Biomedical subjects

A Aviv

Publications and source records attributed to A Aviv.

122 records · Page 7Linked to original sources

PubMed1983

Na+-K+-ATPase in rat vascular smooth muscle cell grown in vitro.

This study has focused on the characteristics of the Na+-K+-ATPase in in vitro preparations of vascular smooth muscle cells (VSMCs) derived from the rat carotid artery. The maximum velocity of enzyme reaction (Vmax) for the specific activity of the enzyme in the VSMCs' preparations was 2.36 +/- 0.04 (SE) mumol Pi X mg cell protein-1 X h-1 or 0.82 +/- 0.02 mumol Pi X 10(6) cells-1 X h-1. The activation of the enzyme by potassium, sodium and ATP has been investigated. The half-maximal values for potassium and sodium activation of the enzyme in the preparations were 1.18 and 10-20 meq/l, respectively. The respective Vmax values for potassium and sodium activation were reached at concentrations of 4-10 and 80-100 meq/l. The Michaelis constant for ATP was 0.83 mM. Calcium exerted a potent inhibition on the activity of the enzyme (I50 at 1 mM). It has been concluded that the Na+-K+-ATPase kinetic pattern in in vitro preparations of VSMCs is quite similar to that observed in homogenates or subcellular fractions of other tissues.

Animals↗

PubMed1983

Vanadium, Na-K-ATPase, and potassium adaptation in the rat.

Vanadate is a potent inhibitor of Na-K-ATPase in vitro. It has been suggested that vanadium may function as a cellular regulator of Na-K-ATPase in vivo. To examine this speculation, we studied in rats the effect of high vanadate intake on 1) the tissue levels and distribution of vanadium, 2) basal activity of Na-K-ATPase in various tissues, and 3) the activity of Na-K-ATPase in various organs under conditions of massive chronic potassium loading known to stimulate Na-K-ATPase in the kidney and colon. Despite extremely high tissue levels of vanadium there was no demonstrable effect of the element on the basal activity of Na-K-ATPase. When subjected to chronic potassium loading, rats with high tissue vanadium concentrations underwent potassium adaptation that was associated with a rise in Na-K-ATPase activity in the renal cortex, renal medulla, and colonic mucosa. Further studies are needed to support or refute the thesis that vanadium might be an intracellular regulator of Na-K-ATPase in vivo.

Animals↗

PubMed1983

Vanadate effect on the Na,K-ATPase and the Na-K pump in in vitro-grown rat vascular smooth muscle cells.

The impact of vanadate on the Na,K-ATPase system in the vascular smooth muscle cell is poorly understood. The present study describes the kinetics of the effect of vanadate on Na,K-ATPase and the Na-K pump in in vitro grown rat VSMC's. Vanadate interaction with the Na,K-ATPase system in vascular smooth muscle cells was examined by observing its influence on ouabain-sensitive adenosine triphosphate hydrolysis in disrupted cells rendered permeable by osmotic shock, and the uptake of rubidium by intact cells. The I50 for vanadate inhibition of ouabain-sensitive hydrolysis of adenosine triphosphate occurred at vanadate concentrations of 10(-6) to 10(-7) M. This inhibition was potassium dependent. The maximal inhibitory effect of vanadate occurred at potassium concentrations of 10-20 mEq/liter. Sodium exerted a moderate antagonistic influence on vanadate inhibition of ouabain-sensitive adenosine triphosphate hydrolysis. Rubidium uptake by vascular smooth muscle cells was not altered within 120 minutes when 10(-5) M vanadate was added to the medium containing intact vascular smooth muscle cells. Yet, vanadium concentrations in the vascular smooth muscle cells within this incubation period reached levels 1.48-fold higher than the extracellular vanadate concentrations of 10(-5) M. These observations indicate that vanadate is a potent inhibitor of the VSMC Na,K-ATPase in disrupted vascular smooth muscle cells. However, in intact vascular smooth muscle cells vanadium gaining access into the vascular smooth muscle cell's interior does not inhibit the Na-K pump, probably because of its binding to intracellular proteins and/or conversion from the vanadate to the vanadyl ion.

Animals↗

PubMed1982

Release of some trace metals from disposable coils during hemodialysis.

