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We characterized mouse blood pressure and ion transport in the setting of commonly used rodent diets that drive K + intake to the extremes of deficiency and excess. Male 129S2/Sv mice were fed either K + -deficient, control, high-K + basic, or high-KCl diets for 10 days. Mice maintained on a K + -deficient diet exhibited no change in blood pressure, whereas K + -loaded mice developed an ~10-mmHg blood pressure increase. Following challenge with NaCl, K + -deficient mice developed a salt-sensitive 8 mmHg increase in blood pressure, whereas blood pressure was unchanged in mice fed high-K + diets. Notably, 10 days of K + depletion induced diabetes insipidus and upregulation of phosphorylated NaCl cotransporter, proximal Na + transporters, and pendrin, likely contributing to the K + -deficient NaCl sensitivity. While the anionic content with high-K + diets had distinct effects on transporter expression along the nephron, both K + basic and KCl diets had a similar increase in blood pressure. The blood pressure elevation on high-K + diets correlated with increased Na + -K + -2Cl - cotransporter and γ-epithelial Na + channel expression and increased urinary response to furosemide and amiloride. We conclude that the dietary K + maneuvers used here did not recapitulate the inverse effects of K + on blood pressure observed in human epidemiological studies. This may be due to the extreme degree of K + stress, the low-Na + -to-K + ratio, the duration of treatment, and the development of other coinciding events, such as diabetes insipidus. These factors must be taken into consideration when studying the physiological effects of dietary K + loading and depletion.

Introduction Diabetic ketoacidosis is a life-threatening condition that requires prompt management. Objectives We aimed to assess the impact of adherence to potassium replacement protocol according to the guidelines of Diabetes Poland on the duration of diabetic ketoacidosis (DKA) treatment. Patients and methods This retrospective analysis included 242 adults (median age, 27 years; range, 21-38 years). Nonadherence to potassium replacement protocol was assessed, along with the relationship between nonadherence and duration of DKA management. Nonadherence to the protocol was defined as too low or too high doses of potassium compared with the recommended potassium replacement protocol. Results The median duration of DKA treatment was longer in the nonadherent group than in the adherent group: 37 hours (interquartile range [IQR], 27-48) and 30 hours (IQR, 17-43), respectively (P = 0.005). Treatment duration correlated positively with nonadherence to potassium replacement protocol (r = 0.18; P = 0.005) and severity of DKA (r = 0.52; P <0.0001). Stepwise multivariate linear regression analysis indicated nonadherence to the protocol (β = 0.14; P = 0.02) and severity of DKA (β = 0.43; P <0.0001) as predictors of treatment duration, after adjustment for body mass index and age (R2 = 0.28; P <0.0001). Conclusions Nonadherence to potassium replacement protocol leads to prolongation of DKA management. Medical staff should be educated about the benefits of potassium replacement and precision in potassium administration and dosing in patients with DKA.

Acute stressor states are linked to neurohormonal activation that includes the adrenergic nervous system. Elevations in circulating epinephrine and norepinephrine unmask an interdependency that exists between K + and Mg 2+ based on their regulation of a large number of Mg 2+ -dependent Na + -K + -ATPase pumps present in skeletal muscle. The hyperadrenergic state accounts for a sudden translocation of cations into muscle with the rapid appearance of hypokalemia and hypomagnesemia. The resultant hypokalemia and hypomagnesemia will cause a delay in myocardial repolarization and electrocardiographic QTc prolongation raising the propensity for supraventricular and ventricular arrhythmias. In this review, we focus on the interdependency between K + and Mg 2+ , which is clinically relevant to acute hyperadrenergic stressor states found in patients admitted to intensive care units., (Copyright © 2017 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

