This study examined firing patterns of single-fiber carotid baroreceptors in response to slow ramp increases in carotid sinus pressure (1-2 mm Hg/sec) in vascularly isolated carotid sinus preparations in thiopental-anesthetized dogs (25 mg/kg, plus 10 mg/kg/hr

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The presence of two types of carotid sinus baroreceptors, as characterized by two different stimulus-response curves in an earlier study, suggests that each type may play a different role in the regulation of blood pressure. The discontinuous hyperbolic curve of the type I baroreceptors, marked by higher firing rates and greater sensitivity than the sigmoidal curve of type II baroreceptors, suggests that these baroreceptors would contribute more to the buffering of arterial pressure changes than the "tonically" active type II baroreceptors, which fired over greater pressure ranges and generally had spontaneous subthreshold discharge. The firing characteristics of type II baroreceptors suggest that these receptors would contribute more to regulation of tonic, baseline levels of arterial pressure. If this functional differentiation exists, the acute resetting characteristics of the two types of baroreceptors could be different. Resetting is defined as a shift in the response curve of a baroreceptor, marked by shifts in pressure threshold, in the same direction as the change in pressure to which it is exposed. Type I baroreceptors would be more likely to reset in response to a sustained acute change in pressure, since their primary role would be to prevent the initial change in pressure. However, type II baroreceptors would not reset to the acute change in pressure, since their primary role would be to maintain consistent information on the level of existing pressure. Therefore, this study was performed to examine the acute resetting ability of both types of baroreceptors by using a vascularly isolated carotid sinus preparation in the dog.(ABSTRACT TRUNCATED AT 250 WORDS)

Female mice treated with 14C-2,4,5,2',4',5'-hexachlorobiphenyl (6-CB) two weeks prior to mating eliminated virtually their entire body burden of the compound through milk during one lactation cycle. 6-CB was shown to distribute among rat and human plasma lipoproteins and protein in vitro. It was readily transferred among plasma constituents and its distribution was related to the triacylglycerol:protein ratio in plasma. At one hour following its intravenous administration to virgin rats, 6-CB was primarily distributed to LDL. With the hypertriglyceridemia of late pregnancy, more than 70% of circulating 6-CB was associated with VLDL. VLDL is a major substrate for mammary gland lipoprotein lipase which is elevated during lactation. When 6-CB was complexed with human VLDL and injected i.v. into late pregnant mice, mammary gland concentrations of 6-CB exceeded those of adipose tissue at all sacrifice times between 5 min and 6 h. No differences between adipose tissue and mammary gland concentrations of 6-CB were observed with Emulphor:ethanol:saline as vehicle until 6 h. Isolated hepatocytes were capable of secreting protein and triacylglycerol in the form of VLDL into serum-free media. Eighty percent of 6-CB released from hepatocytes was in association with VLDL, with the remainder in association with protein. Adipocytes isolated from epididymal fat pads of male rats which were pretreated with 6-CB released progressively less radioactivity to incubation media with time after treatment even though PCB content of these cells increased. 6-CB may not be evenly distributed among adipocyte lipids.

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