In a previous study, we demonstrated that certain disposable coils are contaminated with zinc and release substantial quantities of zinc during hemodialysis, producing high postdialysis plasma zinc concentrations. The present investigation was undertaken to monitor plasma and dialysis fluid zinc and copper throughout dialysis and to estimate plasma zinc and copper uptake. Aluminum, cadmium, and lead release from coils was also determined. Venous plasma, arterial plasma, and coil chamber fluid were sampled periodically during dialysis; the trace metal concentrations were determined by flame atomic absorption spectrophotometry. Release of considerable quantities of zinc from the coils into the dialysis fluid, with uptake into the patient's plasma, was found. Approximately one-half of the plasma zinc uptake occurred within the first 45 min. Coils from different lots released significantly (p less than 0.001) different quantities of zinc. Plasma uptake of zinc ranged from 3.2 mg to 23.0 mg, with a mean (+/-SD) of 15.0 +/- 6.1 mg. Copper release and uptake was low. No detectable release of lead, cadmium, or aluminum was observed. The results suggest that zinc release from disposable dialysis coils should be assessed before recommending that hemodialysis patients receive zinc supplements.

Adult↗

PubMed1982

Balance and tissue distribution of vanadium after short-term ingestion of vanadate.

Forty-six female Sprague-Dawley rats (170-200 g) were randomly assigned to one of six treatment groups receiving 0.1, 5.0, or 25.0 ppm dietary vanadium with either normal (0.13 mEq/g) or high (1.82 mEq/g) dietary potassium. Supplemental vanadium was administered as sodium metavanadate. These diets were fed for 2 weeks, and all feces and urine collected. At the end of the treatment period, brain, liver, renal cortex and medulla, whole blood, and plasma were obtained and analyzed for vanadium by atomic absorption spectrophotometry, as were the urine and feces samples. Tissue vanadium concentration increased significantly (P less than 0.00001) with increasing food vanadium content, but were not affected by dietary potassium in spite of the polyuria induced in animals on the high potassium diets. The highest vanadium concentrations were found in the renal cortex and the lowest, in the brain. Although urinary vanadium excretion was higher in animals fed the high potassium diets, a relatively small percentage of ingested vanadium was excreted in the urine. Rats fed diets containing no supplemental sodium metavanadate (0.1 ppm vanadium) were in negative vanadium balance, but their growth was not inhibited. Animals receiving 5.0 and 25.0 ppm vanadium diets retained 39.7 +/- 18.5% of ingested vanadium and excreted 59.1 +/- 18.8% of ingested vanadium in the feces. These values indicate greater absorption and retention of ingested vanadium than found In previously reported investigations.

Animals↗

PubMed1982

Chronic sodium deficit in the immature rat: its effect on adaptation to sodium excess.

The impact of chronic low-sodium intake during early development on body sodium homeostasis is not sufficiently known. To explore this effect, we have investigated the influence of chronic sodium deficit during the rapid growth period of rats (first phase, age 3-7 wk) and the short-term effect of sodium repletion (second phase, age 8-9 wk) on parameters such as growth rate, urinary aldosterone excretion, 22Na volume of distribution (space), and various renal functions. Three groups were studied: group I (control) and groups II and III. During the first phase the respective sodium intake values for these groups were 8.9, 3.1, and 1.5 meq.kg body wt-1.day-1. During the second phase, all groups had sodium intake of 8.7-8.8 meq.kg body wt-1.day-1. At the end of the first phase, group II showed weight gain and 22Na space values similar to those of group I. Group III demonstrated severe growth retardation and reduced 22Na space. During the second phase, both groups II and III demonstrated expansion of the 22Na space and persistently elevated urinary "acid-labile" aldosterone excretions. Despite the 2 wk of sodium repletion, group III failed to catch up with the body weight of groups I and II. It is concluded that chronic sodium deficit during early development transition is made to a higher sodium intake.

Aging↗

PubMed1982

The fractional hepatic extraction of histidine in acute and chronic renal failure.

