterial haemoglobin saturation. Nonetheless, hypercapnic swine had a statistically significant increase in mean arterial pressure (p = 0.020) and plasma potassium concentration (p = 0.003). The values of PaCO2 achieved during hypercapnia were well tolerated in swine undergoing CO2 pneumoperitoneum for laparoscopy. Permissive hypercapnia increased the duration of the atracurium effect and caused an increase in the intensity of the neuromuscular block in few swine.

Endocrine and haemodynamic changes in resistant hypertension, and blood pressure responses to spironolactone or amiloride: the PATHWAY-2 mechanisms substudies

SummaryBackgroundIn the PATHWAY-2 study of resistant hypertension, spironolactone reduced blood pressure substantially more than conventional antihypertensive drugs. We did three substudies to assess the mechanisms underlying this superiority and the pathogenesis of resistant hypertension.MethodsPATHWAY-2 was a randomised, double-blind crossover trial done at 14 UK primary and secondary care sites in 314 patients with resistant hypertension. Patients were given 12 weeks of once daily treatment with each of placebo, spironolactone 25–50 mg, bisoprolol 5–10 mg, and doxazosin 4–8 mg and the change in home systolic blood pressure was assessed as the primary outcome. In our three substudies, we assessed plasma aldosterone, renin, and aldosterone-to-renin ratio (ARR) as predictors of home systolic blood pressure, and estimated prevalence of primary aldosteronism (substudy 1); assessed the effects of each drug in terms of thoracic fluid index, cardiac index, stroke index, and systemic vascular resistance at seven sites with haemodynamic monitoring facilities (substudy 2); and assessed the effect of amiloride 10–20 mg once daily on clinic systolic blood pressure during an optional 6–12 week open-label runout phase (substudy 3). The PATHWAY-2 trial is registered with EudraCT, number 2008–007149–30, and ClinicalTrials.gov, number NCT02369081.FindingsOf the 314 patients in PATHWAY-2, 269 participated in one or more of the three substudies: 126 in substudy 1, 226 in substudy 2, and 146 in substudy 3. Home systolic blood pressure reduction by spironolactone was predicted by ARR (r2=0·13, p<0·0001) and plasma renin (r2=0·11, p=0·00024). 42 patients had low renin concentrations (predefined as the lowest tertile of plasma renin), of which 31 had a plasma aldosterone concentration greater than the mean value for all 126 patients (250 pmol/L). Thus, 31 (25% [95% CI 17–33]) of 126 patients were deemed to have inappropriately high aldosterone concentrations. Thoracic fluid content was reduced by 6·8% from baseline (95% CI 4·0 to 8·8; p<0·0001) with spironolactone, but not other treatments. Amiloride (10 mg once daily) reduced clinic systolic blood pressure by 20·4 mm Hg (95% CI 18·3–22·5), compared with a reduction of 18·3 mm Hg (16·2–20·5) with spironolactone (25 mg once daily). No serious adverse events were recorded, and adverse symptoms were not systematically recorded after the end of the double-blind treatment. Mean plasma potassium concentrations increased from 4·02 mmol/L (95% CI 3·95–4·08) on placebo to 4·50 (4·44–4·57) on amiloride (p<0·0001).InterpretationOur results suggest that resistant hypertension is commonly a salt-retaining state, most likely due to inappropriate aldosterone secretion. Mineralocorticoid receptor blockade by spironolactone overcomes the salt retention and resistance of hypertension to treatment. Amiloride seems to be as effective an antihypertensive as spironolactone, offering a substitute treatment for resistant hypertension.FundingBritish Heart Foundation and UK National Institute for Health Research.

Selected clinical, biochemical, and electrolyte alterations in anesthetized captive tigers (Panthera tigris) and lions (Panthera leo).