The aim of this study was to determine the intake and food sources of potassium and the molar sodium:potassium (Na:K) ratio in a sample of Australian pre-school children. Mothers provided dietary recalls of their 3.5 years old children (previous participants of Melbourne Infant Feeding Activity and Nutrition Trial). The average daily potassium intake, the contribution of food groups to daily potassium intake, the Na:K ratio, and daily serves of fruit, dairy, and vegetables, were assessed via three unscheduled 24 h dietary recalls. The sample included 251 Australian children (125 male), mean age 3.5 (0.19) (SD) years. Mean potassium intake was 1618 (267) mg/day, the Na:K ratio was 1.47 (0.5) and 54% of children did not meet the Australian recommended adequate intake (AI) of 2000 mg/day for potassium. Main food sources of potassium were milk (27%), fruit (19%), and vegetable (14%) products/dishes. Food groups with the highest Na:K ratio were processed meats (7.8), white bread/rolls (6.0), and savoury sauces and condiments (5.4). Children had a mean intake of 1.4 (0.75) serves of fruit, 1.4 (0.72) dairy, and 0.52 (0.32) serves of vegetables per day. The majority of children had potassium intakes below the recommended AI. The Na:K ratio exceeded the recommended level of 1 and the average intake of vegetables was 2 serves/day below the recommended 2.5 serves/day and only 20% of recommended intake. An increase in vegetable consumption in pre-school children is recommended to increase dietary potassium and has the potential to decrease the Na:K ratio which is likely to have long-term health benefits.

This study investigated the effect of the sodium to potassium ratio on hypertension prevalence and blood pressure. The study population was constructed by pooling the Korean National Health and Nutrition Examination Surveys between 2010 and 2014. The study population was divided into quartiles based on the sodium to potassium ratio, and the effect was inferred by the difference in hypertension prevalence across quartiles by six pairwise comparisons using a propensity score matching technique. The quartiles with the higher sodium to potassium ratio had higher hypertension prevalence rates based on the following pairwise comparisons: the first vs. third quartile, the first vs. fourth quartile, the second vs. third quartile, and the second vs. fourth quartile. The prevalence differences were 2.74% point (p < 0.05), 3.44% point (p < 0.01), 2.47% point (p < 0.05), and 2.95% point (p < 0.01), respectively. In addition, statistically significant higher systolic (p < 0.05) and diastolic blood pressure (p < 0.01) was observed in the second quartiles compared to the first quartiles. Because a strong association was also detected between the sodium to potassium ratio and blood pressure even at a low level of sodium to potassium ratio, a lower sodium to potassium ratio diet than a usual diet is recommended to control high blood pressure in Korea.

The need to create a stoma is frequent in the daily clinical practice. Usually ileostomies work well within the first 24 hours. However, many times they are associated with important morbidity up to 76%. Although the complications derived from this technique may be surgical, metabolic complications, which are preceded by large losses through the stoma, are the ones going undetected. It is not rare to see patients carrying an ileostomy that come repeatedly to the hospital with severe metabolic impairments and in whom the underlying cause remains untreated. The case reported herein is just one of a series published in this journal making us aware of the need for a multidisciplinary approach of the ileostomies and the prevention of major complications derived from their poor functioning.

After confirming the high prevalence rates in our hemodialysis unit of the following nursing diagnoses: nutritional imbalances--both excesses and shortages, willingness to improve nutrition and fear related to the consequences of excessive intake of potassium and manifested by the inhibition in some people towards the enjoyment of food, we decided to plan an educational strategy which later resulted in a nursing intervention for these diagnoses, with the objective of providing adequate resources for the monitoring of balanced diets with a restriction of potassium. Inspired by dietary rations, as well as recognized dietary programs of learning by points, we decided to incorporate these ideas to design an educational tool to facilitate advice to our patients on how to follow diet plans as well as the choice of appropriate foods. The result was a set of cards incorporating nutritional information of various kinds, aimed at our patients covering different aspects of the diet appropriate food rations using household measurements, promoting good food preparation, appropriate dietary advice for different chronic diseases and a scoring system of foods according to their potassium content. Together they form a board game available during the hemodialysis sessions that also takes into consideration other issues of importance related to conditions such as cognitive stimulation, coping with the disease, improving the therapeutic performance or resources to increase patient motivation. Although initially it was only an educational exercise, the result has turned out to be both enjoyable and entertaining.

A 39-year-old woman with an unremarkable history presented to the emergency department with three episodes of collapse. Each episode was witnessed by her son who described a loss of consciousness followed by rapid and complete recovery. The patient appeared well and examination was unremarkable. Her ECG showed a marked QTc prolongation of 642 ms (normal <470 ms) and low serum potassium at 1.8 mmol/l (3.5-5.3 mmol/l). The patient was moved to the coronary care unit and started on potassium replacement. On the ward a thorough history was taken and the patient confessed to being very conscious about his body shape and weight and admitted to episodes of binge eating and self induced vomiting. Her history suggested bulimia nervosa which is known to cause electrolyte disturbances and cardiac arrhythmia. Over the following 2 days the patient's potassium increased and the QTc interval normalised; the patient was discharged with an outpatient referral for a psychiatric opinion.

