sodium-bicarbonate and Hypertension

Individuals with CKD are at a higher risk of cardiovascular morbidity and mortality. Acidosis is positively correlated with CKD progression and elevated systolic BP. Sodium bicarbonate is an efficacious treatment of acidosis, although this may also increase systolic BP. In this systematic review and meta-analysis, we summarize the evidence evaluating systolic BP and antihypertensive medication change (which may indicate systolic BP change) in response to sodium bicarbonate therapy in individuals with CKD.. Medical Literature Analysis and Retrieval System Online, Excerpta Medica database, Cumulative Index to Nursing and Allied Health Literature, Allied and Complementary Medicine Database, Cochrane Central Register of Controlled Trials, and World Health Organization (WHO) trials registry databases were searched for randomized control trials where sodium bicarbonate was compared with placebo/usual care in CKD stage G1-5 non-dialysis-dependent populations. Random effects meta-analyses were used to evaluate changes in systolic BP and BP-modifying drugs after sodium bicarbonate intervention.. Fourteen randomized control trials (2110 individuals, median follow-up 27 [interquartile range 97] weeks, mean age 60 [SD 10] years, mean systolic BP 136 [SD 17] mm Hg, mean eGFR 38 [SD 10] ml/min, mean serum bicarbonate 22 [SD 4] mmol/L) were eligible for inclusion. Meta-analysis suggested that sodium bicarbonate did not influence systolic BP in individuals with CKD stage G1-5. Results were consistent when stratifying by dose of sodium bicarbonate or duration of intervention. Similarly, there was no significant increase in the use of antihypertensive medication or diuretics in individuals taking sodium bicarbonate, whereas there was a greater decrease in antihypertensive medication use in individuals taking sodium bicarbonate compared with controls.. Our results suggest, with moderate certainty, that sodium bicarbonate supplementation does not adversely affect systolic BP in CKD or negatively influence antihypertensive medication requirements.

Topics: Acidosis; Antihypertensive Agents; Blood Pressure; Humans; Hypertension; Kidney Failure, Chronic; Middle Aged; Sodium Bicarbonate

Topics: Abdominal Pain; Acidosis, Lactic; Aged; Antigens, Neoplasm; Carcinoma; Diabetes Mellitus, Type 2; Drug Resistance; Fatal Outcome; Female; Humans; Hypertension; Ki-1 Antigen; Sodium Bicarbonate; Stomach Neoplasms

Metabolic acidosis is a frequent but asymptomatic complication in chronic kidney disease (CKD). In early stages of CKD acidosis is limited to the renal tissue and progresses to reduced serum bicarbonate levels. Reduced renal tissue pH and increased ammoniagenesis are the key mechanisms of the kidney to enhance acid excretion to the urine. The expressed protein patterns in the proximal tubular epithelial cells change remarkably, the proximal convoluted tubule develops hypertrophy, and an intra-renal enhanced renin-angiotensin-system leads to interstitial fibrosis. Since nephrons are numerically reduced in CKD each remaining functional unit has to progressively increase these mechanisms to keep up the equilibrium. The adverse effects of chronic metabolic acidosis include aside from acceleration of progression of kidney disease, the development or exacerbation of bone disease, increased degradation of muscle with muscle wasting, enhanced protein degradation and inflammation. Genome wide association studies demonstrated that tubular acid-base transporters are involved in the development of arterial hypertension. Several retrospective analyses have indicated that low serum bicarbonate predicts death in cohorts with CKD and cardiovascular disease. All studies confirmed a U-shaped association of mortality and serum bicarbonate, indicating that both, acidosis and alkalosis are associated with increased mortality. Randomized controlled trials showed that base substitution, either by modification of the diet or by simply adding alkalizing agents, might halt the decline of kidney function in subjects with CKD. In 2012 a meta-analysis concluded that alkali therapy might provide a long-term favorable effect on renal function in patients with CKD.

Topics: Acid-Base Equilibrium; Acidosis, Renal Tubular; Bone and Bones; Humans; Hypertension; Insulin Resistance; Meta-Analysis as Topic; Muscle, Skeletal; Proteins; Randomized Controlled Trials as Topic; Renal Insufficiency, Chronic; Sodium Bicarbonate; Treatment Outcome

Poisoning with flecainide acetate is rare and associated with a high mortality. This usually occurs after massive ingestion but can also be observed during therapeutic overdose in patients with renal failure or with amiodarone therapy. The prognostic depends on the haemodynamic and rhythmic effects of the overdose one sign of which is widening of the QRS complexes. Major sodium bicarbonate or lactate infusion is the generally prescribed treatment. The authors report one case of a patient with renal failure on amiodarone who survived a severe flecainide acetate overdose.

