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PubMed1979

Effect of potassium chloride on plasma renin activity and plasma aldosterone during sodium restriction in normal man.

The present study was designed to evaluate the spectrum of responses of PRA and plasma aldosterone (PAldo) to a range of oral potassium intakes (0 to 300 mEq of potassium chloride per day) in 20 normal human subjects receiving an electrolyte-free diet. Potassium exhibited a dose-dependent natriuretic effect. The results of the PRA studies indicate that normal dietary amounts (50 mEq/day) of potassium chloride do not prevent the increase in PRA with absolute sodium deprivation and that PRA is maximally stimulated on 150 mEq of potassium chloride per day. The rise in PRA is directly correlated with serum potassium concentration. The results of the PAldo studies indicate that potassium chloride deprivation attenuates PAldo increases due to sodium deprivation and that PAldo is maximally stimulated on 150mEq of potassium chloride per day. The rise in PAldo is directly correlated with serum potassium concentration and with PRA. The administration of 300 mEq/day of potassium chloride caused significant hyperkalemia and blunted both PRA and PAldo increases. Our results suggest that potassium chloride has an important role in the regulation of PRA and PAldo, and that only following potassium chloride deprivation is the PRA/PAldo response dissociated.

Aldosterone↗
PubMed1984

Oral potassium chloride and amiloride in hydrochlorothiazide-induced potassium loss.

To compare the effect of amiloride with that of oral potassium chloride (KCl) in hypokalemia, metabolic balance studies were carried out in hospitalized subjects with mild hypertension without edema who developed negative potassium balance after 4 days on hydrochlorothiazide (HCTZ). Subjects' diets contained measured amounts of sodium and potassium. While HCTZ treatment continued, oral preparations of either KCl solution or amiloride was added for 5 additional days. Potassium balance in the KCl-treated group further decreased by -44.9 +/- 32.3 mEq K+, while subjects on amiloride went into positive balance that averaged +51.7 +/- 24.1 mEq K+. Hypokalemia after HCTZ did not respond to KCl, while K+ levels rose from 3.32 +/- 0.22 to 3.67 +/- 0.26 mEq/l after amiloride.

Administration, Oral↗
PubMed1977

Effects of potassium chloride on isolated, blood-perfused canine atrial or ventricular muscle preparations.

The effects of potassium chloride were studied on pacemaker activity in the sinoatrial (SA) node and on contractility in isolated, blood-perfused atrial and left ventricular preparations of dogs, which were suspended in the bath and perfused with arterial blood from the carotid artery of the heparinized support dog. Potassium chloride given directly into the sinus node artery in a dose range of 100 micrograms--1 mg produced a dose-related positive chronotropic and a negative inotropic effect in isolated atrium preparations. Potassium chloride into the cannulated anterior descending branch of the left coronary artery caused only a negative inotropic effect in isolated ventricular preparations. A larger dose of potassium chloride caused temporary atrial or ventricular arrest. These effects of potassium chloride were not modified by pretreatment with atropine or propranolol.

Animals↗
PubMed2004

Intravesical potassium chloride sensitivity test in men with chronic pelvic pain syndrome.

PURPOSE: Intravesical potassium chloride has been reported to cause pain in patients with interstitial cystitis and male chronic prostatitis (CP)/chronic pelvic pain syndrome (CPPS). We performed the potassium chloride sensitivity test (PST) in subjects with CP/CPPS and healthy men without pelvic pain. MATERIALS AND METHODS: We recruited 40 men with CP/CPPS and 63 healthy men. The National Institutes of Health CPPS symptom index was used to measure the severity of symptoms. We instilled 100 ml physiological saline (NaCl 0.9%) intravesically. The bladder was emptied and 100 ml potassium chloride solution (KCl 40 mEq) were instilled. The subjects were asked to score urgency (0 to 10) and pain (0 to 10) sensations after each instillation. A positive PST was defined by 5 different cut-off points as the difference in score between KCl and NaCl instillations. Logistic regression analyses and area under the receiver operating characteristics curve were used to determine the predictive power of PST in CP/CPPS. RESULTS: There was no difference in pain and urgency scores between the men with CP/CPPS and controls (p >0.05 for each). Men with CP/CPPS had higher pain and urgency scores with KCl than with NaCl (p = 0.011 and 0.033, respectively). The rates of positive PST were 50% and 36.5% in the CP/CPPS and control groups, respectively (p = 0.160). There was no significant correlation of potassium chloride sensitivity scores with National Institutes of Health symptom scores (p >0.05 for each). The sensitivity, specificity, and positive predictive and negative predictive values of PST were 50%, 63.5%, 46.5% and 66.7%, respectively. CONCLUSIONS: Although there was a significant increase in pain and urgency scores following KCl instillation in patients with CP/CPPS, these scores and the rate of positive PST were not statistically different from those of healthy subjects. Thus, PST does not have a good predictive value in the diagnosis of CP/CPPS.