Kidneys produce ammonium to buffer and excrete acids through metabolism of glutamine. Expression of the glutamine transporter Slc38a3 (SNAT3) increases in kidney during metabolic acidosis (MA), suggesting a role during ammoniagenesis. Potassium depletion and high dietary protein intake are known to elevate renal ammonium excretion. In this study, we examined SNAT3, phosphate-dependent glutaminase (PDG), and phosphoenolpyruvate carboxykinase (PEPCK) regulation during a control (0.36%) or low-K(+) (0.02%) diet for 7 or 14 days or a control (20%) or high-protein (50%) diet for 7 days. MA was induced in control and low-K(+) groups by addition of NH(4)Cl. Urinary ammonium excretion increased during MA, after 14-day K(+) restriction alone, and during high protein intake. SNAT3, PDG, and PEPCK mRNA abundance were elevated during MA and after 14-day K(+) restriction but not during high protein intake. SNAT3 protein abundance was enhanced during MA (both control and low K(+)), after 14-day low-K(+) treatment alone, and during high protein intake. Seven-day dietary K(+) depletion alone had no effect. Immunohistochemistry showed SNAT3 staining in earlier parts of the proximal tubule during 14-day K(+) restriction with and without NH(4)Cl treatment and during high protein intake. In summary, SNAT3, PDG, and PEPCK mRNA expression were congruent with urinary ammonium excretion during MA. Chronic dietary K(+) restriction, high protein intake, and MA enhance ammoniagenesis, an effect that may involve enhanced SNAT3 mRNA and protein expression. Our data suggest that SNAT3 plays an important role as the glutamine uptake mechanism in ammoniagenesis under these conditions.

Although renal tubular acidosis (RTA), secondary to autoimmune interstitial nephritis, develops in a large proportion of patients with Sjögren's syndrome (SS), most of the subjects are asymptomatic. Here, we shall present a 39-year-old female patient who came to us with hypokalemic periodic paralysis (HPP), and who was later diagnosed with distal RTA. The patient, who had xerostomia and xerophthalmia for a long period of time, was diagnosed with primary SS from serologic and histologic findings. The patient recovered by being prescribed potassium replacement therapy. Although renal biopsy was not performed, corticosteroids were administered because HPP indicated severe interstitial nephritis. HPP did not reoccur during a 2-year follow-up period. We also review cases with SS-related distal RTA and HPP.

Thyrotoxic periodic paralysis is a rare endocrine disorder seen predominantly in men of Asian origin. The case is reported of a patient who presented to the accident and emergency department with sudden onset of weakness of his lower limbs. Hypokalaemia was identified and treated with resolution of symptoms. Additional tests identified the patient as being thyrotoxic. He was treated with oral antithyroid drugs. It is important to consider the diagnosis of thyrotoxic periodic paralysis in patients presenting with acute onset of weakness. The report discusses the epidemiology, presentation, treatment, and complications of this condition.

To evaluate the actual role of potassium depletion on blood pressure, 11 hypertensive patients were placed on a 10-day isocaloric diet providing a daily potassium intake of either 18 or 80 mmol, with each subject serving as his or her own control; the intake of sodium (220 mmol/day) and other minerals was kept constant. On day 11 each patient was also subjected to central volume expansion by water immersion associated with either normal or low potassium intake. After a 10-day period of low potassium intake, systolic blood pressure increased (P < 0.02) by 5 mm Hg, whereas serum potassium decreased (P < 0.001) by 0.9 mmol/L; no significant changes in urinary sodium and a marked increase in urinary calcium excretion (P < 0.001) were found during the 10-day low potassium intake. PRA (P < 0.02) and plasma aldosterone (P < 0.04) concentrations also decreased during low potassium intake in hypertensive patients. Even though an identical natriuretic response was found during the water immersion experiments with either high or low potassium in the whole hypertensive group, the evaluation of hypertensive subjects in relation to salt sensitivity enabled us to disclose pronounced differences in the natriuretic and calciuretic response. In fact, although an impaired natriuretic ability and moderate calcium loss were particularly found during water immersion in those hypertensive subjects exhibiting a lower salt sensitivity index, a predominant calcium depletion appeared to be the most important consequence of potassium depletion in the hypertensive subjects with a higher salt sensitivity index. By confirming that potassium depletion may exacerbate essential hypertension, our data also suggest that not only sodium restriction, but also potassium and calcium supplementation, could be particularly advisable in salt-sensitive hypertensive patients.