Topics: Aged; Amiodarone; Anti-Arrhythmia Agents; Atrial Flutter; Biological Availability; Calcium Gluconate; Charcoal; Combined Modality Therapy; Consciousness Disorders; Diabetic Nephropathies; Drug Interactions; Drug Therapy, Combination; Flecainide; Heart Block; Hemofiltration; Humans; Hypertension; Hypotension; Intestinal Pseudo-Obstruction; Kidney Failure, Chronic; Male; Poisoning; Pulmonary Edema; Renal Dialysis; Respiration, Artificial; Sodium Bicarbonate; Sodium Channel Blockers; Uremia

This paper reviews the evidence that salt sensitivity of blood pressure is related both to the anion ingested with sodium as well as to other components of the diet. In several experimental models of salt-sensitive hypertension and in humans, blood pressure is not increased by a high sodium intake provided with anions other than chloride. Salt-induced increase of blood pressure depends on the concomitant ingestion of both sodium and chloride. Both epidemiologic and clinical evidence suggest that sodium chloride-induced increases of blood pressure are augmented by diets deficient in potassium or calcium. In experimental animals, a high intake of simple carbohydrates also augments sodium chloride sensitivity of blood pressure. These observations indicate that the effect of dietary sodium on blood pressure is modulated by other components of the diet.

Topics: Animals; Blood Pressure; Citrates; Dietary Sucrose; Humans; Hypertension; Potassium, Dietary; Sodium Bicarbonate; Sodium Chloride, Dietary; Sodium Citrate; Sodium, Dietary

In conclusion, a complete RAS is present in the mammalian proximal tubule that is potentially autocrine and paracrine in nature. Maneuvers that stimulate renin in JG cells and renal vasculature appear to also stimulate renin in the proximal tubule. The subcellular localization of the different components and the regulation of this epithelial RAS still remain to be defined. This RAS may be important in regulation of proximal tubule NaCl and NaHCO3 transport. Finally, one can speculate that activation of this RAS may play a pathogenetic role in some patients with essential hypertension and in the hypertension and cyst growth seen in autosomal dominant polycystic kidney disease.

Topics: Animals; Humans; Hypertension; Kidney Tubules, Proximal; Polycystic Kidney, Autosomal Dominant; Renin; Renin-Angiotensin System; Sodium Bicarbonate; Sodium Chloride; Water-Electrolyte Balance

Topics: Adolescent; Adult; Aldosterone; Bicarbonates; Blood Pressure; Child; Diet, Sodium-Restricted; Diuretics; Female; Glomerular Filtration Rate; Humans; Hyperkalemia; Hypertension; Kidney Tubules; Male; Mannitol; Middle Aged; Mineralocorticoids; Potassium; Renin; Sodium; Sodium Bicarbonate; Syndrome

The aim of our study was to evaluate renal function assessed by serum creatinine as well as novel biomarkers in 142 patients with stable coronary heart disease and normal serum creatinine undergoing percutaneous coronary interventions (PCI) depending on the type of hydration: physiological saline vs. sodium bicarbonate (1:1 randomization).. Serum and urinary NGAL were evaluated before and after 8-12, and 24 hours after PCI. Serum cystatin C, serum creatinine, estimated glomerular filtration rate using different formulae were assessed before PCI, and 24 hours after the procedure.. Only 2 patients (2.8%) from the saline-hydrated group fulfilled the criteria for CI-AKI. In patients hydrated with sodium bicarbonate serum creatinine declined significantly (p<0.01). In patients hydrated with sodium bicarbonate a significant fall in serum NGAL after 8-12 hours was found. In sodium bicarbonate group cystatin C decreased non significantly after 8-12 hours, then returned to the baseline values. In patients hydrated with physiological saline serum NGAL before PCI and after 24 hours correlated positively with cystatin C and eGFR by CKD-EPI. In patients hydrated with sodium bicarbonate baseline serum NGAL correlated with NGAL baseline cystatin C and eGFR by CKD-EPI, similarly serum NGAL after 24 hours correlated with cystatin C.. We suggest to rather use sodium bicarbonate in a hydration protocol in patients undergoing PCI. However, the value of NGAL in this setting remains to be elucidated and volume expansion remain the unquestionable prevention methods of CI-AKI.

Topics: Acute-Phase Proteins; Aged; Biomarkers; Coronary Artery Disease; Creatinine; Cystatin C; Female; Fluid Therapy; Glomerular Filtration Rate; Glucose Intolerance; Humans; Hypertension; Kidney Function Tests; Lipocalin-2; Lipocalins; Male; Middle Aged; Percutaneous Coronary Intervention; Prevalence; Proto-Oncogene Proteins; Risk Factors; Sodium Bicarbonate; Sodium Chloride

