Between May 1988 and September 1989, 829 human immunodeficiency virus type 1 (HIV-1)-seropositive donors were identified from 3,919,000 units of blood donated at 20 United States (US) blood centers. Of the 829,512 (62%) were interviewed to assess behavioral characteristics of the largest subgroup, men reporting sex with men, use of the confidential unit exclusion (CUE) and reasons for donation among all donors. Among 216 men reporting sex with men, 97 percent had male and 72 percent had female sexual contact since 1978. The majority identified themselves as bisexual (29%) or heterosexual (26%). Although 61 percent of 512 donors were aware of their risk behavior at donation, including 57 percent of those infected through heterosexual transmission, only 5 percent used the CUE. Reasons for donation included failure to read carefully (46%) or comprehend (15%) the deferral materials, pressure to donate (27%), a desire to be tested for HIV-1 (15%), and a reliance on screening to identify infected blood (10%). Reasons given for a perception of being at low risk included no recent risk behaviors, infrequent risk behaviors, or modification of risk behaviors. To reach high-risk donors, centers should assess whether referral materials provide necessary medical information and are clearly written for persons with diverse cultural and language backgrounds. Staff should be encouraged to avoid the use of culturally stigmatized terms and behaviors that may be perceived as high pressure.
Chloride (Cl-) channels were characterized in vascular smooth muscle cells (VSMC) using radioisotope flux and patch-clamp electrophysiological techniques. Transmembrane 125iodine (125I) efflux from subcultured (Passage 1-5) rat aortic VSMCs was used as an indicator of Cl- movements to study the relationship between intracellular calcium concentration ([Ca2+]i) and Cl- channel activity. Angiotensin II (Ang II) (10(-7) M) and adenosine 5'-triphosphate (ATP) (10(-4) M) induced rapid increases (9.7- and 14.9-fold, respectively) in 125I efflux rates. We found that both Ang II- and ATP-stimulated 125I efflux and [Ca2+]i increases were completely abolished after brief incubation (20 microM, 20 min) with the acetoxymethyl ester of 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM), a membrane-permeable Ca2+ chelator. However, when external EGTA was used to blunt agonist-stimulated Ca2+ influx, 125I efflux was still increased in response to Ang II and ATP. These data suggest that Ca2+ release from intracellular sites is sufficient to activate Cl- channels in response to Ang II and ATP. Using standard patch-clamp electrophysiological techniques, we found that Ang II, a Ca(2+)-mobilizing agonist, stimulated outward Cl- currents (gCl = 75 pS) in cell-attached (C/A) patches of primary and subcultured VSMCs. Collectively, these data suggest that Ang II and other vasoconstrictor agents stimulate Cl- channel activity via increases in [Ca2+]i. Cl- channel activation may help to depolarize the VSMC membrane leading to increased Ca2+ influx during agonist stimulation.
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