A prospective study to assess changes in selected plasma biochemistry and electrolyte values, plasma insulin and aldosterone concentrations, and electrocardiography (ECG) was performed on eight female captive tigers (Panthera tigris) and three lions (Panthera leo) undergoing general anesthesia for elective laparoscopic ovariectomy. Each animal was sedated with medetomidine (18-25 microg/kg) and midazolam (0.06-0.1 mg/kg) intramuscularly, and anesthesia was induced with ketamine (1.9-3.5 mg/kg) intramuscularly and maintained with isoflurane. Venous blood samples were collected and analyzed for plasma biochemistry parameters and insulin and aldosterone concentrations. An ECG was recorded at the time of each blood sample collection. Mean plasma potassium, glucose, phosphorus, and aldosterone concentrations increased during anesthesia (P < or = 0.05). One tiger developed hyperkalemia (6.5 mmol/L) 2.5 hr after anesthetic induction. Plasma insulin concentrations were initially below the low end of the domestic cat reference interval (72-583 pmol/L), but mean insulin concentration increased (P < or = 0.05) over time compared with the baseline values. Three tigers and two lions had ECG changes that were representative of myocardial hypoxemia. Based on these results, continuous monitoring of clinical and biochemical alterations during general anesthesia in large nondomestic felids is warranted, and consideration should be given to reversal of medetomidine in these animals should significant changes in electrolytes or ECG occur.

Plasma Potassium Concentration Changes Associated with Trimethoprim used for Urinary Tract Infections

ABSTRACTBackgroundHyperkalaemia has been reported with high‐dose trimethoprim (20 mg/kg/day) and standard‐dose trimethoprim (6 mg/kg/day) plus sulfamethoxazole use.AimTo investigate changes in plasma potassium concentrations in patients prescribed standard‐dose trimethoprim 300 mg daily for urinary tract infections.MethodA retrospective cohort study of hospital patients with urinary tract infections treated with trimethoprim or other antibacterials (control group) for more than 5 days. Plasma potassium concentration, creatinine and urea were compared at baseline and at the completion of treatment.ResultsThere were 31 patients in the trimethoprim group and 65 patients in the control group. End–of–therapy mean plasma potassium concentrations increased significantly from baseline in the trimethoprim group (4.2 ± 0.4 mmol/L to 4.5 ± 0.5 mmol/L; p = 0.002) but not in the control group. End–of–therapy mean plasma potassium concentrations were also higher in the trimethoprim group (4.5 ± 0.5 mmol/L vs 4.2 ± 0.5 mmol/L; p = 0.007). 65% of the trimethoprim group developed end–of–therapy hyperkalaemia versus 39% of the control group. Mean creatinine concentration in the trimethoprim group increased by an average of 21% from baseline but did not change in the control group. The trimethoprim group showed no change in mean urea concentration but a decrease was noted in the control group.ConclusionTreating urinary tract infections with trimethoprim 300 mg daily for more than 5 days was associated with an increase in plasma potassium concentration.

Potassium Depletion and Diastolic Dysfunction

Changes in extracellular potassium concentration affect nearly all aspects of myocardial function. Reductions in potassium concentration alter the resting membrane potential, membrane conductance for sodium and potassium, repolarization time, relative refractory time, and conduction velocity. The arrhythmogenic consequences of these effects of potassium depletion are well recognized by the medical community. However, the potential influence of hypokalemia on mechanical function of the heart has not been as thoroughly appreciated. More than 10 years ago, Fitzovich et al1,2 analyzed changes in left ventricular mechanical function of dogs who were either potassium replete or moderately depleted as a result of 7 days of low-potassium intake together with a high-sodium intake and thiazide diuretics. The depleted dogs had a mean plasma potassium concentration of 3.2 mmol/L. The investigators observed in the depleted dogs significant impairment of both systolic and diastolic function, with the most striking effect noted in peak rate of ventricular filling, reduced by &49% during acute elevation of preload. The same group extended the study to normal volunteers age 22 to 30 years whose cardiac mechanical function was studied noninvasively by echo and Doppler techniques.2,3 Compared with the potassium replete state, during potassium depletion (plasma potassium reduced by 1.0 mmol/L), the peak rate of ventricular filling was …

Effects of dexamethasone and isoflupredone acetate on plasma potassium concentrations and other biochemical measurements in dairy cows in early lactation

