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Biomedical subjects

M Levi

Publications and source records attributed to M Levi.

At least 289 records · Page 16Linked to original sources
PubMed1991

Ontogeny of renal renin release in spontaneously hypertensive rat and Wistar-Kyoto rat.

The role of renin-angiotensin system in generation of genetic hypertension is unclear. Renal renin secretion was examined in renal superficial cortical slices from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) at 4 wk (prehypertensive), 6 wk (early hypertensive), and 12 wk (established hypertension) of age. Basal renin release in SHR was greater at 4 wk (749 +/- 55 vs. 480 +/- 50 ng/mg, P less than 0.005) and at 6 wk (428 +/- 70 vs. 266 +/- 60 ng/mg, P less than 0.02). Basal renin release declined by 43% between 4 and 6 wk and by 34% between 6- and 12-wk time periods in SHR. In SHR and WKY at all ages, renin responses to stimulation with isoproterenol (ISO, 10(-5) and 10(-6) M, respectively) were similar. Angiotensin II (ANG II) resulted in a significant reduction in renin release in both SHR and WKY at 10(-7) M in all age groups. The ANG II-induced percent change in renin release from control of SHR was less compared with WKY rats at 10(-8) and 10(-9)M at 4 wk of age. When ANG II was tested in presence of beta-adrenergic stimulation, a comparable renin inhibitory response was observed in both SHR and WKY. The number of ANG II-binding sites in proximal tubular brush-border membrane (BBM) was increased in SHR vs. WKY rats (458 +/- 18 vs. 235 +/- 12 fmol ANG II/mg BBM protein, P less than 0.001) at 4 wk of age. These data document increased basal renin release and ANG II-binding sites in proximal tubular BBM in 4 wk SHR compared with age-matched WKY rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1991

Dietary calcium modulates renal BBM angiotensin II binding and Na(+)-H+ antiporter activity in SHR.

Dietary Ca is an important modulator of blood pressure in the spontaneously hypertensive rat (SHR). Since the kidney plays a key role in the pathogenesis of hypertension, the purpose of this study was to determine the potential renal mechanisms of the blood pressure-lowering effect of increasing dietary Ca content. In 21-day-old SHR fed 0.1 vs. 3.6% Ca diet for 14 days, increasing dietary Ca had no significant effects on basal [704 +/- 50 in 0.1% Ca vs. 784 +/- 61 ng angiotensin I (ANG I).mg-1.h-1 in 3.6% Ca, P = not significant (NS)], isoproterenol-stimulated (1,057 +/- 52 in 0.1% Ca vs. 1,104 +/- 59 ng ANG I.mg-1.h-1 in 3.6% Ca, P = NS), or angiotensin II (ANG II)-inhibited (370 +/- 50 in 0.1% Ca vs. 411 +/- 39 ng ANG I.mg-1.h-1 in 3.6% Ca, P = NS) renal superficial cortical slice renin release. In contrast, in apical brush-border membrane (BBM) vesicles isolated from the superficial cortex, increasing dietary Ca caused a significant decrease in ANG II binding, which was mediated by a decrease in the number of binding sites (Bmax, 376 +/- 14 in 0.1% Ca vs. 234 +/- 6 fmol ANG II/mg BBM protein in 3.6% Ca, P less than 0.01), and no change in the affinity [dissociation constant (Kd), 17.8 +/- 1.4 in 0.1% Ca vs. 13.4 +/- 2.8 nM ANG II in 3.6% Ca, P = NS].(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1991

Chronic K depletion stimulates rat renal brush-border membrane Na-citrate cotransporter.

Chronic K depletion (KD) causes hypocitraturia. In the present studies, the effect of KD, induced by a low-K diet for 14 days (serum [K] 4.1 +- 0.1, control vs. 2.2 +/- 0.1 meq/l, KD, P less than 0.01), on renal cortical brush-border membrane (BBM) Na-citrate cotransporter activity was examined. KD significantly decreased fractional citrate excretion (3.90 +/- 0.68 vs. 0.53 +/- 0.10%, P less than 0.01). This was paralleled by a significant increase in the initial linear rate of BBM Na-dependent citrate transport (81 +/- 4 vs. 141 +/- 6 pmol citrate.5 s-1.mg protein-1, P less than 0.01). Kinetic studies varying extravesicular citrate concentration demonstrated that KD increased the maximal activity (Vmax) (152 +/- 17 vs. 296 +/- 14 pmol citrate.5 s-1.mg protein-1, P less than 0.01) with no difference in citrate affinity (118 +/- 23, control vs. 135 +/- 22 microM citrate, KD). Similarly, when extravesicular Na concentration was varied, KD increased the Vmax (132 +/- 9 vs. 206 +/- 6 pmol citrate.5 s-1.mg protein-1, P less than 0.01) with no difference in Na affinity (29 +/- 3, control vs. 28 +/- 1 mM Na, KD). The effect of KD on Na-citrate cotransport was specific in that KD did not alter Na-glucose (84 +/- 12, control vs. 89 +/- 5 pmol glucose.5 s-1.mg protein-1, KD) or Na-proline (87 +/- 3, control vs. 84 +/- 5 pmol proline.5 s-1.mg protein-1, KD) cotransport. In conclusion, KD increases the Vmax of the proximal tubule apical membrane Na-citrate cotransporter.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1991