From our previous nutritional assessment, low potassium (K) intake among northeastern Thai males has been clearly demonstrated. This prompted us to undertake a survey of the K content of local foods. Food samples comprised of 57 animal and 142 plant products which were collected from various places in the northeast of Thailand. The dry ashing method was used to prepare the samples for K analysis using an atomic absorption spectrophotometer. Foods could be divided into 7 groups according to their K levels. Foods containing K > or = 1000 mg per 100 g fresh food were categorized in group 1. These were mainly foods in the legume group, i.e., soybean, cowpea and mungbean. While rice (polished) and rice products, the main staple, were in group 7, the lowest K group of less than 100 mg per 100 g fresh food. Comparison studies of the natural foods between those collected from the northeast and from the central regions of the country, and between the cooked foods purchased from the rural villages and from the urban areas of Khon Kaen municipality, showed that, for most food items, the K content was similar wherever it came from. However, when the K content in various parts or in different stages of growth of the same kind of plants or animals was compared, a great variation was clearly seen, for example, young tamarind leaves contained K in group 6 whereas ripe tamarind fruit contained K in group 1. According to our food consumption data, the analysis of food components of 48 meals taken during the hot season by 13 rural volunteers revealed that food items eaten with the highest frequencies and in the largest amount were those in the low K food groups, i.e., glutinous rice (group 7) and green papaya (group 6). Our results suggest that the low K intake of these northeast rural Thai people is not due to a low K content of foods in this region, but rather that their food habits and low socioeconomic status restricts consumption of those food items with higher K contents.

Electron microscopy and roentgen microanalysis were used to study the ultrastructure and electrolytic balance of K+, Na+ and Cl- of the animal myocardial tissue during general body hyperthermia. It was established that long-term effect of heating microclimate causes a distinct reduction of K+ in the cardiomyocytes accompanied by essential changes of the ultrastructure of ischemic character.

An imbalance of potassium in cardiac muscle causes an alteration of heart function. The distribution and concentration of potassium in rat papillary heart muscle was studied using cryofixation and X-ray microanalysis. Freeze-dried cryosections and sections of freeze-dried, embedded tissue were analysed. Bulk frozen specimens were freeze-dried either in a vacuum or by a new technique using liquid propane as a cryodehydration medium. These two methods of freeze-drying were tested for elemental retention in other specimens, with comparable results. A potassium concentration of 120 mmol/l was measured in normal myocytes of cardiac papillary muscle compared to 80 mmol/l in myocytes of animals stressed by a temperature of 45 degrees C for 1 h. The presumed physiological significance of the findings is discussed.

Prostaglandin E2 (PGE2) impairs the hydrosmotic effect of vasopressin in toad bladder and mammalian kidney. Because some studies in animals have suggested that potassium depletion enhances renal PGE2 production, the present study examined whether the renal concentrating defect of potassium depletion in humans is mediated by PGE2. Five normal volunteers were studied before and after moderate potassium depletion achieved by 10 days of dietary potassium restriction and administration of a polystyrene sulfonate potassium exchange resin (Kayexalate). Maximal urinary osmolality (Umax) decreased from 1,094 +/- 58 (mean +/- SEM) to 820 +/- 26 mmol/kg (mOsm/kg) (P less than 0.01) following potassium depletion, but urinary PGE2 excretion did not change (496 +/- 145 and 435 +/- 186 ng/d, respectively). Indomethacin suppressed PGE2 excretion significantly, but failed to increase Umax in either the normal or the potassium-depleted state (1,094 +/- 34 and 825 +/- 56 mmol/kg, respectively). It is concluded that the renal concentrating defect produced by moderate potassium restriction in humans is not mediated by PGE2.