To determine whether administration of isoflupredone acetate (ISO) to healthy cows increases the frequency of severe hypokalemia and whether dexamethasone (DEX) has detectable mineralocorticoid properties. 33 cows at 20 to 25 days of lactation. Cows were randomly allocated to 5 treatment groups and received 2 IM injections (on days 0 and 2) of sterile saline (0.9% NaCl) solution (10 mL each), an injection of ISO (20 mg) or DEX (20 mg) followed by 10 mL of saline solution, or 2 injections of ISO or DEX. Milk production was measured, physical examinations were performed, and blood and urine samples were collected daily on days 0 through 7. Physical examination parameters did not differ among groups; however, 1 cow developed atrial fibrillation on day 4. Both corticosteroids significantly increased plasma glucose concentrations, and ISO significantly decreased plasma potassium concentrations and increased total carbon dioxide concentrations with time. One dose of ISO decreased mean plasma potassium concentration by 25% on day 2, compared with day 0, and severe hypokalemia (serum potassium concentration < 2.3 mEq/L) developed in 1 of 6 cows. Mean plasma potassium concentration was 46% lower on day 3 than on day 0 in cows receiving 2 doses of ISO, and 5 of 7 cows became severely hypokalemic. Mean urinary fractional excretion of potassium significantly increased from that on day 0 in cows receiving 2 doses of ISO. Both corticosteroids had glucocorticoid activity; however, only ISO had mineralocorticoid activity. Compared with saline solution, administration of 2 doses of ISO significantly increased the frequency of severe hypokalemia.

Iatrogenic hypocalcaemia during parenteral fluid therapy of diarrhoeic calves

Acid-base balance and electrolyte concentrations, including ionised calcium, were monitored during intravenous fluid therapy of 1 1 collapsed diarrhoeic suckler calves aged five to 10 days. Six healthy calves of...

Use of indapamide in hospital and community clinics and its effect on plasma potassium in Chinese patients.

To investigate the usage pattern of indapamide and other antihypertensive drugs in patients attending a community-based government outpatient clinic (GOPC) or a hospital-based specialist clinic (SC). The plasma potassium concentrations of patients receiving indapamide and other diuretics were also examined. Prescriptions from the SC and the GOPC were reviewed and collected during January 1998. Patients' plasma potassium concentrations and the date of initiation of each medication were retrieved from the hospital computer databases at SC. An age- and sex-matched control group of patients on non-diuretic antihypertensive drugs was identified. A total of 1648 and 773 prescriptions were collected from the SC during a 1-week period and GOPC during a 1-month period, respectively. Approximately half (45%) of the patients received antihypertensive treatment. Indapamide was five times more frequently prescribed in GOPC than SC (84.7 vs. 17.7%, P<0.001). Calcium channel blocking agents were the commonest antihypertensive drugs used in both clinics. The mean plasma potassium concentration of patients taking indapamide was lower than that of the control group (P = 0.037). Multiple linear regression analysis showed that consumption of indapamide (P =0.002) and duration of diuretic therapy (P = 0.023) were significantly related to changes in plasma potassium concentrations [multiple regression equation for potassium level = 4.09-0.145 (thiazide = 1)-0.377 (indapamide = 1) -0.00468 (duration of diuretic therapy in months)]. Indapamide was used extensively in the community clinic and less in the hospital-based outpatient clinic. Patients receiving indapamide had a significantly lower plasma potassium concentration as compared to other diuretics or antihypertensive groups and this was predicted by a multiple linear regression model. Monitoring plasma electrolytes before initiation of indapamide treatment and at regular intervals thereafter is essential for detecting the hypokalaemia that may occur in Chinese patients.

Hypokalaemia related to acute chloroquine ingestion

Summary Large doses of chloroquine can cause poisoning. Our aim was to determine the possible relation between the plasma potassium concentration on admission with the severity of acute chloroquine poisoning and to assess the mechanism of chloroquine-induced hypokalaemia. We conducted a retrospective study of 191 consecutive cases. The main data included the occurrence of vomiting before admission, plasma, and urinary potassium concentration at admission, whole blood chloroquine concentration on admission, haemodynamic parameters and ECG, administration of catecholamines and outcome. Mean blood chloroquine level was 20·1 μmol/L (SD 14·3) (therapeutic level ≤6 μmol/L). Mean plasma potassium concentration was 3·0 mmol/L (0·8) and was lower in the subjects who died than in those who survived (p=0·0003). Plasma potassium varied directly with the systolic blood pressure and inversely with the QRS and QT. Plasma potassium varied inversely with the blood chloroquine (p=0·0001; τ=-0·42). Acute chloroquine intoxication is responsible for a hypokalaemia which correlates with the gravity of the intoxication and may be due to a transport-dependent mechanism. Plasma potassium concentrations should be carefully observed, particularly among patients who also receive catecholamine infusions. We should keep in mind, however, that overzealous repletion invokes the risk of subsequent hyperkalaemia and thus should be avoided.

