Central lead administration induces natriuretic and kaliuretic effects in rats

Physiology and Behavior

Volumn 65, Issue 2, 1998, Pages 321-326

  Fregoneze, J B ^a   Luz, C P ^a   Sarmento, C ^a   Gonzalez, V ^a   Oliveira, P ^a   Santana Jr , P ^a   Marinho, C A ^a   Castro, L ^a   Nascimento, T ^a   De Paula, S ^a   Lima, A K S ^a   De Oliveira, I R ^a   De Castro E Silva, E ^a  

^a FEDERAL UNIVERSITY OF BAHIA   (Brazil)

Author keywords

Brain angiotensin; Calcium; Calcium channels; Gadolinium; Kaliuresis; Lead; Lead intoxication; Lead neurotoxicity; Losartan; Natriuresis

Indexed keywords

ANGIOTENSIN 1 RECEPTOR; CALCIUM; CALCIUM CHANNEL; GADOLINIUM; LEAD ACETATE; LOSARTAN;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; INTRACEREBROVENTRICULAR DRUG ADMINISTRATION; KALIURESIS; KIDNEY FUNCTION; LEAD POISONING; MALE; NATRIURESIS; NEUROTOXICITY; NONHUMAN; PATHOPHYSIOLOGY; PRIORITY JOURNAL; RAT;

EID: 0031794750     PISSN: 00319384     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0031-9384(98)00172-3     Document Type: Article

References (45)