Potassium distribution and content were studied in different compartments of rat heart papillary muscle by X-ray microanalysis. A higher concentration of potassium was measured in normal rat as compared to that in animals treated with high physiological temperature (45 degrees C), to be 120 and 80 mM, respectively.

Very low calorie diets used to treat moderate and severe obesity produce average weight losses of 20 kg in 12 weeks. This paper reviews the development of very low calorie diets from research on fasting in the late 1950s and examines data on the amount of dietary protein needed to achieve positive nitrogen balance. The desirability of including carbohydrate in the diet, the choice of protein sources (formula versus animal protein), and the anorectic value of ketosis are discussed, as are patient selection and the clinical course of the diet. As contrasted to the earlier "liquid protein" diets that were associated with at least 60 deaths, very low calorie diets of high-quality protein appear safe when limited to 3 months or less under careful medical supervision. Evidence of this safety is provided by the results of 24-hour Holter monitoring and the fact that no diet-related fatalities have been reported in over 10 000 cases. The major problem to be resolved is the maintenance of the large weight losses achieved with these diets.

Diabetes mellitus is the most common pathological state in which secondary magnesium deficiency occurs. Magnesium metabolism abnormalities vary according to the multiple clinical forms of diabetes: plasma magnesium is more often decreased than red blood cell magnesium. Plasma Mg levels are correlated mainly with the severity of the diabetic state, glucose disposal and endogenous insulin secretion. Various mechanisms are involved in the induction of Mg depletion in diabetes mellitus, i.e. insulin and epinephrine secretion, modifications of the vitamin D metabolism, decrease of blood P, vitamin B6 and taurine levels, increase of vitamin B5, C and glutathione turnover, treatment with high levels of insulin and biguanides. K depletion in diabetes mellitus is well known. Some of its mechanisms are concomitant to those of Mg depletion. But their hierarchic importance is not the same: i.e., insulin hyposecretion is more important versus K+ than versus Mg2+. Insulin increases the cellular inflow of K+ more than that of Mg2+ because there is more free K+ (87%) than Mg2+ (30%) in the cell. The consequences of the double Mg-K depletion are either antagonistic: i.e. versus insulin secretion (increased by K+, decreased by Mg2+) or agonistic i.e. on the membrane: (i.e. Na+K+ATPase), tolerance of glucose oral load, renal disturbances. The real importance of these disorders in the diabetic condition is still poorly understood. Retinopathy and microangiopathy are correlated with the drop of plasma and red blood cell Mg. K deficiency increases the noxious cardiorenal effects of Mg deficiency. The treatment should primarily insure diabetic control.(ABSTRACT TRUNCATED AT 250 WORDS)

Current issues related to oral potassium supplementation are reviewed, with emphasis on recommendations for the appropriate use of potassium supplementation for both replacement and preventive therapy. Dietary potassium intake, potassium-sparing diuretics, and the various forms of oral potassium supplements are reviewed in terms of indications for use, advantages, and limitations. Attention is given to controversial areas, i.e., gastrointestinal tolerance of controlled-release potassium oral dosage preparations and the need for potassium supplementation in hypertensive patients treated with diuretics.

Although chronic potassium deficiency is a common clinical problem, the hemodynamic consequences of chronic sustained potassium depletion have not been clearly delineated. In this study, the hemodynamic consequences of chronic potassium depletion were evaluated in the conscious rat. Potassium-depleted rats had a decrease in mean arterial pressure which was caused by a decrease in systemic vascular resistance. In association with these changes in systemic hemodynamics, renal blood flow (RBF) was also decreased. The decreased renal blood flow was caused by an increased renal vascular resistance (RVR). Because plasma renin activity was increased the role of angiotensin II as a renal vasoconstrictor was evaluated by utilizing two angiotensin antagonists. Although the administration of saralasin to potassium-depleted rats did not alter systemic hemodynamics, RVR was decreased and RBF was increased. Similar results were obtained with the converting enzyme inhibitor teprotide. Because products of endoperoxide metabolism may cause renal vasoconstriction, the role of prostaglandins and thromboxanes as renal vasoconstrictors were evaluated by utilizing cyclo-oxygenase and thromboxane synthetase inhibitors. None of these agents altered systemic hemodynamics. Following the administration of indomethacin, RVR was decreased and RBF was increased in potassium-depleted rats. Similar results were obtained with another cyclo-oxygenase inhibitor, meclofenamate, and with imidazole, an inhibitor of thromboxane synthetase. Because neither angiotensin II nor products of endoperoxide metabolism could alone account for the increased renal vascular resistance of potassium depletion, studies were performed in potassium-depleted rats treated with indomethacin plus either saralasin or teprotide. In these potassium-depleted animals, renal blood flow was restored to normal. In conclusion, the decrease in renal blood flow and the increase in renal vascular resistance in potassium depletion is mediated by angiotensin II and a product of prostaglandin endoperoxide metabolism, most likely, thromboxane.