Treatment of hyperkalemia in children with intravenous salbutamol

The aim of this study is to investigate the efficacy and safety of intravenous salbutamol in hyperkalemia. Fourteen children with chronic renal failure, three with acute renal failure and hyperkalemia were treated by intravenous infusions of 4 micrograms/kg salbutamol. Reductions in the mean plasma potassium (K+) concentrations obtained at 40 to 120 min after therapy were statistically significant when compared with the mean plasma K+ concentration at the beginning of therapy (P < 0.01).

Adrenocortical function in neonatal and weanling Beagle pups

Abstract Adrenocortical function was assessed in 27 Beagle pups at 2, 4, 6, 8, 10, and 12 weeks of age by determination of plasma sodium, potassium, and chloride concentrations; serum aldosterone and cortisol concentrations; and plasma ACTH concentrations. Serum cortisol concentration was measured before and 1 and 2 hours after IM administration of 2.2 IU of acth/kg of body weight. Serum progesterone concentration also was determined for all pups at 2, 4, and 6 weeks of age. Mean baseline cortisol concentration was lower for pups 8 weeks old or younger than for mature dogs. Nevertheless, mean serum ACIH-stimulated cortisol concentration in dogs of all age groups increased into the adult reference range after administration of acth. For pups 4 weeks old or younger, increase in cortisol concentration was maximal at 2 hours after acth administration. However, in pups between 6 and 12 weeks of age, the increase in cortisol concentration was maximal 1 hour after acth administration in about a third of the pups, whereas the remaining pups had peak values at 2 hours. Mean plasma sodium, potassium, and chloride concentrations for each age group were within the reference ranges established for mature dogs, with the exception of lower mean plasma sodium and chloride concentrations in pups 4 weeks old or younger. Mean serum aldosterone concentration in pups of each age group was substantially higher than the range of aldosterone concentrations for clinically normal mature dogs. Median progesterone concentration was uniformly less than 0.2 ng/ml for all pups 6 weeks old or younger. The normal endogenous acth concentration and adequate cortisol responses to exogenous acth seen in our pups would support functional pituitary gland and adrenal cortex for cortisol production. The low baseline cortisol concentration observed in the pups of this study may be related to reduced binding of cortisol to plasma proteins, as exists in human infants. The hyponatremia and increased aldosterone concentration may be explained by reduced renal tubular response to aldosterone, as also evidenced in the human infant kidney.

Weight, water, and cation losses in horses competing in a three-day event

Summary Body weight of 48 horses competing in a 3-day event was measured the day before the event (baseline), following the dressage phase of the event (day 1), after the endurance phases of the event (day 2), and 18 to 24 hours after the endurance phases (day 3). Plasma sodium and potassium concentrations were measured the evening before, immediately after, and 10 minutes after the endurance phases. Total body water, water loss, and net exchangeable cation loss were then calculated. Body weight and total body water were significantly decreased, compared with baseline values, at all times during the event, and significant water loss was detected. The largest changes were recorded after the endurance phases of the event. Water deficits were still detected 18 to 24 hours after the endurance phases of the event. Mean plasma sodium concentration was significantly increased immediately after the endurance phases of the event, compared with concentration measured the evening before, and remained increased after the 10-minute recovery period, presumably because of dehydration. Mean plasma potassium concentration was significantly increased immediately after the endurance phases of the event, compared with concentration measured the evening before, but was not increased after the 10-minute recovery period.

Treatment of hyperkalaemia using intravenous and nebulised salbutamol.

In 11 children (aged 5-18 years) with end stage chronic renal failure, the effect on plasma potassium of two doses of salbutamol (separated by two hours) given intravenously (4 micrograms/kg) and on a separate date, of salbutamol administered by nebuliser (2.5 mg if the child weighed below 25 kg, 5 mg if above) was observed. Within 30 minutes of the first dose, the mean plasma potassium concentration fell significantly by 0.87 and 0.61 mmol/l after intravenous and nebulised administration respectively. Sixty minutes after the second dose the plasma potassium was significantly reduced by a further 0.28 and 0.53 mmol/l respectively. There was a significant difference between the two methods of administration at 300 minutes after the first dose favouring nebulisation. No major side effects were observed. Nebulised salbutamol should be the first choice emergency treatment of hyperkalaemia.