Administration, Intravesical↗
PubMed1982

Relative potency of spironolactone, triamterene and potassium chloride in thiazide-induced hypokalaemia.

1 The influence of spironolactone 50 mg and 100 mg daily, triamterene 100 mg and 200 mg daily, potassium chloride 32 mmol and 64 mmol daily and placebo on plasma potassium and other variables was examined in a random crossover study of nine hypertensive patients taking bendrofluazide 10 mg daily. 2 Spironolactone and triamterene had significant and parallel dose-response curves for plasma potassium, with a relative potency for triamterene:spironolactone of 0.25:1, significantly lower than the accepted 0.5:1 ratio. These drugs also lowered serum sodium, bicarbonate and body weight, and increased serum urea and creatinine. 3 Potassium chloride increased plasma potassium above placebo values, but the dose-response was not significant and was not parallel with those of the potassium-sparing drugs. Seven of nine patients remained hypokalaemic despite treatment with 64 mmol potassium chloride daily. 4 The relative expense, convenience and toxicity of the potassium-sparing drugs should be assessed at equivalent doses, namely spironolactone 50 mg:triamterene 200 mg:amiloride 20 mg. Potassium chloride does not correct moderate diuretic-induced hypokalaemia even at doses of 64 mmol daily.

Adult↗
PubMed1982

Effects of magnesium on the vasoconstrictor responses to norepinephrine and potassium chloride in the rat mesenteric artery.

In the perfused rat mesenteric vascular bed, the effects of magnesium and calcium on the vasoconstrictor responses to norepinephrine or potassium chloride were studied. Higher concentrations of magnesium in the perfusate attenuated the vascular responses to norepinephrine and potassium chloride in a dose-related manner. Higher concentrations of calcium in the perfusate enhanced greatly the vascular responses to potassium chloride, while the response to norepinephrine was only slightly potentiated by increasing calcium concentration. The attenuating effect of magnesium on the responses to norepinephrine and to potassium chloride were reversed by elevation of calcium concentration in the perfusate. The potentiating effects of calcium on the responses to potassium chloride were also reversed by increasing the concentration of magnesium. However, an inhibitory effect of magnesium on the responses to norepinephrine was not observed in the presence of higher concentrations of calcium. These results indicate that magnesium acts antagonistically on calcium movement in vascular contractions due to potassium chloride, but that the relationship between magnesium and calcium is more complex in vascular contractions induced by norepinephrine.

Animals↗
PubMed1992

Concentration changes of electrolytes in serum of chronic chagasic myocardiopathic patients. Sodium, potassium, chloride, calcium, inorganic phosphorus and magnesium.

Sodium, potassium, chloride, calcium, inorganic phosphorus (Pi) and magnesium contents in the serum of 75 myocardiopathic chagasic patients together with that in 29 healthy controls were determined. Blood samples were taken by catheterization from the superior cava vein (SCV), coronary sinus (CS), pulmonary artery (PA) and a peripheral artery, usually the femoral (FA). The results show that the average serum sodium, potassium, chloride, calcium and PI were invariably different in most samples, except the levels of potassium in SCV and Pi levels in FA. The serum concentration of magnesium was significantly different only in the blood of CS. In general one can observe that in the chagasic patients the serum sodium, chloride and calcium tend to diminish while serum potassium, Pi and magnesium tend to increase, especially in CS blood. The coronary gradient indicates that sodium, chloride and calcium tend to deposit in heart tissues, whereas the other elements (potassium, magnesium and Pi) tend to be released from this tissue. The systemic and peripheric gradients suggest that the chemical elements under study tend either to deposit in/or be released from different tissues depending on the course of development of the chagasic myocardiopathy.

Adult↗
PubMed1995

Dose-dependent promotion effects of potassium chloride on glandular stomach carcinogenesis in rats after initiation with N-methyl-N'-nitro-N-nitrosoguanidine and the synergistic influence with sodium chloride.