An examination of 76 patients with obstructive jaundice of cholelithic and tumor origin indicated an association of manifest hypocoagulation properties of blood with the absolute kalium deficiency in blood. In 54 patients postoperatively following restoration of bile passage in the bowel a progressive decrease in kalium concentration and an increase of sodium in erythrocytes were associated with a simultaneous enhancement of coagulation properties, and vice versa an increased kalium and decreased sodium content in erythrocytes was associated with a hypocaugulation tendency. It is evident that activation or suppression of hemocoagulation is dependent on the state of multiple factors of blood coagulation system in altered electrolytic medium and on eletrolytic reconstruction of erythrocytes.

Administration of KC1 0.5 mmol/kg/day to subjects undergoin prolonged starvation reduced daily urinary ammonium and beta-hydroxybutyrate excretion by one-third. These changes were accompanied by an improvement in potassium balance and an increased rate of chloride excretion. A similar fall in ammonium excretion occurred in a second group of subjects after administration of KHCO3 0.5 mmol/kg/day. Ketone body and bicarbonate excretion remained unchanged in this group while potassium balance improved. In both the first and second groups urine pH fell significantly as the rate of excretion of urinary buffer (ammonium) decreased. When the dose of KHCO3 was increased to 1.5-2.0 mmol/kg/day in fasting subjects, the urine was alkalinized, and ammonium excretion fell to negligible levels, resulting in nitrogen sparing of 2.0 g/day. The results indicate that one-half of the increase in ammonium excretion observed in starvation is due to potassium deficiency. Nitrogen wastage caused by losses of urinary ammonium during starvation can be virtually eliminated by potassium supplementation and urinary alkalinization. The decrease in beta-hydroxybutyrate excretion after potassium chloride administration was not caused by a fall in the rate of nonionic diffusion of this organic acid related to the reduction in urine pH. The reason for the fall in beta-hydroxybutyrate excretion is not apparent, though it was associated with an increase in chloride excretion.

Renal potassium excretion as the factor mainly responsible for potassium balance is reviewed. Clinical syndromes related to potassium wasting, abnormal distribution between intra- and extracellular space and potassium retention are outlined with reference to the pathophysiologic mechanisms. Some therapeutic considerations are presented.

Following nephrectomy and acute potassium loading, animals previously maintained on a high potassium diet have a smaller increment in plasma potassium than do animals on a control diet. The mechanism of this "extrarenal potassium adaptation" is not known. To explore the role of potassium depletion in this process, we studied rats adapted to either a high potassium (HK) or control (C) diet. When dietary potassium was withdrawn, urinary potassium losses in HK rats greatly exceeded those in C rats for at least two days, leading to greater potassium depletion in HK than C animals. A smaller increment in plasma potassium in HK compared to C rats was seen only after prolonged fasting preceded nephrectomy and acute potassium loading. Correction of potassium depletion incurred during fasting abolished extrarenal potassium adaptation. We conclude: after withdrawal of dietary potassium, urinary potassium losses are much greater in HK than in C rats; if the duration of dietary potassium deprivation is sufficient, these urinary potassium losses will cause potassium-adapted animals to paradoxically become more potassium depleted than controls; and this paradoxical potassium depletion may be responsible for extrarenal potassium adaptation.

In a patient who had primary aldosteronism and severe total-body potassium depletion muscular tonic contractures developed during induction of anesthesia. After correction of the potassium deficit, the patient underwent uneventful anesthesia and transabdominal right adrenalectomy. Neither serum potassium level nor EKG seems to provide a reliable index of correction of potassium deficit. Measurement of potassium balance provided a method of quantitating the potassium depletion and of determining when the potassium deficit had been corrected. Balance studies should be utilized preoperatively when long-term potassium loss is suspected to reduced complication secondary to hypokalemia.

