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Biomedical subjects

A B Weder

Publications and source records attributed to A B Weder.

67 records · Page 4Linked to original sources
PubMed1987

Antihypertensive and hypotensive effects of atrial natriuretic factor in men.

Synthetic atrial natriuretic factor (ANF) was administered in ascending doses (0.03, 0.20, 0.45 microgram/kg/min) to eight mildly essential hypertensive men on high (200 mEq/day) or low (10 mEq/day) sodium diets. Responses of blood pressure, heart rate, urinary volume and electrolyte excretion, renin, and aldosterone were measured. For the entire group, ANF lowered blood pressure and increased heart rate during the 0.20 and 0.45 microgram/kg/min infusions, and the antihypertensive effect of the peptide persisted for at least 2 hours after the infusions ended. Four patients (2 at 0.20 microgram/kg/min and 2 at 0.45 microgram/kg/min) experienced sudden bradycardia and hypotension at the end of or shortly after completion of ANF infusion. Renal excretion of water, sodium, chloride, calcium, and phosphorus increased in a dose-dependent fashion in response to infused ANF. Patients on the 200 mEq/day sodium diet had greater increases in urinary volume (11.1 +/- 2.8 vs 3.0 +/- 2.0 ml/min; p less than 0.05), sodium (870 +/- 134 vs 303 +/- 27 microEq/min; p less than 0.05), and chloride (801 +/- 135 vs 176 +/- 75 microEq/min; p less than 0.02) compared with patients on the low sodium diet. The apparent direct suppressive effect of a 0.03 microgram/kg/min infusion of ANF on renin and aldosterone levels was overcome at higher doses by counterregulation provoked by the depressor action. Renin was slightly (-12%) suppressed during the 0.03 microgram/kg/min infusion of ANF but increased at the 0.20 (+50%) and 0.45 microgram/kg/min (+90%; p less than 0.03) rates. Aldosterone declined significantly during the 0.03 microgram/kg/min infusion (-45%; p less than 0.01) of ANF but not during the two higher dose infusions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Red blood cell Li+-Na+ countertransport, Na+-K+ cotransport, and the hemodynamics of hypertension.

Red blood cell Li+-Na+ countertransport and Na+-K+ cotransport activities, home blood pressure, invasive systemic hemodynamics, and limb venous compliance were measured in 65 white men (23 normotensive, 22 borderline hypertensive, and 20 mild essential hypertensive subjects). Li+-Na+ countertransport activity was positively and significantly correlated with subject-determined home systolic blood pressure (r = 0.31, p less than 0.02) and with directly measured systolic (r = 0.29, p less than 0.02) and diastolic (r = 0.27, p less than 0.03) blood pressures in the hemodynamic laboratory, independent of potential confounding variables. Analysis of the hemodynamic determinants of blood pressure revealed a significant positive correlation of countertransport with vascular resistance (r = 0.30, p less than 0.02) but not with cardiac output or cardiac index. High red blood cell Na+-K+ cotransport activity was not independently associated with hypertension or with a characteristic hemodynamic pattern but was related to decreased venous compliance. Red blood cell Li+-Na+ countertransport deserves further study as a marker for the genetic substrate of human essential hypertension. Red cell Na+-K+ cotransport may be altered secondarily by factors related to high blood pressure and seems to be a valid marker for abnormalities of the venous system in hypertension.

Adult↗
PubMed1986

Red-cell lithium-sodium countertransport and renal lithium clearance in hypertension.

Red-cell lithium-sodium countertransport is increased in patients with essential hypertension. It has been proposed that sodium-hydrogen ion exchange in the brush border of the renal proximal tubules is analogous to red-cell countertransport. To investigate the rate of sodium reabsorption by the proximal renal tubules in hypertension, we measured lithium clearance (a measure of proximal tubular reabsorption of sodium), as well as red-cell countertransport, in 14 patients with untreated essential hypertension and in 31 controls. As a group, the hypertensive patients had a higher average (+/- SEM) rate of red-cell countertransport (0.378 +/- 0.030 mmol of lithium per liter of cells per hour, P less than 0.01) and a lower renal fractional lithium clearance (13.96 +/- 0.69 percent, P less than 0.01) than normotensive subjects (0.317 +/- 0.015 mmol of lithium per liter of cells per hour and 17.75 +/- 0.81 percent, respectively). Within the normotensive group, subjects with hypertension in at least one first-degree relative had significantly lower fractional lithium clearances than subjects with no hypertensive relatives (15.37 +/- 0.84 percent vs. 19.06 +/- 1.07 percent, P less than 0.05). We conclude that hypertensive patients have heightened proximal tubular reabsorption of sodium and that red-cell countertransport is a marker of the renal abnormality. Enhanced proximal tubular sodium reabsorption may precede the development of essential hypertension.

Adult↗
PubMed1986

Lithium-sodium countertransport: physiological moorings for red cell transport disorders in hypertension.

Erythrocyte lithium-sodium countertransport, a mode of ouabain-insensitive monovalent cation metabolism, is increased in human essential hypertension, but no pathophysiological link to hypertension has yet been established. Similarities between red cell lithium-sodium countertransport and renal proximal tubular sodium-hydrogen ion exchange suggest a possible role for a countertransport analogue in the control of proximal fluid reabsorption. To test this hypothesis, we measured red cell countertransport and renal lithium clearance, a reliable measure of proximal tubular sodium reabsorption, in normotensives and hypertensives. We found that lithium clearance is (a) inversely correlated with red cell countertransport, (b) decreased in essential hypertensives (reflecting increased proximal sodium reabsorption), and (c) lower in normotensive subjects with a family history of hypertension than in those without such a history. The mechanism by which enhanced proximal tubular sodium reabsorption is related to essential hypertension is unknown, but in addition to its connection to lithium clearance, red cell countertransport is correlated with total peripheral resistance and diastolic compliance of the left ventricle. It is therefore possible that alterations of transport demonstrated in red cells reflect generalized membrane characteristics shared by cardiovascular and renal tissues. Measurements of lithium clearance provide a useful tool for further characterizing the control of renal proximal tubular fluid reabsorption in hypertension. Studies using these measurements may help to explain mechanisms of salt sensitivity and differential responses to antihypertensive therapies as well as yield insights into the heritable basis of human hypertension.