Current guidelines recommend Na(+)-based alkali for CKD with metabolic acidosis and plasma total CO2 (PTCO2) < 22 mM. Because diets in industrialized societies are typically acid-producing, we compared base-producing fruits and vegetables with oral NaHCO3 (HCO3) regarding the primary outcome of follow-up estimated GFR (eGFR) and secondary outcomes of improved metabolic acidosis and reduced urine indices of kidney injury.. Individuals with stage 4 (eGFR, 15-29 ml/min per 1.73 m(2)) CKD due to hypertensive nephropathy, had a PTCO2 level < 22 mM, and were receiving angiotensin-converting enzyme inhibition were randomly assigned to 1 year of daily oral NaHCO3 at 1.0 mEq/kg per day (n=35) or fruits and vegetables dosed to reduce dietary acid by half (n=36).. Plasma cystatin C-calculated eGFR did not differ at baseline and 1 year between groups. One-year PTCO2 was higher than baseline in the HCO3 group (21.2±1.3 versus 19.5±1.5 mM; P<0.01) and the fruits and vegetables group (19.9±1.7 versus 19.3±1.9 mM; P<0.01), consistent with improved metabolic acidosis, and was higher in the HCO3 than the fruits and vegetable group (P<0.001). One-year urine indices of kidney injury were lower than baseline in both groups. Plasma [K(+)] did not increase in either group.. One year of fruits and vegetables or NaHCO3 in individuals with stage 4 CKD yielded eGFR that was not different, was associated with higher-than-baseline PTCO2, and was associated with lower-than-baseline urine indices of kidney injury. The data indicate that fruits and vegetables improve metabolic acidosis and reduce kidney injury in stage 4 CKD without producing hyperkalemia.

Topics: Acid-Base Equilibrium; Acidosis; Administration, Oral; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Biomarkers; Diet; Female; Fruit; Glomerular Filtration Rate; Humans; Hypertension; Kidney; Male; Middle Aged; Potassium; Renal Insufficiency, Chronic; Sodium Bicarbonate; Texas; Time Factors; Treatment Outcome; Vegetables

The neutralization of dietary acid with sodium bicarbonate decreases kidney injury and slows the decline of the glomerular filtration rate (GFR) in animals and patients with chronic kidney disease. The sodium intake, however, could be problematic in patients with reduced GFR. As alkali-induced dietary protein decreased kidney injury in animals, we compared the efficacy of alkali-inducing fruits and vegetables with oral sodium bicarbonate to diminish kidney injury in patients with hypertensive nephropathy at stage 1 or 2 estimated GFR. All patients were evaluated 30 days after no intervention; daily oral sodium bicarbonate; or fruits and vegetables in amounts calculated to reduce dietary acid by half. All patients had 6 months of antihypertensive control by angiotensin-converting enzyme inhibition before and during these studies, and otherwise ate ad lib. Indices of kidney injury were not changed in the stage 1 group. By contrast, each treatment of stage 2 patients decreased urinary albumin, N-acetyl β-D-glucosaminidase, and transforming growth factor β from the controls to a similar extent. Thus, a reduction in dietary acid decreased kidney injury in patients with moderately reduced eGFR due to hypertensive nephropathy and that with fruits and vegetables was comparable to sodium bicarbonate. Fruits and vegetables appear to be an effective kidney protective adjunct to blood pressure reduction and angiotensin-converting enzyme inhibition in hypertensive and possibly other nephropathies.

Topics: Acids; Adult; Diet; Female; Fruit; Glomerular Filtration Rate; Humans; Hypertension; Kidney Diseases; Male; Middle Aged; Renal Insufficiency, Chronic; Sodium Bicarbonate; Vegetables

In most patients with hypertensive nephropathy and low glomerular filtration rate (GFR), the kidney function progressively declines despite the adequate control of the hypertension with angiotensin-converting enzyme inhibition. Previously we found that 2 years of oral sodium citrate slowed GFR decline in patients whose estimated GFR (eGFR) was very low (mean 33 ml/min). This treatment also slowed GFR decline in an animal model of surgically reduced nephron mass. Here, we tested if daily oral sodium bicarbonate slowed GFR decline in patients with hypertensive nephropathy with reduced but relatively preserved eGFR (mean 75 ml/min) in a 5-year, prospective, randomized, placebo-controlled, and blinded interventional study. Patients matched for age, ethnicity, albuminuria, and eGFR received daily placebo or equimolar sodium chloride or bicarbonate while maintaining antihypertensive regimens (including angiotensin-converting enzyme inhibition) aiming for their recommended blood pressure targets. After 5 years, the rate of eGFR decline, estimated using plasma cystatin C, was slower and eGFR was higher in patients given sodium bicarbonate than in those given placebo or sodium chloride. Thus, our study shows that in hypertensive nephropathy, daily sodium bicarbonate is an effective kidney protective adjunct to blood pressure control along with angiotensin-converting enzyme inhibition.

Topics: Administration, Oral; Adult; Albuminuria; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Blood Pressure; Cystatin C; Double-Blind Method; Drug Therapy, Combination; Female; Glomerular Filtration Rate; Humans; Hypertension; Kidney; Kidney Diseases; Longitudinal Studies; Male; Middle Aged; Prospective Studies; Sodium Bicarbonate

To test the hypothesis that NaCl and NaHCO3 have divergent effects on blood pressure, we carried out a randomly allocated, placebo-controlled, crossover trial in 10 mildly hypertensive and 10 normal subjects. They ingested a fixed daily basal diet of 60 mmol sodium and chloride, 60 mmol potassium and 14 mmol calcium. After balance was achieved (4 days), the subjects were randomly assigned to drink 3 liters/day of a NaHCO3-containing mineral water (26.2 mmol/l sodium and 33.03 mmol/l HCO3) or a control solution containing equimolar amounts of cations as the chloride salt for 7 days (total daily sodium 138 mmol). All urine was collected. Blood pressure was determined by an automated device. One month later the opposite regimen was followed. NaCl did not influence blood pressure, whereas NaHCO3 decreased systolic blood pressure (by 5 mmHg) in the hypertensive subjects. Both regimens decreased plasma renin activity in the hypertensive subjects but did not consistently influence plasma aldosterone or catecholamines. However, urinary calcium excretion, which was greater in hypertensives than in normotensives, and greater in white than in black subjects, increased consistently with NaCl but not with NaHCO3. The excretion of urate was not influenced by the regimens; however, urate excretion was consistently greater in whites than in blacks. The data show that NaCl increases calcium excretion whereas NaHCO3 does not, even at modest levels of intake. NaCl and NaHCO3 may therefore differ in their effects on blood pressure.