Chronic potassium deficiency in the rat results in a decrease in the pressor sensitivity to exogenous angiotensin II (AII). To define the mechanism of this resistance to AII, studies were performed in conscious rats after 14-21 d of dietary potassium deficiency. The pressor response to graded doses of AII was 50% less in potassium-deficient than control animals. In contrast, the pressor response to graded doses of norepinephrine was preserved in potassium-deficient rats; therefore, the decreased response to AII was not due to a generalized defect in vascular reactivity. Pretreatment with either the converting enzyme inhibitor, teprotide, or the prostaglandin synthesis inhibitor, indomethacin, failed to normalize the response to AII. Thus, neither prior receptor occupancy with endogenous AII nor the presence of vasodilatory prostaglandins caused the decreased AII response in potassium deficiency. Since the pressor response to AII involves angiotensin interaction with its vascular receptor, binding studies of mesenteric artery and uterine smooth muscle AII receptors were performed. Scatchard analysis showed that potassium deficiency resulted in a decrease in binding affinity (50% increase in Kd) in both uterine (6.00 vs. 3.82 nM; P less than 0.05) and vascular (1.39 vs. 0.973 nM; P less than 0.005) smooth muscle. Furthermore, despite increased circulating AII, there was an increase in AII receptor number in potassium-deficient uterine (308 vs. 147 fmol/mg protein; P less than 0.005) and vascular (470 vs. 316 fmol/mg protein; 0.05 less than P less than 0.1) smooth muscle. Although potassium deficiency resulted in alterations in receptor-binding parameters, the changes in binding affinity and number were directionally opposite, so that in potassium deficiency there was either no change or an increase in total AII binding. We conclude that the decrease in angiotensin pressor sensitivity in potassium-deficient rats is mediated by a postreceptor defect since it occurs subsequent to the binding of AII to its vascular smooth muscle receptor.

It is generally believed that patients operated on for gross obesity with jejunoileal shunt develop electrolyte malabsorption. In follow-up studies electrolyte abnormalities have been reported in 6-37% of the cases. We have not been able to find any description of simple diagnostic tools to help indicate which patients should be treated with electrolyte supplements. The aim of this study was to evaluate different diagnostic tools to determine whether they would identify which patients to treat. Ten patients with end-to-side jejunoileostomies were investigated. Our attempt failed. We were not able to identify the patients who needed supplementary therapy. The reason for this may be absence of severe electrolyte abnormalities or insufficient diagnostic methods.

Three groups of patients with suspected potassium depletion were studied. Twenty-nine obese patients were observed before and up to 1 year after an intestinal shunt operation. During the first week after operation they lost almost 3 grams of potassium per day. The percentage potassium loss was much larger than the percentage weight loss. A significant decrease of serum potassium was also noted during the first week after operation. In contrast to the total body potassium, however, the serum potassium remained within normal limits in all patients except two. Fourteen patients subjected to a cardiac operation also showed a significant decrease of total body potassium concentration 1 week after operation. The serum potassium remained within normal limits. In 187 patients with suspected potassium depletion the total body potassium had been measured, and the results were examined retrospectively. In 38 of these patients the measured total body potassium was outside a 94% confidence interval for an individually predicted value, even though 26 of these 38 patients were taking oral potassium chloride tablets. In 23 of these 38 patients two or three risk factors - hypoalbumin-emia, treatment with diuretics, and treatment with digitalis - were present simultaneously, and in 10 patients one factor was present. Only 8 of the 38 patients had a low serum potassium value. It may therefore be concluded that the total body potassium measurement, when compared with an individually predicted value, seems to be more sensitive in estimation of potassium depletion than the commonly used serum potassium method.

Potassium excretion following cardiopulmonary bypass has been studied in 11 patients. After an initial period of 4 to 5 hours, potassium excretion was found to be directly related to urine flow provided diuretics had not been administered. Triamterene altered the slope of the regression line so that, for any given urine flow rate, less potassium was excreted. A simple program for postoperative potassium therapy is described.