|
|
Environ Health Perspect. 1988 June; 78: 91–99. | PMCID: PMC1474616 |
Research Article Cardiovascular actions of lead and relationship to hypertension: a review. S J Kopp, J T Barron, and J P Tow Department of Physiology, Chicago College of Osteopathic Medicine, IL 60615. Abstract Chronic and acute lead poisoning cause overt, clinical symptoms of cardiac and vascular damage with potentially lethal consequences. Morphological, biochemical, and functional derangements of the heart have all been described in patients following exposure to excessive lead levels. Disturbances in cardiac electrical and mechanical activity and postmortem evidence of morphological and biochemical derangements of the myocardium have all been reported following excessive exposure to lead in humans. In addition, signs of vascular degeneration, abnormal vascular smooth muscle function, and altered vessel compliance have been described in humans chronically and acutely exposed to toxic lead levels. Similar cardiovascular complications have been detected following excessive lead exposure in experimental animals. Myocarditis, electrocardiographic disturbances, heightened catecholamine arrhythmogenicity, altered myocardial contractile responsiveness to inotropic stimulation, degenerative structural and biochemical changes affecting the musculature of the heart and vasculature, hypertension, hypercholesterolemia, atherosclerosis, and increased vascular reactivity to alpha-adrenergic agonists have been among the reported cardiovascular disturbances linked to lead poisoning. Less certain are the cardiovascular effects of subclinical lead poisoning. Although controversial, chronic low-level lead exposure has been linked to hypertension and other cardiovascular disturbances in both clinical and experimental studies. In general, it can be concluded that lead over a wide range of exposure intensities can induce significant changes in the function of the cardiovascular system. Evidence points to the involvement of multiple sites of action. Cardiac and vascular sites, as well as sites within the central nervous system, have all been implicated in the sequelae of cardiovascular effects. The exact pathogenic mechanisms that underlie the actions of lead in the cardiovascular system, however, have yet to be elucidated definitively.(ABSTRACT TRUNCATED AT 250 WORDS) Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.4M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References. These references are in PubMed. This may not be the complete list of references from this article. - Harlan WR, Landis JR, Schmouder RL, Goldstein NG, Harlan LC. Blood lead and blood pressure. Relationship in the adolescent and adult US population. JAMA. 1985 Jan 25;253(4):530–534. [PubMed]
- Pirkle JL, Schwartz J, Landis JR, Harlan WR. The relationship between blood lead levels and blood pressure and its cardiovascular risk implications. Am J Epidemiol. 1985 Feb;121(2):246–258. [PubMed]
- Williams BJ, Griffith WH, 3rd, Albrecht CM, Pirch JH, Hejtmancik MR., Jr Effects of chronic lead treatment on some cardiovascular responses to norepinephrine in the rat. Toxicol Appl Pharmacol. 1977 Jun;40(3):407–413. [PubMed]
- Revis NW, Major TC, Horton CY. The effects of calcium, magnesium, lead, or cadmium on lipoprotein metabolism and atherosclerosis in the pigeon. J Environ Pathol Toxicol. 1980 Sep;4(2-3):293–303. [PubMed]