The modifying effects of potassium chloride (KCl) ingestion on glandular stomach carcinogenesis were investigated in male Wistar rats induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and were compared with those of sodium chloride (NaCl). A total of 120 male 6-week-old Wistar rats were divided into six groups, each consisting of 20 animals. After initiation of treatment with a MNNG solution (100 parts/million) as their drinking water for 10 weeks, rats were fed a diet supplemented with 5% NaCl, 2.5% NaCl, 2.5% NaCl plus 2.5% KCl, 5% KCl, 2.5% KCl, or a basal diet alone for the following 62 weeks. Under this experimental condition, there were no statistical differences in the final body weights between groups. The incidences of adenocarcinomas in the glandular stomachs were significantly higher in the 5% NaCl and combined 2.5% NaCl-plus-2.5% KCl groups (P < 0.05 and 0.01) than in the MNNG alone (control) group. The incidences of atypical or precancerous hyperplasias in the glandular stomachs were increased significantly by the 5% NaCl, 2.5% NaCl-plus-2.5% KCl, and 5% KCl treatments (P < 0.05 or 0.01). The multiplicities of adenocarcinomas were significantly greater in the 5% NaCl, 2.5% NaCl, and combined NaCl-plus-KCl groups (P < 0.05 or 0.01) compared with the control value. The multiplicity data for atypical hyperplasias were most striking; namely, their multiplicities were increased significantly by the treatments of NaCl or KCl (P , 0.01) in a clear dose-dependent manner and enhanced synergistically by the combined treatment of NaCl and KCl. Because the concentrations of KCl used in this study were about 1.3 times lower than those of NaCl on a molar basis, although the doses of each chemical were exactly the same on a weight-percent basis, it is suggested that the enhancing effects of KCl might not be much different from those of NaCl. The results in the present study thus indicate that, similarly to NaCl, KCl ingestion exerts dose-dependent promoting effects and a synergistic influence with NaCl when given during the postinitiation phase of two-stage glandular stomach carcinogenesis in rats.

Animals↗
PubMed1994

Concentrated potassium chloride infusions in critically ill patients with hypokalemia.

Although concentrated infusions of potassium chloride commonly are used to treat hypokalemia in intensive care unit patients, few studies have examined their effects on plasma potassium levels. Forty patients with hypokalemia were given infusions of 20 mmol of potassium chloride in 100 mL of normal saline over 1 hour; 26 patients received the infusions through the central vein and 14 patients through the peripheral vein. Plasma potassium ([K]p) was measured at 15-minute intervals during and after the infusion in 31 patients. delta K was defined as the difference between each potassium determination and baseline plasma potassium concentration. Continuous electrocardiographic recording was carried out during the infusion and during the 1-hour period immediately preceding the infusion. Mean baseline [K]p was 2.9 mmol/L and all subsequent plasma concentrations significantly increased from baseline. Mean peak [K]p was 3.5 mmol/L, [K]p (1 hour postinfusion) was 3.2 mmol/L, and mean postinfusion delta K was 0.48 mmol/L (range -0.1-1.7 mmol/L). Arrhythmias, changes in cardiac conduction intervals, and other complications did not occur. The frequency of premature ventricular beats decreased significantly during the infusion compared with that of the control period. The high concentration (200 mmol/L) and rate of delivery (20 mmol/hr) of the potassium chloride infusions were well tolerated, decreased the frequency of ventricular arrhythmias, and did not cause transient hyperkalemia.

Adult↗
PubMed2005

Evaluation of the implementation of the alert issued by the UK National Patient Safety Agency on the storage and handling of potassium chloride concentrate solution.

OBJECTIVES: To assess the effectiveness of the response of NHS hospital trusts to an alert issued by the National Patient Safety Agency designed to limit the availability of concentrated potassium chloride in hospitals in England and Wales, and to determine the nature of any unintended consequences. DESIGN: Multi-method study involving interviews and a physical inspection of clinical areas. SETTING: 207 clinical areas in 20 randomly selected acute NHS trusts in England and Wales between 31 October 2002 and 31 January 2003. PARTICIPANTS: Senior managers and ward based medical and nursing staff. MAIN OUTCOME MEASURES: Degree of staff awareness of and compliance with the requirements of the national alert, withdrawal of concentrated potassium chloride solutions from non-critical areas, provision of pre-diluted alternatives, storage and recording in accordance with controlled drug legislation. RESULTS: All trusts required that potassium chloride concentrate be stored in a separate locked cup-board from common injectable diluents (100% compliance). Unauthorized stocks of potassium chloride were found in five clinical areas not authorized by the trust (98% compliance). All trusts required documentation control of potassium chloride concentrate in clinical areas, but errors were recorded in 20 of the 207 clinical areas visited (90% compliance). Of those interviewed, 78% of nurses and 30% of junior doctors were aware of the alert. CONCLUSIONS: The NPSA alert was effective and resulted in rapid development and implementation of local policies to reduce the availability of concentrated potassium chloride solutions. The success is likely to be partly due to the nature of the proposed changes and it cannot be assumed that future alerts will be equally effective. Continued vigilance will be necessary to help sustain the changes.

