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Biomedical subjects

E Songu-Mize

Publications and source records attributed to E Songu-Mize.

32 records · Page 2Linked to original sources
PubMed1990

Race, sex, and family history of hypertension and erythrocyte sodium pump [3H]ouabain binding.

We studied the binding properties of [3H]ouabain to erythrocytes from normotensive children (n = 83) between the ages of 10 and 18 years (mean resting arterial pressure: 102/57 mm Hg) from normotensive and essential hypertensive parents. Arterial blood pressures of 101/57 and 104/57 mm Hg (subjects with normotensive and hypertensive parents, respectively) were not significantly different between the two groups. Forty-four children had normotensive parents and 39 had hypertensive parents, 51 were white and 32 were black, and 41 were girls and 42 were boys. By using the [3H]ouabain-binding technique, we determined the density of sodium pump sites and the equilibrium dissociation constants in erythrocytes from these children. Possible effects of race, sex, or parental hypertension status on pump sites and dissociation constants were tested with a three-way analysis of variance (ANOVA). Race had a major effect on the dissociation constant: blacks had a significantly higher value than did whites (p = 0.002). We also found a race by sex by parental hypertension status interaction (p = 0.04) with black girls with hypertensive parents having the highest value. There was no effect of race, sex, or status on sodium pump site density. Age, height, weight, resting arterial blood pressure, and plasma Na+ and K+ concentrations did not correlate with the dissociation constants. These data suggest that, among the groups we studied, black girls with hypertensive parents had erythrocytes with the lowest binding affinity for ouabain.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Comparative ability of digoxin and an aminosugar cardiac glycoside to bind to and inhibit Na+,K+-adenosine triphosphatase. Effect of potassium.

We compared the abilities of digoxin and aminogalactose digitoxigenin (ASI-222) to bind to, or inhibit, purified dog heart Na+,K+-ATPase in the presence of 1, 10, or 80 mM potassium chloride. Changing the potassium concentration from 1 to 10 mM increased the dose producing 50% inhibition of enzyme activity (IC50) by 9- and 2.5-fold for digoxin and ASI-222 respectively. Raising the potassium concentration to 80 mM increased the IC50 for digoxin 3-fold but did not alter significantly the IC50 for ASI-222. Equilibrium binding studies showed that this enzyme exhibited a single class of specific binding sites for both digoxin and ASI-222. Raising the potassium concentration did not affect the maximum number of binding sites (Bmax) but increased the apparent dissociation constant (KD) for digoxin. Potassium differentially affected the affinity and number of binding sites for ASI-222; raising the potassium concentration from 1 to 10 mM did not affect the Bmax or the KD, but raising it to 80 mM increased both. The effect of i.v. infusion of potassium chloride upon cardiac upon cardiac arrhythmias produced by i.v. infusion of digoxin or ASI-222 in anesthetized dogs was also determined. Infusion of potassium chloride reversed the cardiac arrhymias due to digoxin to normal rhythm, but not those due to ASI-222. In conclusion, the interaction of digoxin and the polar digitalis agent, ASI-222, with dog heart Na+,K+-ATPase was differentially affected by potassium. These agents also also produced cardiac arrhythmias, which were differentially affected by potassium.

Animals↗
PubMed1988

Quantitative immunocytochemistry using an image analyzer. II. Concentration standards for transmitter immunocytochemistry.

Image analyzers can measure both the optical density and geometry of immunocytochemically labeled cells and fibers, as reviewed in a companion paper (Mize et al., 1988). In this paper, we report a procedure which allows us to estimate the concentration of a neurotransmitter based upon the optical density of antibody labeling produced by immunocytochemistry. To accomplish this, we developed a standard which binds conjugated neurotransmitters. Several artificial media for the standard were compared, including agar, gelatin, and agar-gelatin. A 3% agar matrix was found to be most suitable because it cut well and was nearly transparent. The agar sections were activated with cyanogen bromide/acetonitrile to promote coupling to the antigen. To test the standard, we used gamma-aminobutyric acid (GABA) conjugated to bovine serum albumin (BSA) as the antigen. The antibody was directed against this conjugate. Activated agar sections were incubated in serial dilutions of the tritium-labeled GABA/BSA conjugate. The radioactivity of some of these sections was measured to estimate the amount of coupled antigen. The remaining sections were incubated in the GABA antibody and processed for immunocytochemistry. The optical density of these sections was measured with an image analyzer. A linear relationship was found between GABA concentration and optical density over a range of at least 0.01 to 1 nmol/mg of agar. These results show that the concentration of bound GABA can be estimated from the optical density of sections labeled by antibody immunocytochemistry. The applicability of this technique to fixed brain tissue is discussed.