Topics: Adult; Bicarbonates; Blood Pressure; Female; Humans; Hypertension; Male; Mineral Waters; Randomized Controlled Trials as Topic; Sodium; Sodium Bicarbonate; Sodium Chloride; Sodium, Dietary; Water-Electrolyte Balance

Effervescent formulations of paracetamol containing sodium bicarbonate have been reported to associate with increased blood pressure and a higher risk of cardiovascular diseases and all-cause mortality. Given the major implications of these findings, the reported associations were re-examined.. Using linked electronic health records data, a cohort of 475 442 UK individuals with at least one prescription of paracetamol, aged between 60 and 90 years, was identified. Outcomes in patients taking sodium-based paracetamol were compared with those taking non-sodium-based formulations of the same. Using a deep learning approach, associations with systolic blood pressure (SBP), major cardiovascular events (myocardial infarction, heart failure, and stroke), and all-cause mortality within 1 year after baseline were investigated.. A total of 460 980 and 14 462 patients were identified for the non-sodium-based and sodium-based paracetamol exposure groups, respectively (mean age: 74 years; 64% women). Analysis revealed no difference in SBP [mean difference -0.04 mmHg (95% confidence interval -0.51, 0.43)] and no association with major cardiovascular events [relative risk (RR) 1.03 (0.91, 1.16)]. Sodium-based paracetamol showed a positive association with all-cause mortality [RR 1.46 (1.40, 1.52)]. However, after further accounting of other sources of residual confounding, the observed association attenuated towards the null [RR 1.08 (1.01, 1.16)]. Exploratory analyses revealed dysphagia and related conditions as major sources of uncontrolled confounding by indication for this association.. This study does not support previous suggestions of increased SBP and an elevated risk of cardiovascular events from short-term use of sodium bicarbonate paracetamol in routine clinical practice.

Topics: Acetaminophen; Aged; Aged, 80 and over; Antihypertensive Agents; Blood Pressure; Cardiovascular Diseases; Female; Humans; Hypertension; Male; Middle Aged; Myocardial Infarction; Sodium; Sodium Bicarbonate

Topics: Acidosis; Diet; Female; Fruit; Humans; Hypertension; Male; Renal Insufficiency, Chronic; Sodium Bicarbonate; Vegetables

The human SLC4A5 gene has been identified as a hypertension susceptibility gene based on the association of single nucleotide polymorphisms with blood pressure (BP) levels and hypertension status. The biochemical basis of this association is unknown particularly since no single gene variant was linked to hypertension in humans. SLC4A5 (NBCe2, NBC4) is expressed in the collecting duct of the kidney and acts as an electrogenic ion-transporter that transports sodium and bicarbonate with a 1:2 or 1:3 stoichiometry allowing bicarbonate reabsorption with relatively minor concurrent sodium uptake. We have mutated the Slc4a5 gene in mice, which caused a persistent increase in systolic and diastolic BP. Slc4a5 mutant mice also displayed a compensated metabolic acidosis and hyporeninemic hypoaldosteronism. Analysis of kidney physiology revealed elevated fluid intake and urine excretion and increased glomerular filtration rate. Transcriptome analysis uncovers possible compensatory mechanisms induced by SLC4A5 mutation, including upregulation of SLC4A7 and pendrin as well as molecular mechanisms associated with hypertension. Induction of metabolic alkalosis eliminated the BP difference between wild-type and Slc4a5 mutant mice. We conclude that the impairment of the function of SLC4A5 favors development of a hypertensive state. We reason that the loss of sodium-sparing bicarbonate reabsorption by SLC4A5 initiates a regulatory cascade consisting of compensatory bicarbonate reabsorption via other sodium-bicarbonate transporters (e.g. SLC4A7) at the expense of an increased sodium uptake. This will ultimately raise BP and cause hypoaldosteronism, thus providing a mechanistic explanation for the linkage of the SLC4A5 locus to hypertension in humans.

