SUMMARY Erythrocyte contents and ouabain-insensitive transport pathways were measured hi 120 white and black normotensives and hypertensives. Mean maximal sodium-stimulated lithiumsodium 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. (Hypertension 6: 115-123, 1984) KEY WORDS • race • countertransport • cotransport • erythrocyte E RYTHROCYTE lithium-sodium countertransport and sodium-potassium cotransport have been proposed as markers for human essential hypertension. 1 2 Virtually all reports have included only white subjects. For lithium-sodium countertransport, Canessa and colleagues' 3 have consistently demonstrated enhanced maximal activity in white hypertensives and others 4 "* have confirmed the observation, although agreement is not universal. 9 Canessa et al.'°r eported that black hypertensives had values similar to those of black normotensives. Etkin et al." observed increases in tracer sodium influx rates in the erythrocytes of white essential hypertensives but not in blacks and suggested that tracer influx rate is closely correlated with the acitivity of the lithium-sodium countertransport system. 12 However, Trevisan et al. 13 found a significant correlation between lithium-sodium countertransport and blood pressure in black schoolchildren, and Woods et al. l4 found higher countertransport rates in blacks by comparing the normotensive sons of two hypertensive parents and the normotensive sons of normotensive parents.

The fate of nonsuppressible insulin-like activity (NSILA-S) was studied by injecting a tracer of 125I-NSILA-S iv into rats. Ten minutes after injection of 125I-NSILA-S alone, 20% of the label is found in serum, whereas after the injection of 125-I-insulin or 125I-NSILA-S together with an excess of cold NSILA-S only 8% of the label are recovered. Sephadex G-200 chromatography at neutral pH of serum after injection of 125I-NSILA-S reveals 2 peaks of radioactivity in the high molecular weight region at 67 and 47% bed volume. Five minutes after injection the peak at 67% starts to disappear, whereas the one at 47% persists with a half-life of 3 h. The latter peak was submitted to Sephadex G-200 chromatography at acidic pH which dissociates NSILA-S from its binding protein. The labeled material obtained by this procedure still exhibits the same binding characteristics to chick embryo fibroblasts as standard 125 I-NSILA-S. A third peak at 90% bed volume corresponding to low molecular NSILA-S is no longer detectable 20 min after injection. A fourth peak at 100% bed volume becomes apparent after 1 h. The half-life and chromatographic pattern of iv injected 125 I-NSILA-S are not changed by the simultaneous administration of insulin or growth hormone. These findings confirm the existence of a specific serum carrier protein for NSILA-S and may explain why endogenous NSILA-S does not exert insulin-like effects under physiological conditions in vivo.

Background. The prevalence of obesity has increased dramatically over the last decades, and its association with asthma is being increasingly recognized. Aims. Our hypothesis is that increased leptin and decreased adiponectin levels in obese subjects play a direct role in regulating inflammation in asthmatics. We wanted to examine the hypothesis that cysteinyl leukotrienes (cys-LT), inflammatory mediators that are regulated by adipokines, are involved in the pathogenesis of asthma. Methods. We studied a population of asthmatics and nonasthmatics, who in turn were divided into obese and nonobese categories. We examined leptin and its ratio to adiponectin, in asthmatics and nonasthmatics, with and without obesity. In addition, we measured cys-LT levels in exhaled breath condensate (EBC) and in peripheral blood monocytes (PBM) in these groups. Results. Leptin levels were increased in obese asthmatics compared to obese nonasthmatics. The leptin/adiponectin (L/A) ratio was higher in obese asthmatics compared to obese nonasthmatics. EBC cys-LT levels were elevated in asthmatics compared to nonasthmatics. Discussion. Proinflammatory adipokines, released from adipose tissue, may promote an asthma phenotype through enhanced cys-LT production that may result in more prevalent and difficult to control airway disease.

SUMMARY 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 < 0.02) and with directly measured systolic (r = 0.29, p<0.02) and diastolic (r=0.27, p<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<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. (Hypertension 9: 459-466, 1987) KEY WORDS • lithium-sodium countertransport • sodium-potassium cotransport bumetanide • vascular resistance • venous compliance I NCREASED systemic vascular resistance is the hemodynamic hallmark of established human essential hypertension. Borderline hypertension results from elevated cardiac output in about a third of patients, but even in such "hyperkinetic" hypertensive patients, vascular resistance is considered to be inappropriately elevated for the prevailing cardiac output.' Although structural changes may reinforce and amplify the development of elevated vascular resistance, 2 the events initiating hypertension can more plausibly

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