Reduction of contact activation related fibrinolytic activity in factor XII deficient patients. Further evidence for the role of the contact system in fibrinolysis in vivo.

In this study the contribution of activation of the contact system to activation of the fibrinolytic system in vivo was investigated in healthy volunteers and in factor XII deficient patients. The plasminogen activating activity in plasma from healthy volunteers after infusion of desamino D-arginine vasopressin (DDAVP) was only partially blocked (for 77%) with specific antibodies to tissue-type plasminogen activator and urokinase type plasminogen activator. The residual activity could be quenched by a monoclonal antibody that inhibits factor XII activity and was not present in patients with a factor XII deficiency. The formation of plasmin upon the DDAVP stimulus as reflected by circulating plasmin-alpha 2-antiplasmin complexes was lower in factor XII deficient patients than in healthy volunteers. Activation of the contact system occurred after DDAVP infusion in healthy volunteers and was absent in factor XII deficient patients. These results indicate that DDAVP induces a plasminogen activating activity that is partially dependent on activation of the contact system and that contributes to the overall fibrinolytic activity as indicated by the formation of plasmin-alpha 2-antiplasmin complexes. This fibrinolytic activity is impaired in factor XII deficient patients which may explain the occurrence of thromboembolic complications in these patients.

Adult↗
PubMed1990

Effect on thrombus growth and thrombolysis of two types of osmolar contrast media in rabbits.

Thromboembolic complications have been reported after diagnostic or interventional radiological procedures. However, contrast media inhibit platelet function and blood coagulation in vitro. To investigate these characteristics in vivo, we determined the effect of nonionic and ionic low osmolar contrast media on thrombus growth and thrombolysis in rabbits in a randomized study design. Rabbits received either ionic low osmolar contrast medium (ioxaglate), nonionic low osmolar contrast medium (iohexol) or saline. Thrombus growth was determined by the accretion of 125I-labeled fibrinogen on to autologous, nonradioactive, preformed thrombi in rabbit jugular veins. Thrombolysis was assessed by measurement of the decrease in radioactivity of standard sized preformed 125I-fibrinogen labeled thrombi. Ioxaglate significantly inhibited thrombus growth (60% inhibition, P less than 0.005 vs. saline), in contrast to iohexol, which had no significant effect (33% inhibition, P less than 0.2 vs. saline). Neither ioxaglate nor iohexol affected thrombolysis.

Animals↗
PubMed1990

Early selective effects of gentamicin on renal brush-border membrane Na-Pi cotransport and Na-H exchange.

Gentamicin nephrotoxicity is associated with impairments in proximal tubular function. This study determined whether gentamicin administration to the rat, before a reduction in glomerular filtration rate (GFR), causes early and selective alterations in renal cortical brush-border membrane (BBM) enzyme and transport activity, lipid composition, and fluidity. Three days of gentamicin administration caused significant decreases in the Vmax of alkaline phosphatase, the Vmax of sodium gradient-dependent phosphate transport (Na-Pi cotransport), and the Vmax of pH gradient-dependent sodium transport (Na-H exchange). Gentamicin did not affect BBM-bound maltase or leucine aminopeptidase activities and sodium gradient-dependent glucose or proline transport activities. Gentamicin also caused a significant decrease in BBM sphingomyelin, significant increases in BBM phosphatidylcholine and phosphatidylinositol, a significant decrease in the phospholipid fatty acid saturation index, and a significant increase in BBM fluidity, i.e., decrease in the fluorescence anisotropy of diphenylhexatriene. These BBM functional and compositional effects of gentamicin were independent of endogenous parathyroid hormone activity. We conclude that gentamicin causes early and specific alterations in BBM enzyme and transport activity and also lipid composition, which may play an important role in the progression of renal cell injury.