Topics: Acid-Base Equilibrium; Acidosis, Renal Tubular; Aldosterone; Animals; Atrial Natriuretic Factor; Blood; Blood Chemical Analysis; Blood Pressure; Gene Expression Regulation; Glomerular Filtration Rate; Hydrogen-Ion Concentration; Hypertension; In Situ Hybridization; Kidney; Kidney Tubules; Male; Mice; Mutation; Sequence Deletion; Sodium; Sodium Bicarbonate; Sodium-Bicarbonate Symporters; Urination; Urine

Topics: Adrenergic beta-2 Receptor Agonists; Albuterol; Anti-Arrhythmia Agents; Anticonvulsants; Antihypertensive Agents; Antiparkinson Agents; Antipsychotic Agents; Anxiety Disorders; Atropine; Bradycardia; Calcium Chloride; Diabetes Mellitus; Diagnosis, Differential; Drug Therapy, Combination; Humans; Hyperkalemia; Hypertension; Hypoglycemic Agents; Hypolipidemic Agents; Male; Middle Aged; Muscle Weakness; Polypharmacy; Renal Dialysis; Renal Insufficiency; Sodium Bicarbonate; Sodium Chloride

We tested the hypothesis that the Na(+) component of dietary NaCl can have a pressor effect apart from its capacity to complement the extracellular osmotic activity of Cl(-) and, thus, expand plasma volume. We studied 35 mostly normotensive blacks who ingested a low-NaCl diet, 30 mmol/d, for 3 weeks, in the first and third of which Na(+) was loaded orally with either NaHCO(3) or NaCl, in random order (250 mmol/d). In subjects adjudged to be salt sensitive (n=18; Delta mean arterial pressure: >or=5 mm Hg with NaCl load), but not in salt-resistant subjects (n=17), loading with NaHCO(3) was also pressor. The pressor effect of NaHCO(3) was half that of NaCl: mean arterial pressure (millimeters of mercury) increased significantly from 90 on low NaCl to 95 with NaHCO(3) and to 101 with NaCl. The pressor effect of NaCl strongly predicted that of NaHCO(3.) As judged by hematocrit decrease, plasma volume expansion with NaCl was the same in salt-resistant and salt-sensitive subjects and twice that with NaHCO(3), irrespective of the pressor effect. In salt-sensitive subjects, mean arterial pressure varied directly with plasma Na(+) concentration attained with all Na(+) loading. In salt-sensitive but not salt-resistant subjects, NaHCO(3) and NaCl induced decreases in renal blood flow and increases in renal vascular resistance; changes in renal blood flow were not different with the 2 salts. Responses of renal blood flow and renal vascular resistance to NaHCO(3) were strongly predicted by those to NaCl. In establishing the fact of "sodium-selective" salt sensitivity, the current observations demonstrate that the Na(+) component of NaCl can have pressor and renal vasoconstrictive properties apart from its capacity to complement Cl(-) in plasma volume expansion.

Topics: Adult; Black People; Blood Pressure; Female; Humans; Hypertension; Male; Middle Aged; Plasma Volume; Renal Circulation; Sodium; Sodium Bicarbonate; Sodium Chloride, Dietary; Vascular Resistance

Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Electrocardiography; Enalapril; Humans; Hyperkalemia; Hypertension; Kidney Failure, Chronic; Male; Potassium; Renal Dialysis; Sodium Bicarbonate; Sympathomimetics

A 59-year-old man was referred to the hospital for psychiatric reasons. To control hypertension and chronic heart failure he had been treated with 5 mg ramipril and 12.5 mg hydrochlorothiazide. In addition, he received 25 mg spironolactone. A prostate disease was diagnosed two months ago.. Laboratory analysis revealed a severe hyperkalemia (9.3 mmol/l) as well as an increase in creatinine (24.3 mg/dl) and urea nitrogen (349.0 mg/dl). The ECG showed a bradycardia with increased T-wave amplitudes. Abdominal sonography revealed a full urinary bladder.. Administration of terbutaline, sodium bicarbonate, and glucoseinfusion lowered potassium level to 6.3 mmol/l before hemodialysis was started. Hyperplasia of the prostate gland was found to be the reason for acute renal failure. Dialysis treatment was only temporarily necessary; afterwards, the patient was transferred to the urology department for subsequent therapy.. Hyperkalemia is a life-threatening emergency that requires immediate therapy. Conservative treatment allows to partially correct water-electrolyte imbalance until hemodialysis can be performed. Hyperkalemia often results from the administration of combination therapy with ACE-inhibitors/AT (1)-antaganonists and antikaliuretic diuretics (spironolactone) in renal failure.

Topics: Acute Kidney Injury; Adrenergic beta-Agonists; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Bradycardia; Diuretics; Drug Therapy, Combination; Electrocardiography; Emergencies; Glucose; Heart Failure; Humans; Hydrochlorothiazide; Hyperkalemia; Hypertension; Male; Mental Disorders; Middle Aged; Prostatic Hyperplasia; Ramipril; Renal Dialysis; Sodium Bicarbonate; Terbutaline