- Fell GS. Lead toxicity: problems of definition and laboratory evaluation. Ann Clin Biochem. 1984 Nov;21 (:453–460. [PubMed]
- Kopp SJ, Baker JC, D'Agrosa LS, Hawley PL. Simultaneous recording of His bundle electrogram, electrocardiogram, and systolic tension from intact modified Langendorff rat heart preparations. I: effects of perfusion time, cadmium, and lead. Toxicol Appl Pharmacol. 1978 Nov;46(2):475–487. [PubMed]
- Kopp SJ, Bárány M. Influence of isoproterenol and calcium on cadmium- or lead-induced negative inotropy related to cardiac myofibrillar protein phosphorylations in perfused rat heart. Toxicol Appl Pharmacol. 1980 Aug;55(1):8–17. [PubMed]
- Prentice RC, Kopp SJ. Cardiotoxicity of lead at various perfusate calcium concentrations: functional and metabolic responses of the perfused rat heart. Toxicol Appl Pharmacol. 1985 Dec;81(3 Pt 1):491–501. [PubMed]
- Rosenblum WI. Effects of lead and other cations on pial arteries of the mouse. Acta Neuropathol. 1965 Oct 4;5(1):54–60. [PubMed]
- Favalli L, Chiari MC, Piccinini F, Rozza A. Experimental investigations on the contraction induced by lead in arterial smooth muscle. Acta Pharmacol Toxicol (Copenh) 1977;41 Suppl 2:412–420. [PubMed]
- Piccinini F, Favalli L, Chiari MC. Experimental investigations on the contraction induced by lead in arterial smooth muscle. Toxicology. 1977 Aug;8(1):43–51. [PubMed]
- Webb RC, Winquist RJ, Victery W, Vander AJ. In vivo and in vitro effects of lead on vascular reactivity in rats. Am J Physiol. 1981 Aug;241(2):H211–H216. [PubMed]
- Tomera JF, Harakal C. Mercury- and lead-induced contraction of aortic smooth muscle in vitro. Arch Int Pharmacodyn Ther. 1986 Oct;283(2):295–302. [PubMed]
- Stöfen D. Letter: Environmental lead and the heart. J Mol Cell Cardiol. 1974 Jun;6(3):285–290. [PubMed]
- Hejtmancik MR, Jr, Williams BJ. Effect of chronic lead exposure on the direct and indirect components of the cardiac response to norepinephrine. Toxicol Appl Pharmacol. 1979 Nov;51(2):239–245. [PubMed]
- SCHROEDER HA, BALASSA JJ. INFLUENCE OF CHROMIUM, CADMIUM, AND LEAD ON RAT AORTIC LIPIDS AND CIRCULATING CHOLESTEROL. Am J Physiol. 1965 Aug;209:433–437. [PubMed]
- Revis NW, Zinsmeister AR, Bull R. Atherosclerosis and hypertension induction by lead and cadmium ions: an effect prevented by calcium ion. Proc Natl Acad Sci U S A. 1981 Oct;78(10):6494–6498. [PMC free article] [PubMed]
- READ JL, WILLIAMS JP. Lead myocarditis: report of a case. Am Heart J. 1952 Nov;44(5):797–802. [PubMed]
- KLINE TS. Myocardial changes in lead poisoning. AMA J Dis Child. 1960 Jan;99:48–54. [PubMed]
- MYERSON RM, EISENHAUER JH. Atrioventricular conduction defects in lead poisoning. Am J Cardiol. 1963 Mar;11:409–412. [PubMed]
- Silver W, Rodriguez-Torres R. Electrocardiographic studies in children with lead poisoning. Pediatrics. 1968 Jun;41(6):1124–1127. [PubMed]
- Dimitrova M. Modifications de la fonction contractile du myocarde dans le saturnisme chronique. Arch Mal Prof. 1972 Jul–Aug;33(7):383–388. [PubMed]
- Bertel O, Bühler FR, Ott J. Lead-induced hypertension: blunted beta-adrenoceptor-mediated functions. Br Med J. 1978 Mar 4;1(6112):551–551. [PMC free article] [PubMed]
- Kirkby H, Gyntelberg F. Blood pressure and other cardiovascular risk factors of long-term exposure to lead. Scand J Work Environ Health. 1985 Feb;11(1):15–19. [PubMed]
