Taurine plays an important role in the modulation of cardiovascular function by acting not only within the brain but also within peripheral tissues. We found that IV injection of taurine to male rats caused hypotension and tachycardia. A single injection of taurine significantly lowered the systolic, diastolic, and mean arterial blood pressure in freely moving Long-Evans control rats. We further confirm the vasoactive properties of taurine using isolated aortic ring preparations. Mechanical responses of circular aortic rings to pharmacological agents were measured by an isometric force transducer and amplifier. We found that bath application of taurine to the aortic rings caused vasodilation which was blocked by picrotoxin. Interestingly, picrotoxin alone induced a constriction of the aortic ring in the absence of exogenously added taurine, suggesting a tonic activation of GABA(A)receptors by circulating either taurine or GABA. Additionally, we found that the endothelial cells express high levels of taurine transporters and GABA(A)receptors. We have previously shown that taurine activates GABA(A)receptors and thus we suggest that the functional implication of GABA(A)receptor activation is the relaxation of the arterial muscularis, vasodilation, and a decrease in blood pressure. Interestingly however, the effects of acute taurine injection were very different than chronic supplementation of taurine. When rats were supplemented taurine (0.05%, 4 weeks) in their drinking water, taurine has significant hypertensive properties. The increase in blood pressure was observed however only in females; males supplemented with taurine did not show an increase in systolic, diastolic, or mean arterial pressure. In both genders however, taurine supplementation caused a significant tachycardia. Thus, we suggest that acute administration of taurine may be beneficial to lowering blood pressure. However, our data indicate that supplementation of taurine to females caused a significant increase in blood pressure. The effect of taurine supplementation on hypertensive rats remains to be seen.
This paper investigates the small sample performance of the Least Squares Dummy Variable (LSDV) estimator of the dynamic panel data models for period, T, greater than the cross sections, N and its large sample performance in the direction of T as N remains finite, and compares it with the performance of the instrumental variable- generalize method of moments (IV-GMM) estimators using the properties of root mean squares error(RMSE) of the model , root mean squares error of the autoregressive term ? (RMSE?), the bias of ? (bias?) and the Akaike Information Criterion (AIC) with the motive of ascertaining the usefulness of the LSDV estimator in determining the parameters of a dynamic panel model as T? and finite N, for which it is regarded as consistent.
Background: Developmental lead (Pb2+) exposure has been historically shown to alter the pathological functions of the cardiovascular system at high blood lead levels (i.e.,>15 μg/dL). However, given the time that has elapsed in the field (i.e., some 30 years), there is a great need for less clinical and more basic research on the cardiopathology of low blood lead levels (lBLLs; i.e.,<10 μg/dL). Further, most of the prior literature had focused solely on males as they had been reported to be more vulnerable to Pb2+ induced cardiovascular pathology. Aims and Objectives: To generate a model system of Pb2+-induced cardiovascular pathology that would be consistent with past reports, the present study examined male Long–Evans Hooded rats that were perinatally Pb2+ exposed (i.e., via their food with 996 ppm lead acetate in the rat chow) up until weaning (i.e., postnatal day 22; blood lead levels [BLLs]: 10–15 μg/dL) and were then removed from Pb2+ exposure for nearly 1.5 months (i.e., BLLs >3.33 μg/dL). Materials and Methods: Rats were then subjected to cardiovascular measures of systolic and diastolic blood pressures (SBP and DBP) and heart rates. Rats were sacrificed and their hearts were weighed; their thoracic aortas were collected and examined for microstructural and morphological changes through a scanning electron micrograph. Results: The data showed that compared to age matched control rats, the Pb2+ exposed rats have increased SBP, DBP, and heart rate with no differences in heart weight. These data show that early developmental Pb2+ exposure comprising lBLLs can cause significant cardiovascular pathological changes in rats. Conclusion: The present model of developmental Pb2+-exposure occurring early in life caused Pb2+-induced cardiopathology later in life through increased hypertension and reduced elasticity of the aorta media. These cardiovascular pathologies could further increase the likelihood of accelerated fronto executive dysfunctions due to the direct action of Pb2+ on neurons through inhibition of calcium dependent processes and might also contribute to vascular dementias.
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