To evaluate the role of chloride in the pathogenesis of salt-dependent deoxycorticosterone (DOC) hypertension, we studied young Wistar rats chronically loaded with sodium bicarbonate (NaHCO(3)) or sodium chloride (NaCl) which were administered either in the diet or in the drinking fluid. Selective sodium loading (without chloride) increased blood pressure (BP) in DOC-treated animals only if NaHCO(3) was provided in the diet. In contrast, no significant blood pressure changes were induced by DOC treatment in rats drinking NaHCO(3) solution. Hypernatremia and high plasma osmolality occurred only in rats drinking NaCl or NaHCO(3) solutions. Compared to great volume expansion in NaCl-loaded DOC-treated rats, the degree of extracellular fluid volume expansion (namely of its interstitial fraction) was substantially lower in both NaHCO(3)-loaded groups in which significant hypokalemia was observed. NaHCO(3)-drinking rats without significant blood pressure response to DOC treatment represented the only experimental group in which blood volume was not expanded. In conclusion, our data confirm previous observations that NaHCO(3) loading is less potent in eliciting DOC hypertension than NaCl loading, but blood pressure rise in rats fed NaHCO(3) diet clearly demonstrated that selective sodium loading could potentiate the development of DOC hypertension if NaHCO(3) is offered within the appropriate dietary regimen. The reasons for the failure of NaHCO(3)-drinking rats to elevate blood pressure in response to chronic mineralocorticoid treatment are not obvious. However, the absence of a significant plasma volume expansion together with hypernatremia and increased plasma osmolality suggest a considerable degree of dehydration in these animals which fail to increase their fluid consumption compared to water drinking rats.

Topics: Animals; Blood Pressure; Blood Volume; Body Fluids; Body Weight; Chlorides; Desoxycorticosterone; Drinking; Extracellular Fluid; Hematocrit; Hypertension; Male; Osmolar Concentration; Plasma Volume; Potassium; Rats; Rats, Wistar; Sodium; Sodium Bicarbonate; Sodium Chloride, Dietary

Topics: Alkalosis; Circadian Rhythm; Humans; Hypertension; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Sleep Apnea Syndromes; Sodium Bicarbonate; Substance-Related Disorders

The outcomes of 294 orthotopic liver transplants performed in 221 children at The University of Chicago Children's Hospital between October 1984 and October 1992 have been retrospectively reviewed. Medical information for 281 transplant in 210 children was sufficient for inclusion in this analysis. The mean age at transplant was 4.1 +/- 5.0 yr. Forty-four percent of the children were male, and 16% of the transplants were living-related. Four children received combined liver-kidney transplants. Seventy-six percent of the children are currently alive. The incidence of acute renal failure occurring following transplantation and requiring dialysis was 6.2% with a mortality rate of 85%. Early postoperative hypertension was seen in 65% of the children and persistent hypertension of greater than 12 months duration was seen in 28%. Sixteen percent of children developed metabolic acidosis requiring sustained sodium bicarbonate supplementation. Aggregate and longitudinal analysis of serial calculated glomerular filtration rates revealed abnormal renal function in approximately one third of children at any given time period following transplantation. The renal dysfunction was unrelated to age at transplant, type of transplant, gender, previous transplants, rejection episodes, courses of nephrotoxic drugs, presence of hypertension, or cyclosporin dose. This review supports prior studies which document abnormal renal function following orthotopic liver transplantation in a significant proportion of children.

Topics: Acidosis; Acute Kidney Injury; Adolescent; Adult; Age Factors; Child; Child, Preschool; Cyclosporine; Female; Follow-Up Studies; Glomerular Filtration Rate; Graft Rejection; Humans; Hypertension; Immunosuppressive Agents; Incidence; Infant; Kidney; Kidney Diseases; Kidney Transplantation; Liver Transplantation; Living Donors; Longitudinal Studies; Male; Renal Dialysis; Retrospective Studies; Sex Factors; Sodium Bicarbonate; Survival Rate; Treatment Outcome

A patient with a history of cerebrovascular disease, hypertension, and previous gastrectomy developed metabolic alkalosis and myoclonus. His medications included the anti-hypertensive agents nicardipine hydrochloride, delapril, prazosin; dihydroergotoxin and ticlopidine for cerebral infarction; estazolam for insomnia; azuren-L-glutamine compound and S-M powder. In addition, he had taken 12 grams per day of Ohta's Isan antacid, which contained 625 mg sodium bicarbonate per 1.3 g of antacid powder over a 6-month period. This antacid is commonly used in Japan. This is the first report of a case of metabolic alkalosis and myoclonus secondary to ingestion of a commercially available antacid in Japan.

Topics: Aged; Alkalosis; Antacids; Cardiovascular Agents; Cerebral Infarction; Dyspepsia; Gastrectomy; Humans; Hypertension; Hypnotics and Sedatives; Hypokalemia; Male; Myoclonus; Sleep Initiation and Maintenance Disorders; Sodium Bicarbonate

To review the data on pharmacology, pathophysiology and treatment of cocaine toxicity, with particular relevance to the heart and cardiovascular system.. Published epidemiology, laboratory and clinical studies on the pharmacology, electrophysiology and pathophysiology of cocaine toxicity and its treatment.. Cocaine toxicity-related morbidity and mortality are frequent due to the potent pharmacological effects of the drug as an indirect-acting sympathomimetic agent and its class I antiarrhythmic property paradoxically inducing pro-arrhythmia. The cardiac and cardiovascular toxic effects of cocaine include various degrees of myocardial ischemia, cardiac arrhythmias, cardiotoxicity, hypertensive effects, cerebrovascular effects and a hypercoagulable state. Treatment of cocaine toxicity must be based on the multiple factors leading to the toxicity. Sodium bicarbonate appears to have an important role in the acute setting with conduction abnormalities, seizures or acidosis. Unopposed alpha-stimulation provided by beta-blockade should be avoided. Central nervous system hyperexcitability should be treated with diazepam. The use of calcium antagonists appears logical.. Cocaine is an alkaloid with widespread illicit use. The rationale for treating acute cocaine intoxication has become clearer and more logical with increased knowledge of its mechanisms of action.