Image Processing, Computer-Assisted↗
PubMed1988

Mechanisms of altered sodium excretion after preoptic hypothalamic lesions.

These experiments investigated cardiovascular and hormonal responses during the natriuresis and subsequent sodium retention following electrolytic lesions of the periventricular tissue surrounding the anteroventral third ventricle (AV3V-X) in the rat. Four hours following treatment, AV3V-X resulted in a significant increase in blood pressure (18 +/- 3 mmHg), bradycardia (-68 +/- 20 beats/min), and natriuresis (212 +/- 36 mu eq/h), compared with control-operated (control: 2 +/- 4 mmHg, -14 +/- 18 beats/min, 89 +/- 34 mu eq/h) and unanesthetized control (UC) animals (-1 +/- 3 mmHg, -5 +/- 12 beats/min, 74 +/- 25 mu eq/h). Preventing the hypertensive response in AV3V-X rats abolished the natriuresis. Twenty-four hours after treatment, blood pressure, heart rate, urine flow, and sodium excretion were similar between experimental groups. However, sodium excretion by AV3V-X rats was significantly smaller than control 24-48 h following treatment. AV3V-X rats had significantly elevated plasma concentrations of aldosterone and corticosterone 4, 24, and 48 h and increased plasma renin 24 and 48 h after treatment. These data suggest that the acute natriuresis following AV3V-X is mediated by increased arterial blood pressure, whereas the subsequent sodium retention could be due to activation of the renin-aldosterone system.

Aldosterone↗
PubMed1987

High and low dietary potassium effects on rat vascular sodium pump activity.

Studies of renal and other tissues suggest that chronic elevation or reduction of dietary potassium intake could affect vascular smooth muscle sodium pump (Na-pump) activity. To examine this possibility, the effects of 3 weeks of low (LK: 4 mmole KCl/kg chow), normal (NK; 162 mmole/kg), and high (HK; 1350 mmole/kg) dietary potassium intake on Na-pump activity, the Na-pump activity response to changes in extracellular potassium concentration, and Na-pump site density were determined in tail arteries of rats. Plasma potassium concentration was elevated by 21% in HK rats and reduced by 45% in LK rats. When incubated in autologous plasma, compared to arteries from NK rats, Na-pump activity was decreased in the tail arteries from LK rats but not altered in those from HK rats. When arteries from NK and LK rats were incubated in autologous plasma with the potassium concentration increased to equal that of the HK rats, Na-pump activity exceeded that of HK rat arteries: Na-pump activity of arteries incubated in autologous plasma did not differ from that of arteries incubated in Krebs-Henseleit buffer with the potassium concentration adjusted to equal that of the plasma. Tail artery Na-pump activity for all three dietary potassium groups increased as potassium concentration of the incubation medium was increased from 1 to 12 mM; Na-pump activity was similar for the NK and LK rats at all potassium concentrations, but Na-pump activity of HK rat arteries was less than that of NK arteries at high extracellular potassium concentrations. Na-pump site density was not altered by either HK or LK diet. It is concluded that in tail arteries of rats fed the LK diet, chronically decreased extracellular potassium results in chronically decreased Na-pump activity. In contrast, an adaptive change occurs in tail arteries of rats fed HK diet, such that Na-pump activity remains at normal levels despite elevated extracellular potassium; this adaptive response to chronically increased dietary potassium does not appear to be the result of decreased Na-pump site density.

Animals↗
PubMed1987

Effect of DOCA-salt treatment duration and anteroventral third ventricle lesions on a plasma-borne sodium pump inhibitor in rats.

We determined the effect of plasma obtained from rats treated with DOCA-salt for 6 and 28 days on sodium pump activity, measured as ouabain-sensitive Rb+ uptake in tail arteries from these rats. The effect of an electrolytic lesion in the area of the anteroventral third cerebral ventricle (AV3V) before DOCA-salt treatment was investigated in relation to the ability of plasma to inhibit vascular Na+ pump activity. Systolic blood pressures, plasma sodium and potassium concentrations, body weights and haematocrit were also measured. Six days after DOCA-salt treatment, there was a 22% suppression of vascular Na+ pump activity in these rats. This suppression was due to a plasma factor since plasma from these rats produced a similar degree of suppression in arteries isolated from untreated control rats. Furthermore, tail arteries from DOCA-salt rats treated for 6 days displayed normal Na+ pump activity when incubated in plasma from control rats or in Krebs-Henseleit buffer. There was no elevation of systolic blood pressure at the end of 6 days of treatment with DOCA-salt. Placement of an electrolytic brain lesion in the AV3V area before treatment with DOCA-salt abolished the ability of plasma to inhibit the vascular Na+ pump. Treatment with DOCA-salt for 28 days resulted in a significant increase in systolic blood pressure, a decrease in plasma potassium concentration, and a significant increase in vascular Na+ pump activity (26%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Phasic vascular sodium pump changes in deoxycorticosterone-hypertensive rats.

