Abstract
We studied the effects of the acute administration of small doses of lead over time on hemodynamic parameters in anesthetized rats to determine if myocardial contractility changes are dependent or not on the development of hypertension. Male Wistar rats received 320 µg/kg lead acetate iv once, and their hemodynamic parameters were measured for 2 h. Cardiac contractility was evaluated in vitro using left ventricular papillary muscles as were Na+,K+-ATPase and myosin Ca2+-ATPase activities. Lead increased left- (control: 112 ± 3.7 vs lead: 129 ± 3.2 mmHg) and right-ventricular systolic pressures (control: 28 ± 1.2 vs lead: 34 ± 1.2 mmHg) significantly without modifying heart rate. Papillary muscles were exposed to 8 µM lead acetate and evaluated 60 min later. Isometric contractions increased (control: 0.546 ± 0.07 vs lead: 0.608 ± 0.06 g/mg) and time to peak tension decreased (control: 268 ± 13 vs lead: 227 ± 5.58 ms), but relaxation time was unchanged. Post-pause potentiation was similar between groups (n = 6 per group), suggesting no change in sarcoplasmic reticulum activity, evaluated indirectly by this protocol. After 1-h exposure to lead acetate, the papillary muscles became hyperactive in response to a β-adrenergic agonist (10 µM isoproterenol). In addition, post-rest contractions decreased, suggesting a reduction in sarcolemmal calcium influx. The heart samples treated with 8 µM lead acetate presented increased Na+,K+-ATPase (approximately 140%, P < 0.05 for control vs lead) and myosin ATPase (approximately 30%, P < 0.05 for control vs lead) activity. Our results indicated that acute exposure to low lead concentrations produces direct positive inotropic and lusitropic effects on myocardial contractility and increases the right and left ventricular systolic pressure, thus potentially contributing to the early development of hypertension.
Highlights
Lead is a toxic metal and an environmental pollutant related to the development of hypertension, in addition to having harmful effects on the neural, renal and cardiovascular systems, among others [1,2,3,4]
Our results indicated that acute exposure to low lead concentrations produces direct positive inotropic and lusitropic effects on myocardial contractility and increases the right and left ventricular systolic pressure, potentially contributing to the early development of hypertension
The force and both time derivatives increased after lead exposure
Summary
Lead is a toxic metal and an environmental pollutant related to the development of hypertension, in addition to having harmful effects on the neural, renal and cardiovascular systems, among others [1,2,3,4]. Navas-Acien et al [6] reviewed the link between lead exposure and cardiovascular events in various population studies, highlighting the elevation of arterial pressure [7,8,9]. Lead-induced hypertension involves an increase of sympathetic nerve activity and a reduction of baroreflex sensitivity [10,11,12]. The cardiovascular effects of lead are not limited to increases in blood pressure. While lead-induced hypertension has been well described, only a few reports have described the direct effects of lead on cardiac muscle [13]. Carmignani et al [14] reported a positive inotropic effect and the increased activity of angiotensinconverting enzyme in rats exposed to 60 ppm, as drinking water, of lead acetate for 10 months.
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