Treatment of hyperkalaemia with intravenous salbutamol.

Thirteen children with hyperkalaemia were treated by intravenous infusions of salbutamol, 4 micrograms/kg over 20 minutes. Reductions in the mean (SD) plasma potassium concentrations, of 1.48 (0.5) and 1.64 (0.5) mmol/l were obtained at 40 and 120 minutes, respectively, after completion of the infusions. No side effects were noted.

Effects of cilazapril on renal function and hormones in hypertensive patients with renal disease

The effects of cilazapril 2.5 to 5.0 mg every 24 hours orally for one month on blood pressure, renal hemodynamics, and plasma and urinary hormones were investigated in 11 patients with renal disease and hypertension. Six patients had renal failure (pretreatment creatinine clearance of less than 1 ml/second). Both systolic and diastolic blood pressures were significantly decreased in all patients and seven of the 11 required 5.0 mg daily. There was no significant change in the effective renal plasma flow, glomerular filtration rate, or creatinine clearance, although the renal vascular resistance was significantly reduced. Albuminuria was reduced in most patients but the mean change was not significant. The mean plasma potassium concentration rose significantly, but no changes in electrolyte excretion or weight were noted. Mean ambulant plasma renin activity was normal before treatment and rose significantly. Mean ambulant angiotensin II concentrations did not change. Mean ambulant plasma aldosterone concentration and mean urinary aldosterone excretion decreased significantly. Plasma arginine vasopressin and cortisol concentrations did not change. No changes were noted in plasma glucose concentrations, liver function tests, hemoglobin concentrations, or white blood cell or platelet counts. A slight looseness of bowel motions occurred in two patients and was the only side effect recorded. Cilazapril appears to be an effective and safe antihypertensive drug in patients with hypertension and renal disease.

Effects of cilazapril on renal function and hormones in hypertensive patients with renal disease*1

The effects of cilazapril 2.5 to 5.0 mg every 24 hours orally for one month on blood pressure, renal hemodynamics, and plasma and urinary hormones were investigated in 11 patients with renal disease and hypertension. Six patients had renal failure (pretreatment creatinine clearance of less than 1 ml/second). Both systolic and diastolic blood pressures were significantly decreased in all patients and seven of the 11 required 5.0 mg daily. There was no significant change in the effective renal plasma flow, glomerular filtration rate, or creatinine clearance, although the renal vascular resistance was significantly reduced. Albuminuria was reduced in most patients but the mean change was not significant. The mean plasma potassium concentration rose significantly, but no changes in electrolyte excretion or weight were noted. Mean ambulant plasma renin activity was normal before treatment and rose significantly. Mean ambulant angiotensin II concentrations did not change. Mean ambulant plasma aldosterone concentration and mean urinary aldosterone excretion decreased significantly. Plasma arginine vasopressin and cortisol concentrations did not change. No changes were noted in plasma glucose concentrations, liver function tests, hemoglobin concentrations, or white blood cell or platelet counts. A slight looseness of bowel motions occurred in two patients and was the only side effect recorded. Cilazapril appears to be an effective and safe antihypertensive drug in patients with hypertension and renal disease.

Effect of glucose intake on human leucocyte 86Rb influx and [ 3H]-ouabain binding

86Rb influx and [ 3H] ouabain binding by human leucocytes were measured in eight normal nonobese fasting subjects before and after a challenge with 75 g glucose orally. The mean ouabain-sensitive 86Rb influx increased significantly from 194 to 283 mmol/kg protein/h ( P < .01), and [ 3H]-ouabain binding increased from 236 to 403 fmol/mg protein. The mean plasma potassium concentration fell from 4.2 to 3.9 mmol/L ( P < .05). Following intravenous glucose infusion, the median 86Rb transport increased from 186 to 267 mmol/kg protein/h, while median plasma potassium concentration fell from 4.3 to 3.9 mmol/L. Therefore, glucose intake acutely increases Na-K ATPase units, stimulates potassium (Rb) transport, and causes a concomitant fall in plasma potassium concentrations. Nutritional intake is probably an important determinant of Na-K ATPase units and activity in the human leucocyte.