We determined the sodium pump activity, measured as ouabain-sensitive 86Rb+ uptake, in the tail arteries of rats treated with deoxycorticosterone and sodium chloride for 6, 9, 14, 28, and 50 days. Systolic blood pressures, plasma sodium, potassium, and creatinine concentrations were measured, and the body weights were recorded. Vascular sodium pump activity was suppressed (by 27%) at the 6th day of deoxycorticosterone and sodium chloride treatment, a prehypertensive state. By the 9th day, blood pressure of deoxycorticosterone-treated and sodium chloride rats had increased, but sodium pump activity was not different from that of control animals. However, increases in sodium pump activity were noted after 14 and 28 days of deoxycorticosterone and sodium chloride treatment (18 and 21%, respectively). By 28 days, a fully developed hypertension was noted. At 50 days, rats displayed lower vascular sodium pump activity (by 23%) than the controls. These rats, although hypertensive, had significantly lower systolic blood pressures than the rats treated for 28 days. They had high plasma creatinine levels, low potassium and sodium concentrations, and low body weights compared to the controls, suggesting the presence of a malignant state. Our data indicate that there are time-related changes in the vascular sodium pump activity with this type of hypertension.

Animals↗
PubMed1984

The vasopressor response to centrally administered ouabain.

Ouabain (80 micrograms/kg) injected into the lateral cerebroventricles (ICV) of rats produced a prompt and sustained increase in arterial blood pressure. A diastolic blood pressure increase of about 40 mm Hg began within 10 minutes of injection and lasted at lest 1 hour. This dose of ouabain had no effect on arterial pressure when given intravenously. The vasopressor response to intracerebroventricularly administered ouabain was not blocked by prior intravenous administration of phentolamine (1 mg/kg) or hexamethonium (3 mg/kg). However, continuous intravenous infusion of saralasin (2 micrograms/kg per min) prevented the pressor response to intracerebroventricularly administered ouabain. In addition, bilateral nephrectomy, adrenalectomy, pretreatment with intravenously administered propranolol (2 mg/kg) or captopril (10 mg/kg) abolished the increase in blood pressure evoked by intracerebroventricularly administered ouabain. Plasma renin and epinephrine levels at the peak of the pressor response to intracerebroventricularly administered ouabain were respectively, about 2.5- and 2-fold higher than in control rats. Our data indicate that ouabain administered into the central nervous system produces a hypertensive effect which does not primarily involve peripheral alpha-adrenergic receptors, but appears to be due to angiotensin II produced by renin of renal origin. These data suggest that digitalis agents can interact with sites in the central nervous system to induce a release of renin from the kidney; this release appears to involve activation of beta-adrenergic receptors by catecholamines from the adrenal medulla, perhaps through a direct adrenal-kidney vascular network.

Animals↗
PubMed1983

Metabolism and cardiac actions of a polar aminocardenolide and digoxin in the conscious dog.

We studied the metabolism and cardiac actions of a polar aminocardenolide, 3-beta-O-(4-amino-4,6-dideoxy-beta-D-galactopyranosyl) digitoxigenin (ASI-222), in conscious, chronically instrumented dogs and compared the cardiac actions of this compound with those of digoxin. Chloroform-soluble metabolites and the excretion patterns of ASI-222 in urine and feces were identified and measured using thin-layer chromatography. The deaminated metabolite of ASI-222 appeared both in the urine and the feces together with the genin, digitoxigenin and the parent drug which constituted the majority of the radioactivity excreted. There was a secondary rise in the plasma concentration of ASI-222 starting 2 hr after the i.v. administration, which strongly suggests its enterohepatic recycling. The secondary increase in the plasma concentration was not seen in the dogs receiving digoxin. ASI-222 produced increases in cardiac contractility and systolic blood pressure which were more rapid in onset and shorter in duration than those produced by an equimolar dose of digoxin. Amplitudes of these physiologic responses to these two compounds in conscious dogs were approximately 2 times higher than the effects previously reported to similar doses in anesthetized dogs.

Animals↗
PubMedDate not supplied

Renal cytochrome P450-related arachidonate metabolite inhibits (Na+ + K+)ATPase.

