Renal mechanisms in the cardiovascular effects of chronic exposure to inorganic mercury in rats.

Abstract

Male weanling Wistar rats received 200 pg/mi of mercury (Hg), as HgCl,, in drinking water for 180 days. At the end of the treatment, systemic arterial blood pressure was augmented, cardiac inotropism was reduced, and heart rate was unchanged. Light and electron microscopical studies of the kidney showed a mesangial proliferative glomerulonephritis in about 80% of the glomeruli. Tubular cells showed reduction of the acid phosphatase activity, which was related to functional abnormalities of the lysosomes. In the 24 hour urine samples ofthe Hg exposed rats, there was slight reduction of kallikrein activity, but evident proteinuria was not present in all samples. Plasma renin activity was reduced, that of angiotensin I-converting enzyme was augmented, and plasma aldosterone concentrations were unchanged. Mercury was accumulated mostly in the kidney of the Hg treated animals; and the content of Hg in the heart was higher than in the brain. These data show that chronic exposure to Hg acts on the kidney with complex mechanisms of toxicity; these contribute to modify systemic haemodynamics. The purpose of this study was to investigate some mechanisms of renal toxicity possibly involved in the dysfunction of cardiovascular function, in rats exposed to doses of Hg known to induce both arterial hypertension and autoimmune lesions in the kidney. Materials and methodsSixteen male weanling Wistar rats were randomly divided into two equal groups, housed in stainless steel cages, and fed a standard laboratory diet. One group received 200 pg/ml of Hg (as HgCl2) in deionised drinking water for 180 days and the other group was kept as a control. At the end of the exposure all the rats were placed in metabolism cages for the collection of 24 hour urine samples.The animals were anaesthetised with a single intraperitoneal injection of sodium thiopental (50 mg/kg body weight) in order to perform haemodynamic measurements. The trachea was cannulated to allow spontaneous breathing and polyethylene catheters (containing sodium heparin, 100 USP units/ml) were placed in the left femoral artery to record aortic blood pressure. Specimens of several tissues were also excised for histopathological observation by light microscopy.Samples of blood, brain, heart, and kidney were prepared for determination of Hg content. Mercury was analysed by flameless atomic spectrophotometry after special digestion of tissues and blood.25 The Hg content was quoted as the wet weight of blood and

Mechanisms involved in the transport of mercuric ions in target tissues

“…These include, but are not limited to, the cardiovascular (Carmignani et al 1992; Soni et al 1992; Wakita 1987; Wang et al 2000; Warkany and Hubbard 1953), gastrointestinal (Afonso and De Alvarez 1960; Bluhm et al 1992; Lundgren and Swensson 1949; Murphy et al 1979), neurological (Jaffe et al 1983; Lin and Lim 1993), hepatobiliary (Jaffe et al 1983; Murphy et al 1979; Samuels et al 1982), and renal (Murphy et al 1979; Rowens et al 1991; Samuels et al 1982) systems.…”

Chronic HgCl2 treatment increases vasoconstriction induced by electrical field stimulation: role of adrenergic and nitrergic innervation

“…In fact, acute mercury exposure reduces the development of myocardial force [14] and inhibits myosin ATPase activity [15]. Moreover, chronic mercury exposure increases vascular resistance and induces hypertension [12,16].…”

Molecular and ionic mimicry and the transport of toxic metals

“…However, the extent of the adverse effects induced by Hg in an organism depends on the form of Hg at the time of exposure, the duration of exposure, and the route of exposure. Exposure to all forms of Hg, at least to some extent, has been shown to cause deleterious effects in the cardiovascular system (Carmignani et al, 1992;Soni et al, 1992;Warkany and Hubbard, 1953;Wakita, 1987), gastrointestinal system (Afonso and deAlvarez, 1960;Bluhm et al, 1992;Lundgren and Swensson, 1949;Murphy et al, 1979), liver (Jaffe et al, 1983;Murphy et al, 1979;Samuels et al, 1982), kidneys (Murphy et al, 1979;Rowens et al, 1991;Samuels et al, 1982;Yasutake et al, 1991), and neurological system (Jaffe et al, 1983;Kutsuna, 1968;Lin and Lim, 1993;Tsubaki and Takahashi, 1986).…”