Degradation of the Ferric Chelate of EDTA by a Pure Culture of an Agrobacterium sp.

A pure culture of an Agrobacterium sp. (deposited as ATCC 55002) that mineralizes the ferric chelate of EDTA (ferric-EDTA) was isolated by selective enrichment from a treatment facility receiving industrial waste containing ferric-EDTA. The isolate grew on ferric-EDTA as the sole carbon source at concentrations exceeding 100 mM. As the degradation proceeded, carbon dioxide, ammonia, and an unidentified metabolite(s) were produced; the pH increased, and iron was precipitated from solution. The maximum rate of degradation observed with sodium ferric-EDTA as the substrate was 24 mM/day. At a substrate concentration of 35 mM, 90% of the substrate was degraded in 3 days and 70% of the associated chemical oxygen demand was removed from solution. Less than 15% of the carbon initially present was incorporated into the cell mass. Significant growth of this strain was not observed with uncomplexed EDTA as the sole carbon source at comparable concentrations; however, the ferric chelate of propylenediaminetetraacetic acid (ferric-PDTA) did support growth.

Histamine and serotonin independently elicit drinking in the rat.

Drinking elicited by SC histamine or serotonin (5-HT) was studied in Sprague-Dawley male rats following 0.9% NaCl or combined antagonism of H1 and H2 histamine receptors using dexbrompheniramine (DXB) and cimetidine (C), or following antagonism of 5-HT receptors using methysergide (M). Histaminergic antagonism using IP 1 mg/kg DXB plus 16 mg/kg C abolished drinking elicited by SC 2.5 mg/kg histamine, but it failed to inhibit drinking elicited by the ED50 or by the ED100 for SC 5-HT in the same rats. Serotonergic antagonism using IP 3 mg/kg M abolished drinking elicited by SC 0.63 mg/kg 5-HT, but it failed to inhibit drinking elicited by the ED50 or by the ED100 for SC histamine in the same rats. These findings demonstrate that activation of peripheral 5-HT receptors is not necessary for SC histamine to elicit drinking and that activation of peripheral histamine receptors is not necessary for SC 5-HT to elicit drinking. This demonstrates that histamine and 5-HT activate different receptors to elicit drinking in the rat. The finding that the ED50 for histamine and the ED50 for 5-HT are not additive in their effects on drinking is consistent with the notion that a single mechanism mediates the dipsogenic effects of SC histamine and SC 5-HT in the rat.

Histamine plays no part in schedule-induced polydipsia in the rat.

Twelve Sprague-Dawley male albino rats were tested with or without combined antagonism of peripheral H1 (using 2 mg/kg dexbrompheniramine IP) and H2 (using 32 mg/kg cimetidine IP) receptors for histamine prior to (a) drinking after 2.5 mg/kg histamine SC, (b) drinking after 24-hr water deprivation, and (c) drinking during the acquisition and maintenance of schedule-induced polydipsia (SIP) with a 45 mg Noyes pellet delivered every 90 sec. Such antagonism of histamine receptors abolished drinking elicited by exogenous histamine without inhibiting drinking after water deprivation. Moreover, histaminergic antagonism failed to prevent the acquisition and maintenance of SIP and failed to alter the distribution of contacts with the drinking spout during interpellet intervals. These findings demonstrate no role for endogenous systemic histamine in SIP.

Disordered drinking in developing spontaneously hypertensive rats.

Eating and drinking in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were measured at 5-17 wk of life. The SHR drank significantly more water in 24 h than WKY as early as wk 9, spilled more dry food than did WKY, and exhibited an inverse relation between 24-h water intake and dry food spilled. When eating a meal of dry food after 12 h food deprivation, SHR drank earlier and drank more in a 1-h test than WKY rats. Moreover, SHR exhibited (as early as wk 7) a striking pattern of interrupting eating to drink. This pattern was not present when SHR ate liquid food, and it was attenuated by infusion of water through a cheek fistula. Adult SHR (22 wk) salivated less than WKY in response to intraperitoneal 3.25 mg/kg pilocarpine nitrate. When developing SHR and WKY were maintained on liquid and solid food, SHR gained disproportionately more weight than WKY during development. When young SHR were permitted to drink no more water than WKY rats, the development of hypertension was retarded, and body weight gain was slowed. Because restricted access to food, which produced an equivalent slowing of body weight gain as did restricted access to water, also retarded development of hypertension, it appears that restricted access to water retards development of hypertension due to delayed growth. These results demonstrate that hyperdipsia, apparently caused by deficient salivary function, is not necessary for the development of hypertension in SHR.