Topics: Arrhythmias, Cardiac; Cerebrovascular Disorders; Cocaine; Heart; Humans; Hypertension; Myocardial Ischemia; Sodium Bicarbonate

The effect of the converting enzyme inhibition treatment on the renal acidification function was studied in 5 mild hypertensive subjects. Before and after one week treatment with daily 75 mg of captopril bicarbonate loading was carried out by peroral administration of 68 mmol NaHCO3. The difference between the partial carbon dioxide tension (pCO2) of the urine and blood [(U-B) pCO2], as well as the pH and bicarbonate values were determined at every hour in the course of 3 hours. In the same persons phosphate loadings were also carried out. Although decrease H+ excretion may follow the suppression of aldosterone, which could be expected in response to the short-term captopril treatment, no such change in distal tubular function could be demonstrated by the sensitive methods administered in this study. It seems to be highly probable, that captopril does not limit the urinary acidifying function in patients with healthy kidneys.

Topics: Administration, Oral; Angiotensin-Converting Enzyme Inhibitors; Captopril; Carbon Dioxide; Female; Humans; Hydrogen-Ion Concentration; Hypertension; Kidney; Male; Partial Pressure; Phosphates; Sodium Bicarbonate

The contribution of chloride to the haemodynamic changes of salt-dependent deoxycorticosterone (DOC) hypertension was studied in young Wistar rats subjected to dietary loading with sodium chloride (NaCl) or sodium bicarbonate (NaHCO3). Mean arterial pressure (MAP), cardiac output, systemic resistance (TPR) and arterial rigidity (estimated from pulse pressure/stroke volume ratio, PP/SV) were determined in conscious chronically cannulated rats. DOC-induced increase of MAP and TPR appeared earlier in NaCl-loaded than in NaHCO3-loaded rats. After 4-6 weeks of hypertensive treatment MAP, TPR and PP/SV ratio were higher in DOC-treated rats fed NaCl diet than in those fed NaHCO3 diet. In contrast, after a long-term hypertensive regimen (lasting for 7-9 weeks) there was no significant difference in either MAP or TPR between rats loaded with NaCl or NaHCO3. On the other hand, DOC hypertension induced by a long-term feeding of NaHCO3 diet was not associated with an increase of arterial rigidity which was characteristic for DOC-NaCl hypertensive rats. Thus, a sufficiently long selective dietary sodium loading is capable to increase the systemic resistance but not to alter the arterial rigidity. This was also confirmed by a comparison of blood pressure-matched DOC hypertensive rats fed NaCl or NaHCO3 diets. These animals did not differ in the degree of systemic resistance elevation but the arterial rigidity was increased only in NaCl-loaded rats.

Topics: Animals; Blood Pressure; Cardiac Output; Desoxycorticosterone; Diet; Hemodynamics; Hypertension; Male; Pulse; Rats; Rats, Wistar; Sodium Bicarbonate; Sodium Chloride, Dietary; Vascular Resistance

We report two diabetic patients who developed lactic acidosis following the use of Buformin. Treatment consisted of mechanical ventilation, massive bicarbonate administration, circulatory support with dopamine and peritoneal dialysis. Despite this, both patients died.

Topics: Acidosis, Lactic; Aged; Bicarbonates; Biguanides; Buformin; Diabetes Mellitus; Diabetic Angiopathies; Dopamine; Humans; Hypertension; Male; Peritoneal Dialysis; Respiration, Artificial; Sodium; Sodium Bicarbonate

Topics: Adult; Anemia, Hypochromic; Bicarbonates; Female; Humans; Hypertension; Patient Compliance; Pica; Sodium; Sodium Bicarbonate

The role of sodium and its accompanying anion for the development of DOCA-salt hypertension was studied in uninephrectomized DOCA-treated weanling Wistar rats which were fed a diet containing either sodium chloride or sodium bicarbonate (170 mmol/kg). The blood pressure was increased in both groups of rats with sodium overload as compared to rats fed a low-salt diet only. A decreased cardiac output and substantially elevated systemic resistance were demonstrated in both groups of rats with high sodium intake in comparison with rats kept on a low-salt diet. However, these haemodynamic changes were more pronounced in rats with sodium chloride overload than in animals with a high sodium bicarbonate intake. On the other hand, the rigidity of major arteries which was estimated as the pulse pressure/stroke volume ratio, was increased only in rats fed a diet with sodium chloride but not in rats with sodium bicarbonate overload. Thus high sodium intake was responsible for the changes of systemic resistance in DOCA-treated animals and its action was only slightly augmented by a high chloride intake. In contrast to this, the chloride overload seemed to be essential for the induction of increased arterial rigidity.