1. Al-Saleh, I. A. S. The biochemical and clinical consequences of lead poisoning. Med. Res. Rev. 14:415-486; 1994.
2. Arvidson, B. A review of axonal transport of metals. Toxicology 88:1-14; 1994.
3. Bellinger, D.; Sloman, J.; Leviton, A.; Rabinowitz, M.; Needleman, H. L.; Waternaux, C. Low-level lead exposure and children's cognitive function in preschool years. Pediatrics 87:219-227; 1991.
4. Bellinger, D.; Stiles, K.; Needleman, H. Low-level lead exposure intelligence and academic achievement. A long-term follow-up study. Pediatrics 89:855-861; 1992.
5. Bielarczyk, H.; Tomsig, J. L.; Suszkiw, J. B. Perinatal low-level lead exposure and the septo-hippocampal cholinergic system: Selective reduction of muscarinic receptors and cholineacetyltransferase in the rat septum. Brain Res. 643:211-217; 1994.
6. Bradbury, M. W. B.; Deane, R. Permeability of the blood-brain barrier to lead. Neurotoxicology 4:131-136; 1993.
7. Brooks, V. L.; Malvin, R. L. Intracerebroventricular infusion of angiotensin II increases sodium excretion. Proc. Soc. Exp. Biol. Med. 169:532-537; 1982.
8. Büsselberg, D.; Evans, M. L.; Rahmann, H.; Carpenter, D. O. Lead and zinc block a voltage-activated calcium channel of aplysia neurons. J. Neurophysiol. 65:786-795; 1991.
9. Cory-Slechta, D.; Pokora, M. J.; Widzowski, D. V. Postnatal lead exposure induces supersensitivity to the stimulus properties of a D2-D3 agonist. Brain Res. 508:162-172; 1992.
10. Cory-Slechta, D. A. Postnatal lead exposure and MK-801 sensitivity. Neurotoxicology 18:209-220; 1997.
11. Denton, D. A.; McKinley, M. J.; Weisinger, R. S. Hypothalamic integration of body fluid homeostasis. Proc. Natl. Acad. Sci. USA 93:7397-7404; 1996.
12. Ferreira-do-Vale, C.; Renzi, A.; Camargo, G. P. A.; Saad, W. A.; Luiz, A. C.; Menani, J. V.; Silveira, J. E. N.; Camargo, L. A. A. The role of angiotensin AT1 receptors in the diuretic, natriuretic, kaliuretic and blood pressure responses induced by angiotensin II activation of the median preoptic nucleus in conscious rats. Braz. J. Med. Biol. Res. 28:1097-1101; 1995.
13. Fitzsimons, J. B.; Fuller, L. M. Effects of angiotensin or carbachol on sodium intake and excretion in adrenalectomized or deoxycorticosterone-treated rats. J. Physiol. 359:447-458; 1985.
14. Fregoneze, J. B.; Antunes-Rodrigues, J. Role of opioid peptides and subfornical organ in the renal function of intact and hypophysectomized rats. Physiol. Behav. 51:287-292; 1992.
15. Fregoneze, J. B.; Cunha, M.; Bulcão, C.; Ferreira, H.; De Castro e Silva, E. Acute effect of intracerebroventricular administration of lead on the drinking behavior of rats induced by dehydration or central cholinergic and angiotensinergic stimulation. Physiol. Behav. 56:129-133; 1994.
16. 2+) inhibit the dipsogenic action of central β-adrenergic stimulation by isoproterenol. Braz. J. Med. Biol. Res. 30:419-423; 1997.
17. Goldstein, G. W. Brain capillaries: A target for inorganic lead poisoning. Neurotoxicology 5:167-176; 1994.
18. Goldstein, G. W. Lead poisoning and brain cell function. Environ. Health Perspec. 89:91-94; 1990.
19. Goldstein, G. W. Evidence that lead acts as a calcium substitute in second messenger metabolism. Neurotoxicology 14:97-101; 1993.
20. Goyer, R. A. Nutrition and metal toxicity. Am. J. Clin. Nutr. 61(Suppl.): 646-505; 1995.
21. Goyer, R. A. Results of lead research: Prenatal exposure and neurological consequences. Environ. Health Perspec. 104:1050-1054; 1996.
22. Jonhson, A. K.; Thunhorst, R. L. The neuroendocrinology of thirst and salt appetite: Visceral sensory signals and mechanisms of central integration. Frontiers in Neuroendocrinology 18:292-353; 1997.
23. Lansdown, R.; Yule, W.; Urbanowicz, M. A.; Hunter, J. The relationship between blood-lead concentrations, intelligence, attainment and behaviour in a school population: The second London study. Int. Arch. Occup. Environ. Health 57:225-235; 1986.
24. Lansman, J. B. Blockade of current through single calcium channels by trivalent lanthanide cations. Effect of ionic radius on the rates of ion entry and exit. J. Gen. Physiol. 95:679-696; 1990.
25. Lasley, S. N.; Gilbert, M. E. Presynanaptic glutamatergic function in dentate gyrus in vivo is diminished by chronic exposure to inorganic lead. Brain Res. 736:125-134; 1996.
26. McCann, S. M.; Gutkowska, J.; Franci, C. R.; Favaretto, A. L. V.; Antunes-Rodrigues, J. Hypothalamic control of water and salt intake and excretion. Braz. J. Med. Biol. Res. 27:865-884; 1994.
27. McDowell, J.; Kitchen, I. Perinatal lead exposure alters the develop-ment of δ- but not μ-opioid receptors in rat brain. Br. J. Pharmacol. 94:933-937; 1988.
28. McKinley, M. J. Common aspects of the cerebral regulation of thirst and renal sodium excretion. Kidney Intern. 41(Suppl. 37):S102-S106; 1992.
29. National Academy of Sciences, Committee on Lead in the Human Environment, Washington, DC; 1980.
30. National Research Council. Measuring lead exposure in infants, children and other sensitive Populations. Washington, DC: Natl. Acad.; 1993.
31. Oortigiesen, M.; van Kleef, R. G. D. M.; Vijverberg, H. P. M. Dual, non-competitive interaction of lead with neuronal nicotinic acetylcholine receptors in N1E-115 neuroblastoma cells. Brain Res. 747:1-8; 1997.
32. P'an A. Y. S.; Kennedy, C. Lead distribution in rats repeatedly treated with low doses of lead acetate. Environ. Res. 48:238-247; 1989.
33. 2+ influx and glutamate release in rat cerebrocortical synaptosomes. Neurosci. Lett. 178:155-158; 1994.
34. Rosen, H. Polakiewicz, R. D. Increase in hypothalamic pro-opiomelanocortin gene expression in response to prolonged low-level lead exposure. Brain Res. 493:380-384; 1989.
35. Saavedra, J. Brain and pituitary angiotensin. Endocr. Rev. 13:329-380; 1992.
36. Schwartz, J.; Otto, D. Blood lead hearing thresholds and neurobehavioral development in children and youth. Arch. Environ. Health. 42: 153-160; 1987.
37. Shailesh-Kumar, M. V.; Desiraju, T. Regional alterations of brain biogenic amines and GABA/glutamate levels in rats following chronic lead exposure during neonatal development. Arch. Toxicol. 64:305-314; 1990.
38. Thunhorst, R. L.; Johnson, A. K. Effects of arterial pressure on drinking and urinary responses to intracerebroventricular angiotensin II. Am. J. Physiol. 264:R211-R217; 1993.
39. Unger, T.; Horst, P. J.; Bauer, M.; Demmert, G.; Rettig, R.; Rohmeiss, P. Natriuretic action of angiotensin II in concious rats. Brain Res. 486:33-38; 1989.
40. Verity, M. A. Nervous system. In: Goyer, R. A., Klaassen, C. D.; Waalkes, M.P., eds. Metal toxicology. San Diego: Academic; 1995: 199-224.
41. Widmer, H. R.; Bütikofer, E. E.; Schlumpf, M; Lichtensteiger, W. Preand postnatal lead exposure affects the serotoninergic system in the immature rat brain. Experientia 47:463-466; 1991.
42. Widzowski, D. V.; Cory-Slechta, D. A. Homogeneity of region brain lead concentrations. Neurotoxicol. 15:295-308; 1994.
43. Winneke, G.; Kramer, U.; Brockhaus, A.; Ewers, U.; Kujanek, G.; Lechner, H.; Janke, W. Neuropsychological studies in children with elevated tooth-lead concentrations. Arch. Occup. Environ. Health. 51:231-252; 1983.
44. World Health Organization. Environmental Health Criteria on Inorganic Lead. Geneva: World Health Organization; 1994.
45. Zawia, N. H.; Harry, G. J. Developmental exposure to lead interferes with glial and neuronal differential gene expression in the rat cerebellum. Toxicol. Appl. Pharmacol. 138:43-47; 1996.