Animals↗
PubMed1990

Heterogeneity of Pi transport by BBM from superficial and juxtamedullary cortex of rat.

There is an axial heterogeneity for proximal tubular phosphate (Pi) transport. Sodium gradient-dependent Pi transport (Na-Pi cotransport) is greater in the proximal convoluted tubule (PCT) than in the proximal straight tubule (PST). In brush-border membrane vesicles (BBMV) isolated from the superficial cortex (SC-BBM) and the juxtamedullary cortex (JMC-BBM), we have also found a heterogeneity in BBM Na-Pi cotransport activity. The greater Na-Pi cotransport activity in SC-BBM was not caused by an alteration in the stoichiometry (2 Na+:1 HPO42-) or the activation of the Na-Pi cotransporter by Na+ (KNa = 37 in SC-BBM vs. 44 mM Na in JMC-BBM, P = NS, not significant). Despite a higher affinity for Pi in JMC-BBM (KPi = 156 in SC-BBM vs. 105 microM Pi in JMC-BBM, P less than 0.001), the Vmax for Na-Pi cotransport was higher in the SC-BBM (Vmax = 2,939 in SC-BBM vs. 1,421 pmol Pi.5 s-1.mg BBM protein-1 in JMC-BBM, P less than 0.001). Na gradient-dependent Pi-protectable phosphonoformic acid (Na-PFA) equilibrium binding studies revealed that the higher Vmax for Na-Pi cotransport in SC-BBM was in part due to a higher number of Na-Pi cotransport units (Bmax = 4.24 in SC-BBM vs. 2.67 nmol PFA.30 min-1.mg BBM protein-1 in JMC-BBM, P less than 0.001). In addition, the fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene (rDPH), which is inversely related to fluidity, was lower in SC-BBM (rDPH = 0.247 in SC-BBM vs. 0.254 in JMC-BBM, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Cholesterol modulates rat renal brush border membrane phosphate transport.

In dietary phosphate (Pi) deprivation and in aging there is an inverse correlation between renal proximal tubular brush border membrane (BBM) cholesterol (Chol) content, BBM fluidity, and BBM sodium gradient-dependent Pi transport activity (Na-Pi cotransport). The purpose of this study was to determine whether in vitro enrichment of renal BBM with Chol has a direct modulating effect on Na-Pi cotransport. 12 and 24 mol % increases in Chol content caused dose-dependent decreases in Na-Pi cotransport activity, 2,000 in control, vs. 1,450 in Chol (+12%), vs. 900 pmol/5 s/mg BBM protein in Chol (+24%), all P less than 0.01, which was paralleled by dose-dependent increases in the fluorescence anisotropy of diphenylhexatriene, rDPH, i.e., decrease in BBM fluidity, 0.203 in control, vs. 0.210 in Chol (+12%), vs. 0.219 in Chol (+24%), all P less than 0.01. We found that increasing ambient temperature, which increases BBM fluidity independent of changes in Chol content, increased Na-Pi cotransport. When Na-Pi cotransport was analyzed as a function of BBM fluidity, 1/rDPH, we found that at an equivalent BBM fluidity BBM Chol enrichment still resulted in a dose-dependent decrease in Na-Pi cotransport. Finally, in BBM isolated from rats fed a low Pi diet in vitro enrichment with Chol completely reversed the adaptive increases in Na-Pi cotransport and fluidity. Our study therefore, indicates that Chol is a direct modulator of renal BBM Na-Pi cotransport activity, and that in vivo alterations in BBM Chol content most likely plays an important role in the regulation of renal tubular Pi transport.

Alkaline Phosphatase↗
PubMed1990

Diagnostic accuracy of computerized impedance plethysmography in the diagnosis of symptomatic deep vein thrombosis: a controlled venographic study.

The aim of our study was to evaluate the sensitivity, the specificity, and the positive and negative predictive values of a recently developed computerized impedance plethysmography (CIP) in the diagnosis of deep vein thrombosis (DVT); 117 consecutive outpatients with a clinical suspicion of DVT were evaluated. After informed consent was obtained, a CIP and, within twenty-four hours, a venography of the symptomatic lower limb were performed in each patient. The results of CIP were compared with the results of contrast venography, which was considered as the gold standard. As far as the diagnosis of both proximal and distal DVT was concerned, the accuracy of CIP was 88.5%; the sensitivity and specificity were 95.1% and 83.6%, respectively; the positive and negative predictive values were 81.2% and 95.8%, respectively. When the diagnosis of only proximal deep vein thrombosis was considered, the accuracy of CIP was 88.8%; the sensitivity and specificity were 97.1% and 83.6%, respectively; the positive and negative predictive values were 79.0% and 97.8%, respectively. The authors conclude that the newly developed CIP has a diagnostic accuracy similar to that of traditional impedance plethysmography. Moreover, being completely automated and portable, CIP can play an important role in the bedside diagnosis of DVT.