Drug Storage↗
PubMed1985

Moderate potassium chloride supplementation in essential hypertension: is it additive to moderate sodium restriction?

Twenty patients with mild or moderate essential hypertension and not receiving any drug treatment, who had been moderately restricting their sodium intake to around 70 mmol(mEq) a day for at least one month and whose mean blood pressure was then 163/103 mm Hg, were entered into a double blind, randomised crossover study to compare one month's treatment with slow release potassium chloride tablets (64 mmol potassium chloride a day) with one month's treatment with a matching placebo. Mean (SEM) urinary sodium excretion on entry to the study was 68 (6.8) mmol/24 h. Mean urinary potassium excretion increased from 67 (6.9) mmol(mEq)/24 h with placebo to 117 (4.6) mmol/24 h with potassium chloride. Supine and standing systolic and diastolic blood pressures did not change significantly with potassium chloride supplementation when compared with pressures while receiving placebo or before randomisation. In patients who are able moderately to restrict their sodium intake doubling potassium as a chloride salt has little or no effect on blood pressure.

Adult↗
PubMed1983

Presence of a sodium-potassium chloride cotransport system in the rectal gland of Squalus acanthias.

In order to investigate whether the loop diuretic sensitive, sodium-chloride cotransport system described previously in shark rectal gland is in fact a sodium-potassium chloride cotransport system, plasma membrane vesicles were isolated from rectal glands of Squalus acanthias and sodium and rubidium uptake were measured by a rapid filtration technique. In addition, the binding of N-methylfurosemide to the membranes was investigated. Sodium uptake into the vesicles in the presence of a 170 mM KCl gradient was initially about five-fold higher than in the presence of a 170 mM KNO3 gradient. In the presence of chloride, sodium uptake was inhibited 56% by 0.4 mM bumetanide and 40% by 0.8 mM N-methylfurosemide. When potassium chloride was replaced by choline chloride or lithium chloride, sodium uptake decreased to the values observed in the presence of potassium nitrate. Replacement of potassium chloride by rubidium chloride, however, did not change sodium uptake. Initial rubidium uptake into the membrane vesicles was about 2.5-fold higher in the presence of a 170 mM NaCl gradient than in the presence of a 170 mM NaNO3 gradient. The effect of chloride was completely abolished by 0.4 mM bumetanide. Replacement of the sodium chloride gradient by a lithium chloride gradient decreased rubidium uptake by about 40%; replacement by a choline chloride gradient reduced the uptake even further. Rubidium uptake was also strongly inhibited by potassium. Sodium chloride dependence and bumetanide inhibition of rubidium flux were also found in tracer exchange experiments in the absence of salt gradients. The isolated plasma membranes bound 3[H]-N-methylfurosemide in a dose-dependent manner. In Scatchard plots, one saturable component could be detected with an apparent KD of 3.5 x 10(-6) M and a number of sites n of 104 pmol/mg protein. At 0.8 microM, N-methylfurosemide binding decreased 51% when sodium-free or low-potassium media were used. The same decrease was observed when the chloride concentration was increased from 200 to 600 mM or when 600 1 mM bumetanide or furosemide was added to the incubation medium. These studies indicate that the sodium-chloride cotransport system described previously in the rectal gland is in fact a sodium-potassium chloride cotransport system. It is postulated that this transport system plays an essential role in the secondary active chloride secretion of the rectal gland.

Animals↗
PubMed1978

Effect of beta-sympatholytic agents on vascular responses to noradrenaline and potassium chloride.

Vasoconstrictory responses to noradrenaline (NA) or high potassium chloride (130 mM) usually show a biphasic behaviour: an initial peak is followed by a lower steady state level. The influence of three beta-sympatholytic agents (propranolol, pindolol, practolol) and a "Ca-antagonist" (verapamil) on this particular behaviour of KCl-induced vasoconstrictions was compared with responses to NA. Studies were performed on the intact vascular bed of an isolated intestinal preparation of the rat. 1. Increases in the concentration of propranolol and pindolol from 10(-10) to 10(-6) M attenuated the vascular responses to high KCl. Practolol, however, distinctly enhanced the KCl-responses. NA (1.3 microgram/ml)-elicited vasoconstriction was found to be influenced in a similar manner by the beta-receptor antagonists used, though lower concentrations of pindolol had an enhancing, higher concentrations a reducing effect on the constrictory responses to NA. 2. The extent to which the biphasic response adjusted to the steady state level was concentration-dependently increased KCl-responses and significantly decreased to a monophasic response to NA, in the presence of the beta-sympatholytic agents. 3. By using a quotient of deltaPs (steady-state phase) to deltaPi (initial vasoconstriction) and by comparing the effect of the three beta-sympatholytic agents with that of verapamil on this quotient showed a concentration-dependent decrease in presence of the beta-sympatholytic as well as of the Ca-antagonistic agents. These myotropic actions, i.e. negative influences on the mechanism of vascular smooth muscle activation ranged in the following sequence: Verapamil greater than propranolol greater than pindolol greater than practolol. 4. The mechanism underlying the biphasic responses to high potassium chloride are concluded to be basically different from the NA-responses because they are inversely affected by beta-sympatholytic agents. The steady-state response to KCl was found to be very sensitive to non-specific pharmacological actions of beta-sympatholytic substances. The myotropic action of the beta-receptor antagonists is compared with that of the Ca-antagonist verapamil and the role of calcium in the mechanism of activation of vascular smooth muscle is discussed.