- Boscolo P, Galli G, Iannaccone A, Martino F, Porcelli G, Troncone L. Plasma renin activity and urinary kallikrein excretion in lead-exposed workers as related to hypertension and nephropathy. Life Sci. 1981 Jan 12;28(2):175–184. [PubMed]
- Jhaveri RC, Lavorgna L, Dube SK, Glass L, Khan F, Evans HE. Relationship of blood pressure to blood lead concentrations in small children. Pediatrics. 1979 Apr;63(4):674–676. [PubMed]
- Beevers DG, Cruickshank JK, Yeoman WB, Carter GF, Goldberg A, Moore MR. Blood-lead and cadmium in human hypertension. J Environ Pathol Toxicol. 1980 Sep;4(2-3):251–260. [PubMed]
- Pocock SJ, Shaper AG, Ashby D, Delves T, Whitehead TP. Blood lead concentration, blood pressure, and renal function. Br Med J (Clin Res Ed) 1984 Oct 6;289(6449):872–874. [PMC free article] [PubMed]
- Batuman V, Landy E, Maesaka JK, Wedeen RP. Contribution of lead to hypertension with renal impairment. N Engl J Med. 1983 Jul 7;309(1):17–21. [PubMed]
- Medeiros DM, Pellum LK. Blood pressure and hair cadmium, lead, copper, and zinc concentrations in Mississippi adolescents. Bull Environ Contam Toxicol. 1985 Feb;34(2):163–169. [PubMed]
- Carvalho L, Soares MA, da Costa JN. O chumbo revisitado como factor etiológico da hipertensão arterial. Acta Med Port. 1985 May;6(5):161–164. [PubMed]
- Patel MA. An inquiry into the poisoning with lead nitrate in experimental animals. Indian J Med Res. 1966 Feb;54(2):196–207. [PubMed]
- Kopp SJ, Bárány M, Erlanger M, Perry EF, Perry HM., Jr The influence of chronic low-level cadmium and/or lead feeding on myocardial contractility related to phosphorylation of cardiac myofibrillar proteins. Toxicol Appl Pharmacol. 1980 Jun 15;54(1):48–56. [PubMed]
- Kopp SJ, Perry M, Jr, Glonek T, Erlanger M, Perry EF, Bárány M, D'Agrosa LS. Cardiac physiologic-metabolic changes after chronic low-level heavy metal feeding. Am J Physiol. 1980 Jul;239(1):H22–H30. [PubMed]
- Evis MJ, Kane KA, Moore MR, Parratt JR. The effects of chronic low lead treatment and hypertension on the severity of cardiac arrhythmias induced by coronary artery ligation in anesthetized rats. Toxicol Appl Pharmacol. 1985 Sep 15;80(2):235–242. [PubMed]
- Asokan SK. Experimental lead cardiomyopathy: myocardial structural changes in rats given small amounts of lead. J Lab Clin Med. 1974 Jul;84(1):20–25. [PubMed]
- Moore MR, Meredith PA, Goldberg A, Carr KE, Toner PG, Lawrie TD. Cardiac effects of lead in drinking water of rats. Clin Sci Mol Med. 1975 Oct;49(4):337–341. [PubMed]
- Kopp SJ, Daar AA, Prentice RC, Tow JP, Feliksik JM. 31P NMR studies of the intact perfused rat heart: a novel analytical approach for determining functional-metabolic correlates, temporal relationships, and intracellular actions of cardiotoxic chemicals nondestructively in an intact organ model. Toxicol Appl Pharmacol. 1986 Feb;82(2):200–210. [PubMed]
- Parr DR, Harris EJ. The effect of lead on the calcium-handling capacity of rat heart mitochondria. Biochem J. 1976 Aug 15;158(2):289–294. [PMC free article] [PubMed]
- Silver PJ, Buja LM, Stull JT. Frequency-dependent myosin light chain phosphorylation in isolated myocardium. J Mol Cell Cardiol. 1986 Jan;18(1):31–37. [PubMed]
- Chekunova MP. Sostoianie katekholaminov serdtsa pri deĭstvii nekotorykh promyshlennykh iadov. Gig Tr Prof Zabol. 1974 Feb;18(2):36–40. [PubMed]
- Barron JT, Bárány M, Bárány K. Phosphorylation of the 20,000-dalton light chain of myosin of intact arterial smooth muscle in rest and in contraction. J Biol Chem. 1979 Jun 25;254(12):4954–4956. [PubMed]
|