Diagnosis, Computer-Assisted↗
PubMed1990

Population genetic studies on Jews. I. The alpha 2HS serum glycoprotein, a polymorphism strongly correlated with latitude.

A sample of Jews subdivided according to the birth-place of their parents or grand-parents have been examined for a large number of genetic markers in the course of a long-term project on the genetics of Jews. We report here the findings concerning 794 Jews studied for the AHSG polymorphism. All the subsamples were in Hardy-Weinberg equilibrium. A highly significant difference was found between Sephardic + Near East Jews and Ashkenazi (AHSG*2 frequencies: 0.184 +/- 0.015 and 0.258 +/- 0.016, respectively). For comparative purposes the data available on Caucasoids have been considered. It turned out that they were neatly arranged along a latitude-AHSG gene frequency cline (0.0092 of AHSG*2 gene frequency increase per degree of increase of latitude) in the explored 30 degrees-60 degrees range (r = 0.97; P much less than 0.001). Of the two Jewish frequencies that could be taken into consideration because of their sufficient sizes, that of the Near East + Sephardic Jews was perfectly in line with the above mentioned cline, while that of the Ashkenazi was somewhat displaced in the sense of being more similar than expected to the other, more southern, Jewish group. Since the only AHSG*2 frequency significantly displaced from the regression line is that of the Ashkenazi, whose ancestors lived until centuries ago in more southern areas, this finding is a strong confirmation of the observed cline.

Africa↗
PubMed1989

DDAVP induces systemic release of urokinase-type plasminogen activator.

The desamino-d-arginine vasopressin (DDAVP) induced enhancement of endogenous fibrinolysis is generally attributed to the release of tissue-type plasminogen activator (t-PA) from the vessel wall. The observation of concurrent release of urokinase-type plasminogen activator (u-PA), which eventually might cooperate in the enhanced fibrinolytic activity, has not been reported thus far. In a preliminary study in two healthy human volunteers we found a 1.8-fold increase of urokinase-antigen (UK-antigen) and a 1.7-fold increase of plasmin-activatable pro-urokinase (pro-UK) activity to DDAVP intravenously. The plasma-peak levels coincided with the maximal t-PA level. These responses following infusion of DDAVP were subsequently confirmed in a randomized double blind cross-over study in six human volunteers. We conclude that u-PA is released by DDAVP concurrently with t-PA and that it is presumably from the same origin as t-PA i.e. endothelial cells. u-PA and t-PA may therefore cooperate in the enhanced fibrinolytic activity upon DDAVP infusion.

Deamino Arginine Vasopressin↗
PubMed1989

Additive effect of dDAVP and standard heparin in increasing plasma t-PA.

The aim of this study was to evaluate the existence of an additive effect between standard heparin and dDAVP in the enhancement of endogenous fibrinolysis. Eight healthy volunteers were studied in a randomized double blind placebo controlled cross-over trial. The volunteers were treated i.v. with dDAVP, 0.4 micrograms/kg, over 15 minutes followed by an i.v. bolus dose of either standard heparin, 5,000 I.U., or saline. A 48 hour wash-out period was adopted. The infusion of dDAVP followed by standard heparin resulted in a higher increase in plasma t-PA activity, t-PA antigen, circulating t-PA specific activity and FPLA when compared with dDAVP followed by saline. The difference was already statistically significant at 15 minutes after the infusion of dDAVP and lasted for up to 60 minutes after the end of the infusion of dDAVP. Plasma PAI 1 showed a slightly higher decrease after dDAVP plus standard heparin than after dDAVP plus saline but this difference was not statistically significant. No statistically significant changes of fibrinogen and alpha 2-antiplasmin levels were observed. As expected, the infusion of standard heparin resulted in an increase in plasma anti-Xa activity and in a prolongation of aPTT. Our results demonstrated an additive effect of dDAVP and standard heparin on the increase in circulating t-PA, the effect of dDAVP being potentiated and prolonged by heparin. This observation could prospect a combined use of dDAVP and standard heparin in the prophylaxis and treatment of thromboembolic diseases.

Adult↗