The inheritance of 12-hour overnight total urinary kallikrein excretion and its association with family history of essential hypertension were studied in 405 normotensive adults and 391 youths in 57 Utah pedigrees. Total urinary kallikrein excretion was highly familial with 51% of the total variance attributable to a dominant allele for high total urinary kallikrein excretion and 27% attributable to the combined effects of polygenes and shared family environment. An estimated 28% of the population has one or two copies of the dominant allele for high total urinary kallikrein excretion (2.3 SD units higher than the low homozygotes). About 83% of the population could be assigned to one of the two genotypic populations. Individuals with the high total urinary kallikrein excretion genotype were significantly less likely to have one or two hypertensive parents (relative odds = 0.56, p = 0.042). We conclude that a dominant allele expressed as high total urinary kallikrein excretion may be associated with decreased risk of essential hypertension. Further studies should be performed to confirm this finding and to test for interactions between this apparently protective gene and other genetic and environmental determinants of essential hypertension.

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To investigate the pathophysiology of essential hypertension, detailed biochemical and clinical variables were collected and analyzed for 2091 Utah subjects aged 3 to 83 years. Three different measurements of erythrocyte cation transport were obtained: Na +-Li + countertransport, Li +-K + cotransport, and furosemide-insensitive Li + efflux into MgCI 2. Total plasma cholesterol, triglycerides, and high density lipoprotein cholesterol levels were obtained from fasting subjects. Levels of high density lipoprotein subfractions 2 and 3 were also obtained from 350 subjects. Standardized data collection also included blood pressure, height, weight, and presence or absence of a diagnosis or treatment of essential hypertension. In univariate analyses of all 1420 adults, each of the three transport systems showed the same significant correlations with triglyceride levels (r = 0.33-0.35, p < 0.0001), high density lipoprotein concentration (r =-0.19 to-0.21, p < 0.001), and weight (r = 0.22-0.28, p < 0.0001). In multivariate regression analyses, values for each transport system were significantly higher in hypertensive subjects; values for triglycerides, high density lipo-protein, and usually, the high density lipoprotein subfractions continued to have strong significant independent associations with all three transport systems; and weight remained significantly related only to Na +-Li + countertransport. In separate logistic regressions, plasma triglyceride levels (posi-tively, p < 0.001) and high density lipoprotein subfraction 3 levels (inversely, p < 0.03) were associated with hypertension itself. In multivariate analyses among 671 children, high density lipopro-tein and high density lipoprotein subfraction 3 levels showed significant (p < 0.05) inverse correlations with Na +-Li + countertransport and furosemide-insensitive Li + efflux. These associations of all three cation transport systems with several blood lipids as well as with weight and hypertension suggest that a general relationship exists between blood lipids and membrane cation transport in the pathophysiol-ogy of essential hypertension. (Hypertension 8: 30-36, 1986) KEY WORDS • triglycerides • high density lipoprotein cholesterol • Na +-Li + countertransport • Li +-K + cotransport • weight • hypertension • red blood cell membranes O UABAIN-INSENSITIVE cation fluxes are being studied extensively because of their differing rates in hypertensive and normotensive subjects. '•' The three transport systems discussed herein are Na +-Li + countertransport, Li +-K + cotransport, and furosemide-insensitive Li + efflux into MgCl 2. The Na +-Li + countertransport system exchanges Na + for Li + (another Na + in vivo) across the red blood cell membrane. The Li +-K + cotransport consists of simultaneous outward transport of Li + and K + and seems to be related to the Na +-K + cotransport system, 2 5 6 al

Illicit-drug users may attempt to falsify results by in vitro adulteration of specimens. We investigated eight additives (NaCl, Visine, handsoap, Drano, bleach, vinegar, golden-seal tea, and lemon juice) claimed by drug users to invalidate enzyme immunoassay (EIA) drug assays. We also analyzed adulterated urine specimens to determine if they could be identified, adding adulterants at several concentrations to 222 EIA-positive specimens confirmed by gas chromatography and mass spectrometry (GC/MS) to contain illicit drugs. To identify adulterated urines, we monitored pH, relative density, and urine color and turbidity at adulterant concentrations that falsified EIA results. Specimens contaminated with NaCl had relative densities greater than 1.035. Liquid Drano, bleach, and vinegar shifted urine pH outside the physiological range. Golden-seal tea caused a dark appearance, and specimens containing liquid soap were unusually cloudy. Lemon juice had no effect on the assays. Visine was the only adulterant not detected. The adulterants interfered somewhat differently with each of the drug assays. EIA assays for illicit drugs can be invalidated by specimen adulteration producing false-negative results. Therefore, if urine drug testing is to be conducted, pH, relative density, and appearance should be assessed and suspect specimens should be rejected. Not all adulterants can be detected, so observed collection is strongly recommended.