Biological Transport, Active↗
PubMed1985

Racial differences in bumetanide-sensitive cotransport and N-ethylmaleimide-stimulated potassium efflux.

Racial differences in erythrocyte potassium effluxes mediated by two loop-diuretic sensitive modes of cotransport were compared. In red cells loaded to contain approximately equimolar amounts of sodium and potassium, black subjects had lower bumetanide-sensitive sodium-dependent net potassium effluxes as compared to whites. In fresh, washed erythrocytes pretreated with N-ethylmaleimide (NEM), maximal net potassium efflux was greater in blacks than in whites. NEM-stimulated potassium efflux was partially inhibited by bumetanide but only at very high concentrations. The quantitative differences in these two modes of potassium efflux suggest that NEM-stimulated potassium efflux is not an altered mode of sodium-dependent potassium efflux.

Biological Transport↗
PubMed1984

The antihypertensive effect of calorie restriction in obese adolescents: dissociation of effects on erythrocyte countertransport and cotransport.

Measures of maximal rates of lithium-sodium countertransport and frusemide-sensitive sodium and potassium cotransport have been proposed as biochemical markers for human essential hypertension. The stability of these functions over time within the same individuals has led to the suggestion that maximal transport capacities are genetically determined. The present study confirms the reproducibility of functional assays of countertransport and cotransport in human erythrocytes after overnight storage and over a six-month period in normal volunteers and provides estimates of the magnitude of technical error for each assay. A long-term dietary intervention study in a group of obese adolescents demonstrated marked increases in erythrocyte sodium levels and maximal frusemide-sensitive sodium and potassium fluxes but no changes in cell potassium or water and no effect on lithium-sodium countertransport. A correlation between the decrease in percentage of body fat and the increase in cell sodium content suggests a link between the metabolic effects of dieting and control of erythrocyte cation handling. Although the mechanism linking dietary calorie restriction and changes in erythrocyte cation metabolism is unknown, evaluation of body weight, and especially recent weight loss, is important in studies of erythrocyte transport. Conclusions regarding genetic contributions to the activities of lithium-sodium countertransport and sodium-potassium cotransport systems will be strengthened by clarification of environmental regulators.

Adolescent↗
PubMedDate not supplied

Contemporary antihypertensive therapy.

Pharmacotherapy of human hypertension is effective, safe and well-tolerated. Antihypertensive drugs are of three broad classes: diuretics, sympatholytics and vasodilators. The use of each class is discussed and a summary of therapeutic considerations offered for representative agents. Recent trends in antihypertensive therapy are identified.

Antihypertensive Agents↗
PubMedDate not supplied

Racial differences in erythrocyte cation transport.

Erythrocyte contents and ouabain-insensitive transport pathways were measured in 120 white and black normotensives and hypertensives. Mean maximal sodium-stimulated lithium-sodium countertransport rate was higher in white hypertensives than in white normotensives, and countertransport was significantly positively correlated with mean arterial pressure in whites. Values similar to those in white normotensives were found in both black normotensives and hypertensives, and countertransport was not significantly correlated with blood pressure in blacks. The rate constant for passive lithium efflux was greater in whites as compared to blacks, and the difference was not related to blood pressure level or sex. Ouabain-insensitive, furosemide-sensitive sodium and potassium effluxes were not found to be altered in hypertension. Furosemide-sensitive sodium efflux rate was lower in blacks but furosemide-sensitive potassium efflux was not similarly depressed. While white subjects demonstrated a close correlation between sodium and potassium effluxes, blacks did not. Further study of these differences in the cellular metabolism of sodium and potassium may provide clues to the pathogenesis of racial dissimilarities in total body sodium handling.

Adolescent↗
PubMedDate not supplied

Erythrocyte lithium transport changes induced by deoxycorticosterone acetate treatment in pigs.

Ouabain-insensitive lithium efflux from lithium-loaded pig erythrocytes has sodium-dependent and sodium-independent components. Lithium effluxes into sodium (total efflux) and sodium-free (leak) media, sodium-dependent lithium efflux, defined as the difference between total and leak fluxes, and changes in red cell cation and water contents as well as blood pressure were assessed serially for 3 weeks in pigs implanted with Silastic strips impregnated with deoxycorticosterone acetate or with Silastic alone and maintained on a high salt diet (200 mEq/day). Significant differences developed between the groups in blood pressure, red cell sodium content, red cell water content, leak flux, and sodium-dependent lithium efflux (maximal difference: 648 +/- 60 vs 256 +/- 81 mumoles of lithium per liter of cells per hour, deoxycorticosterone acetate vs controls; p less than 0.01). Increased sodium-dependent lithium efflux paralleled a decrease of the diffusional leak component of lithium efflux; total lithium efflux was unchanged. Deoxycorticosterone acetate hypertension in pigs is a useful model in which to study factors modulating erythrocyte cation content and lithium transport in vivo. Changes in lithium transport characterized in red blood cells in this form of experimental hypertension may reflect generalized membrane phenomena.

Animals↗