The function of the nephron, the anatomical unit of the kidney, is segmented; at least 12 segments have been identified that differ in their morphology, transport properties and hormonal responsiveness. The medullary portion of the thick ascending limb of the loop of Henle (mTALH) has one of the highest concentrations of (Na+ + K+)ATPase found in mammalian tissues, reflecting the importance of this nephron segment in the regulation of extracellular fluid volume, as active sodium transport is driven by (Na+ + K+)ATPase. Here, in cells derived primarily from the mTALH of the outer medulla of rabbit kidney, we have identified a cytochrome P450-dependent monooxygenase system which metabolizes arachidonic acid to two biologically active oxygenated products; one of the products inhibits (Na+ + K+)ATPase and the other relaxes blood vessels. We report that formation of these oxygenated arachidonate metabolites is stimulated by arginine vasopressin (AVP) and salmon calcitonin (SCT).

Animals↗
PubMedDate not supplied

Effect of AV3V lesions on development of DOCA-salt hypertension and vascular Na+-pump activity.

We studied the effects of anteroventral third ventricle (AV3V) lesions on the vascular Na+-pump activity of deoxycorticosterone acetate-salt (DOCA-salt) treated rats. Blood pressures and Na+-pump activity of the isolated tail arteries, measured as ouabain-sensitive 86Rb-uptake, were determined in untreated control rats, DOCA-salt treated rats, rats with AV3V lesions, and rats with AV3V lesions which were treated with DOCA-salt. Control rats receiving DOCA treatment developed higher blood pressures than rats receiving no DOCA treatment. Placement of AV3V lesions prior to administration of DOCA prevented the increase in blood pressure. Vascular Na+-pump activity in the DOCA-treated group was reduced by 20% compared to all other groups. The AV3V lesions prevented the suppression of Na+-pump activity caused by DOCA treatment. Suppression of vascular Na+-pump activity was due to a humoral substance since Na+-pump activity of tail arteries from control rats incubated in plasma from DOCA-salt treated rats was suppressed by 25% when compared to those incubated in control plasma. Our findings support the hypothesis that a circulating pressor substance is at least partially responsible for the development of DOCA-salt hypertension and that the mechanism by which AV3V lesions prevent DOCA hypertension may be through the interruption of secretion, transport, or synthesis of this factor.

Animals↗
PubMedDate not supplied

Effect of anteroventral third ventricle lesions on vascular sodium-pump activity in two-kidney Goldblatt hypertension.

We studied the effects of anteroventral third ventricle (AV3V) lesions on the vascular Na+-pump activity and blood pressure of rats prepared by the two-kidney Goldblatt procedure. Blood pressures and Na+-pump activity of the isolated tail arteries, measured as ouabain-sensitive 86Rb+-uptake were determined in rats with renal artery clips, rats with AV3V lesions, and rats with AV3V lesions. Rats with renal artery clips developed higher blood pressures (40%) and higher vascular Na+-pump activity (20%-35%) than rats with no renal clips. Placement of AV3V lesions prior to the placement of renal clips prevented the increase in blood pressure and the increase in vascular Na+-pump activity. Plasma potassium and creatinine concentrations, nonspecific 86Rb+-uptake, and hematocrit were not different among these groups. Plasma sodium concentration was elevated in the AV3V lesioned control group. These experiments suggest a possible role of this CNS region in the regulation of vascular Na+-pump function during hypertensive states.

Animals↗
PubMedDate not supplied

Renal arachidonic acid metabolism. The third pathway.

Cells were isolated from the outer medulla of the rabbit kidney, primarily from the thick ascending limb of Henle's loop (mTALH). These mTALH cells are heavily invested with a cytochrome P450-linked monooxygenase that represents the third pathway by which arachidonic acid is metabolized. After cell separation, approximately 80% of the cells proved to be mTALH in origin, based on electron microscopic criteria and immunofluorescent localization of Tamm-Horsfall protein, a specific marker for mTALH cells. The specific activity of alkaline phosphatase, a marker for proximal tubular cells, decreased threefold after separation of mTALH cells from outer medullary cells, associated with a fourfold increase in the capacity of the separated mTALH cells to metabolize arachidonic acid. Incubation of mTALH cells with 14C-arachidonic acid resulted in formation of oxygenated metabolites, identified as two peaks (P1 and P2), which accounted for 30 to 40% of the recovered radioactivity. Formation of prostaglandin E2 and F2 alpha accounted for only 3 to 5%. The chromatographic retention times of P1 and P2 were different from products of lipoxygenases. An inhibitor of cytochrome P450-dependent enzymes, SKF-525A (50 microM), reduced product formation by mTALH cells by more than 70%, while induction of cytochrome P450 increased product formation. Formation of P1 and P2 by cell-free homogenates of mTALH was totally dependent on the presence of nicotinamide adenine dinucleotide phosphate, reduced form (NADPH), which suggests a NADPH-dependent cytochrome P450-linked monooxygenase pathway. Vasopressin and calcitonin (10(-10) M to 10(-7) M) stimulated release of arachidonic acid metabolites from mTALH cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