Topics: Animals; Bicarbonates; Chlorides; Desoxycorticosterone; Hemodynamics; Hypertension; Male; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate; Vascular Resistance

Topics: Acidosis; Analgesics; Atropine; Bicarbonates; Bradycardia; Cardiac Complexes, Premature; Critical Care; Diazepam; Digitalis Glycosides; Early Ambulation; First Aid; Furosemide; Heparin; Humans; Hypertension; Lidocaine; Myocardial Infarction; Nitroglycerin; Pacemaker, Artificial; Positive-Pressure Respiration; Sodium; Sodium Bicarbonate; Verapamil

In uninephrectomized rats given desoxycorticosterone (DOC) and a fixed amount of dietary sodium, we sought to determine if the anionic component of the sodium salt consumed could be a pathogenetic determinant of the occurrence and maintenance of hypertension. After two weeks, mean arterial pressure (MAP) in rats given DOC and NaCl was significantly greater than in rats given DOC and NaHCO3, or NaCl without DOC. Replacing dietary NaCl with a near equimolar amount of NaHCO3 corrected the hypertension. Replacing dietary NaHCO3 with a near equimolar amount of NaCl induced hypertension. These findings could not be attributed to changes in caloric intake, weight gain, or external balances of sodium or potassium. These findings demonstrate that, in rats given DOC and a fixed amount of dietary sodium, the anionic component of the sodium salt consumed can determine the occurrence, progression, and reversal of hypertension.

Topics: Animals; Bicarbonates; Blood Pressure; Desoxycorticosterone; Diet; Drug Interactions; Hypertension; Male; Nephrectomy; Rats; Rats, Inbred Strains; Sodium; Sodium Bicarbonate; Sodium Chloride; Time Factors

In 116 patients with coronary heart disease, essential hypertension, acute and chronic glomerulonephritis and pyelonephritis, the authors observed differences in the excretion of the ions of 42K, stable potassium, 24Na, stable sodium, chlorine as well as in the value of diuresis during the administration of equimolar solutions of potassium hydrocarbonate and potassium chloride, sodium hydrocarbonate and sodium chloride labeled with 42K and 24Na respectively. These differences depended on the expression of the basic (alkaline) characteristics of the anions of the administered solutions of potassium and sodium and the osmolarity of the administered amount of liquid. Pronounced ion exchange reactions were observed during the administration of KHCO3 solution only, the multiplicity factor of the excretion of sodium and chlorine ions with urine significantly exceeding that of diuresis. During the administration of KCl solutions in the isotonic NaCl solution and 5% glucose, the excretion of sodium and chlorine ions changed strictly in accordance with the changes of diuresis. Similar changes were noted in the administration of the solutions of sodium hydrocarbonate and sodium chloride.

Topics: Bicarbonates; Coronary Disease; Humans; Hypertension; Injections, Intravenous; Potassium; Potassium Chloride; Potassium Compounds; Potassium Radioisotopes; Sodium; Sodium Bicarbonate; Sodium Chloride; Sodium Radioisotopes; Solutions

The effect of the anion associated with sodium loading on the development of hypertension in the Dahl salt-sensitive rat was determined. For 5 weeks rats were fed a diet containing normal or high concentrations of sodium chloride or high concentrations of sodium provided as a mixture of sodium bicarbonate, phosphate, and amino acids. After 1 week on these diets and until the end of the study the rats receiving high concentrations of sodium chloride had higher systolic blood pressures than the rats in the other two groups. There were no statistically significant group differences in plasma volume, arterial pH, or plasma concentrations of Na+, K+, Cl-, Ca2+, or creatinine, or in renomedullary prostaglandin E2 production. Compared to the animals receiving normal concentrations of sodium chloride, those receiving high concentrations of sodium chloride or amino acids showed decreased plasma renin activity and plasma aldosterone concentrations. Thus, the anion ingested with sodium alters the development and severity of hypertension in the Dahl salt-sensitive rat.

Topics: Animals; Bicarbonates; Blood Pressure; Chlorides; Diet; Hypertension; Kidney; Loop of Henle; Male; Phosphates; Rats; Rats, Inbred Strains; Sodium Bicarbonate; Sodium Chloride

Both the inhibition of renin release by sodium chloride and salt-sensitive hypertension have been attributed to sodium. We evaluated the contribution of chloride to these responses to sodium chloride. In the Sprague-Dawley rat, acute and chronic administration of sodium salts other than sodium chloride failed to suppress plasma renin activity, whereas renin was inhibited by both sodium chloride and by selective chloride (without sodium) loading. Plasma renin activity was stimulated by selective chloride depletion. Similarly, in humans, plasma renin activity was suppressed by sodium chloride but not by sodium bicarbonate infusion. In a preliminary study in the Dahl salt-sensitive rat, in contrast to sodium chloride loading, sodium bicarbonate loading failed to produce hypertension. Thus, both the renin and possibly the blood pressure responses to sodium chloride are dependent on chloride.

Topics: Adult; Animals; Bicarbonates; Blood Pressure; Chlorides; Diet; Dogs; Humans; Hypertension; Male; Nitrates; Potassium; Rats; Renin; Sodium Bicarbonate; Sodium Chloride