The fractional hepatic extraction (FHE) of histidine absorbed from the in vivo-perfused jejunum was measured in rats with chronic renal failure (CRF) and acute renal failure (ARF). CRF rats were compared with two groups: (a) animals pair-fed with the CRF rats, designated as a protein-calorie malnutrition (PCM) group, and (b) animals fed ad libitum. Despite their poor dietary intake, the FHE of histidine in the CRF animals did not differ from that of rat fed ad libitum. As expected, the PCM animals demonstrated a substantial reduction in the FHE of histidine, thereby making the amino acid more available for peripheral tissue utilization. Animals with ARF also manifested no change in the FHE of histidine. The present study was designed to examine the hypothesis that in CRF, the lack of hepatic adaptations to the diminished intake of histidine may contribute to the abnormal metabolism of this amino acid in uremia.

Acute Kidney Injury↗

PubMed1982

The intestinal profile of Na-K-ATPase in two rat models of acute renal failure.

The specific activity of mucosal Na-K-ATPase in segments of the small intestine and colon was examined after BN or BUL. BN resulted in a surge of the specific activity of the enzyme throughout the mucosa of the intestinal tract (duodenum 26%, jejunum 33%, ileum 37%, and colon 68%). BUL induced to significant change in the specific activity of Na-K-ATPase in the small intestinal mucosa and a small rise (32%) in the specific activity of the enzyme in the colon. Kinetic analyses of potassium activation of the enzyme in the two models of ARF indicate that the increase in the specific activity of the enzyme in the colonic mucosa was a function of increased Vmax rather than a change in the apparent Km for potassium by the Na-K-ATPase. It is theorized that the kidney modifies the response of intestinal Na-K-ATPase in AFR.

Acute Kidney Injury↗

PubMed1980

Lead intoxication during development: its late effects on kidney function and blood pressure.

Exposure to lead in early life may result in chronic renal disease in adulthood. To test this hypothesis, we gave Sprague-Dawley rats, from 3 to 9 weeks of age, either tap water or a 1% lead acetate solution, and we studied them (in pairs) 3 and 16 weeks after exposure; that is, at 12 and 25 weeks of age. Lead-intoxicated animals failed to grow. Their GFR's were lower compared with the matched controls and fell between 12 and 25 weeks of age from 4.8 +/- 0.3 to 3.3 +/- 0.4 ml/min/g dry kidney wt (P less than 0.01). Changes in RBF and single nephron GFR were proportional to changes in total kidney GFR, indicating that superficial and deep nephrons were equally affected. The blood pressure in the lead-exposed animals studied at 25 weeks of age was 143.2 +/- 3.7 mm Hg, a value significantly higher than that of 130.4 +/- 3.3 observed in controls (P less than 0.05). These results demonstrate that limited exposure to lead during development can result in progressive renal insufficiency and hypertension.

Animals↗

PubMedDate not supplied

Cytosolic Ca profile of resting and thrombin-stimulated platelets from black women with NIDDM.

In this study, human platelets were used as a cellular model for exploring cytosolic free Ca (Cai) regulation in non-insulin-dependent diabetes mellitus (NIDDM). Cai levels were monitored in resting and thrombin-stimulated platelets from obese females with NIDDM; obese, nondiabetic women, and nonobese, nondiabetic women. All subjects were black. Significant and marked elevation of basal Cai levels was observed in platelets from the diabetic subjects when no aspirin was used during platelet isolation. However, no significant differences were observed in Cai between aspirin-treated platelets from women with NIDDM and platelets from nondiabetic women. The rate of the Cai return to basal level after thrombin stimulation was significantly lower in platelets from the diabetic subjects, suggesting an abnormality in platelet Ca extrusion or sequestration in NIDDM. Platelet Cai levels positively correlated with low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio (LDL/HDL) and fasting blood glucose. These findings suggest abnormalities in platelet Cai homeostasis in NIDDM that are influenced by the serum lipid profile and perhaps glucose.

Adult↗

PubMedDate not supplied

Obesity, cigarette smoking, and telomere length in women.

Obesity and smoking are important risk factors for many age-related diseases. Both are states of heightened oxidative stress, which increases the rate of telomere erosion per replication, and inflammation, which enhances white blood cell turnover. Together, these processes might accelerate telomere erosion with age. We therefore tested the hypothesis that increased body mass and smoking are associated with shortened telomere length in white blood cells. We investigated 1122 white women aged 18-76 years and found that telomere length decreased steadily with age at a mean rate of 27 bp per year. Telomeres of obese women were 240 bp shorter than those of lean women (p=0.026). A dose-dependent relation with smoking was recorded (p=0.017), and each pack-year smoked was equivalent to an additional 5 bp of telomere length lost (18%) compared with the rate in the overall cohort. Our results emphasise the pro-ageing effects of obesity and cigarette smoking.