Adrenergic beta-Antagonists↗
PubMed1991

Stability of amrinone and digoxin, procainamide hydrochloride, propranolol hydrochloride, sodium bicarbonate, potassium chloride, or verapamil hydrochloride in intravenous admixtures.

The stability of amrinone and digoxin, procainamide hydrochloride, propranolol hydrochloride, sodium bicarbonate, potassium chloride, or verapamil hydrochloride in intravenous admixtures was studied. Admixtures of amrinone and digoxin were studied at one concentration. Amrinone admixtures with propranolol hydrochloride, sodium bicarbonate, potassium chloride, and verapamil hydrochloride were studied at two concentrations. In general, 0.45% sodium chloride injection was used as the diluent; 5% dextrose injection was also used for the procainamide hydrochloride experiments. Duplicate solutions of each test admixture and single-drug control admixture were prepared and stored for four hours at 22-23 degrees C under fluorescent light. Samples were analyzed by visual inspection, tested for pH, and assayed by high-performance liquid chromatography. Admixtures containing amrinone 1.25 or 2.5 mg/mL (as the lactate salt) and sodium bicarbonate 37.5 mg/mL precipitated immediately or within 10 minutes. No changes in pH or visual appearance were noted for amrinone admixtures with procainamide hydrochloride, digoxin, propranolol hydrochloride, potassium chloride, and verapamil hydrochloride. Appreciable degradation of both amrinone and procainamide was observed after four hours when the two were mixed in 5% dextrose. No degradation of amrinone or procainamide was seen when the 5% dextrose was replaced by 0.45% sodium chloride. Amrinone and sodium bicarbonate were incompatible in intravenous admixtures. Amrinone was compatible with digoxin, propranolol hydrochloride, potassium chloride, and verapamil hydrochloride. Amrinone and procainamide were compatible in 0.45% sodium chloride injection but not in 5% dextrose injection.

Amrinone↗
PubMed1992

Chemical characterization of a potassium hydroxyapatite prepared by soaking in potassium chloride and carbonate solutions.

A potassium-doped synthetic apatite was prepared by soaking hydroxyapatite in potassium carbonate and potassium chloride solutions. The hydroxyapatite was prepared by firing slip cast ceramic bodies in vacuum at 1100 degrees C. The conical ceramic samples and a crushed material of this were soaked in carbonate and chloride solutions for 2, 4, 6, and 8 weeks. Potassium, calcium, and phosphate were determined by direct current plasma emission spectroscopy. The carbonate content was determined by thermogravimetric analysis and chloride titrimetrically. After 2 weeks, one potassium ion substituted one calcium ion when soaked in a carbonate solution. When soaked in the chloride solution substitution occurred to the same extent. At phosphate sites the substitution of phosphate for carbonate occurred at one sixth of the sites after 2 weeks. Chloride incorporated one half of the OH-sites after 2 weeks. After 4 weeks about one chloride ion was found in the apatite, and after 6 weeks one and a half of the OH-sites were occupied by chloride ions.

Carbonates↗
PubMed1976

Positive chronotropic and negative inotropic effects induced by potassium chloride in the isolated canine atrium.

The effects of potassium chloride on inotropic and chronotropic activity were investigated in five isolated canine atrium preparations which were suspended in a bath and perfused with arterial blood from the carotid artery of the heparinized support dog. Potassium chloride administered into the cannulated sinus node artery in a dose range of 100 mug-1 mg produced a dose-related negative inotropic and a positive chronotropic effect. These effects were not influenced by treatment with either atropine or propranolol. From these results, it is concluded that potassium had a direct negative effect on atrial contractility and a direct positive effect on atrial rate.

Animals↗