Adolescent↗

PubMedDate not supplied

Extraction of copper and zinc from rubber and silicone stoppers.

Drugs and other chemicals are often administered in the drinking water of laboratory animals, and bottles for this purpose usually have rubber stoppers. We studied the ability of solutions of several drugs to extract copper and zinc from rubber and silicone stoppers. Water and isoniazid extracted little copper or zinc from rubber stoppers, whereas EDTA, ethambutol, tetracycline, and chlorpromazine generally extracted considerable quantities of copper and zinc from these stoppers. Neither water nor solutions of the above drugs extracted copper or zinc from silicone stoppers. We routinely use silicone stoppers on water bottles when conducting laboratory studies requiring administration of drugs, toxins, or nutrients in the drinking water.

Copper↗

PubMedDate not supplied

Cadmium effect on the Na,K-ATPase system in cultured vascular smooth muscle cells.

The present study focuses on the interaction between cadmium (Cd) and the Na, K-ATPase system in in vitro grown vascular smooth muscle cells (VSMCs) derived from the rat carotid artery. In disrupted VSMCs rendered permeable by osmotic shock, Cd inhibited Na, K-ATPase; I50 was reached at 10(-5) M Cd. Mg-ATPase was also inhibited by Cd; I50 was attained at concentrations of 10(-4) M Cd. Cd inhibition of Na,K-ATPase in the VSMCs was noncompetitive with respect to Na, K, and ATP. Rubidium transport experiments performed with intact VSMCs demonstrated that within an incubation period of 150 minutes, a concentration of 10(-4) M Cd in the extracellular fluid exerted no acute effect on the Na-K pump. Within this time interval, intracellular Cd attained a concentration eightfold higher than the extracellular Cd concentration. Thus, it appears that under acute conditions Cd exerts its inhibitory effect on Na, K-ATPase only in disrupted VSMCs. The data further suggest that, in the VSMC, conditions under which Cd inhibits Na, K-ATPase are consistent with inhibition from the cytoplasmic side of the cell membrane.

Animals↗

PubMedDate not supplied

Increased membrane permeability of skin fibroblasts from the spontaneously hypertensive rat.

Recently, we have demonstrated several abnormalities in Na+ and K+ homeostasis in cultured vascular smooth muscle cells derived from spontaneously hypertensive rats (SHR). To study whether similar defects can be identified in other cells of this rat strain, 86Rb and 22Na flux experiments as well as measurements of intracellular Na+ and K+ levels were performed in cultured skin fibroblasts of SHR and normotensive Wistar-Kyoto rats (WKY). The efflux rate constant (ke) for Rb+ (K+ analogue) was higher (p less than 0.001) in fibroblasts of SHR than in those of WKY (2.11 +/- 0.03 and 1.66 +/- 0.02 X 10-2/min; mean +/- SEM). The ouabain-insensitive influx rate constant (ki) for Rb+ was also higher (p less than 0.001) in fibroblasts of SHR than in those of WKY (13.26 +/- 0.41 and 10.71 +/- 0.27 X 10-2/min. On the other hand, the activity of the Na+-K+ pump of cells of SHR (44.81 +/- 0.81 X 10-2/min) was not different from that of cells of WKY (44.72 +/- 0.47 X 10-2/min). This parameter was obtained by calculating the ouabain-sensitive Rb+ influx rate constant. There was also no difference in the Na+ uptake (in the presence of ouabain) between cells of the two rat strains. Although there was no statistically significant difference in the measured intracellular total K+ levels between the two groups, on the basis of equilibrium distribution of 86Rb+, we calculated a significantly lower (p less than 0.001) level of exchangeable intracellular K+ in fibroblasts of SHR (98.2 +/- 1.2 mEq/L) as compared with cells of WKY (115.3 +/- 1.5 mEq/L). These findings indicate increased membrane permeability to K+ in fibroblasts of SHR and that this defect is likely to be innate to their membrane structure.

Animals↗