Potencial de economia de energia elétrica através do uso da luz natural e da ventilação híbrida em edifícios comerciais em Florianópolis

O objetivo deste estudo é estimar o potencial de economia de energia elétrica com o uso da luz natural integrada ao sistema de iluminação artificial e a utilização da ventilação híbrida em edifícios comerciais localizados em Florianópolis, SC. O trabalho foi baseado em simulações computacionais nos programas EnergyPlus e Daysim. Foram simulados modelos de ambientes de edificações comerciais, com três geometrias, três dimensões de sala por geometria, dez áreas de janela por modelo e quatro orientações. Os modelos foram examinados por meio de quatro estudos de caso. No Caso 1 (referência), a edificação opera com sistemas de iluminação e de condicionamento artificiais; no Caso 2, ocorre a integração da iluminação natural com a artificial, com condicionamento artificial; já no Caso 3, utilizam-se a ventilação híbrida e a iluminação artificial; no Caso 4, adotam-se a iluminação natural integrada com a artificial e a ventilação híbrida. Os consumos de eletricidade do Caso 1 foram comparados com os demais casos. Assim, foi estimado o potencial de economia de energia elétrica gerado pelo uso da luz natural e ventilação híbrida. Conclui-se que a utilização da iluminação natural e da ventilação híbrida em edificações comerciais localizadas em Florianópolis apresenta potencial de economia de energia elétrica de até 64,9% e que essas estratégias podem ser utilizadas para aumentar a eficiência energética desse tipo de edificação

Direct evidence that thromboxane mimetic U44069 preferentially constricts the afferent arteriole

The thromboxane A2 (TXA2) mimetic U44069 has been demonstrated to reduce the GFR and filtration fraction of the normal isolated perfused rat kidney markedly, suggesting a predominant constriction of preglomerular vessels. To assess this possibility directly, effects of U44069 on the renal microvessels of the isolated perfused hydronephrotic kidney were examined. At 10(-6) mol/L, U44069 elicited a 27 +/- 2% decrease in afferent arteriolar (AA) diameter (from 18.8 +/- 0.3 to 13.7 +/- 0.3 micron, P < 0.001). In contrast, efferent arteriolar (EA) diameter decreased by only 9 +/- 1% (from 16.4 +/- 0.5 to 15.0 +/- 0.5 micron, P < 0.001). These effects on both AA and EA were completely reversed by the TXA2 receptor antagonist SQ29548. The calcium antagonist diltiazem reversed U44069-induced AA constriction by 83 +/- 5%. The U44069-induced EA constriction was insensitive to the vasodilator action of diltiazem at concentrations from 10(-8) to 10(-6) mol/L, but at 10(-5) mol/L, diltiazem increased the EA diameter significantly, albeit modestly. Nifedipine also reversed the U44069-induced AA constriction (81 +/- 7%), but failed to inhibit the EA constriction at concentrations from 10(-9) to 10(-6) mol/L. These findings constitute the first direct evidence that a TXA2 agonist preferentially constricts the afferent arteriole. Furthermore, the ability of both the calcium antagonist and SQ29548 to reverse the renal microvascular actions of TXA2 agonists suggests a potential utility of these agents in ameliorating TXA2-induced renal hemodynamic abnormalities

Divergent effects of KCl-induced depolarization on afferent and efferent arterioles

We have previously proposed that renal microvessels exhibit a unique regional heterogeneity. Studies with calcium channel agonists and antagonists suggest that potential-dependent calcium channels may play a more prominent role in the activation of the afferent arteriole than the efferent arteriole. Because KCl-induced depolarization elicits vasoconstriction exclusively by the activation of potential-dependent calcium channels, we tested this postulate directly by ascertaining the vasoconstrictor effects of KCl and countervailing effects of a calcium channel blocker on the afferent and efferent arteriole of isolated perfused hydronephrotic kidneys. Increasing media potassium concentration from 5 to 30 mM resulted in a marked renal vasoconstriction decreasing renal perfusate flow by 61 +/- 4%. An examination of the microvascular response to KCl revealed a predominant response of the afferent arteriole. Thus afferent arteriolar diameter decreased by 38 +/- 6% (i.e., from 20.7 +/- 1.5 to 13.0 +/- 1.8 microns, P less than 0.005), whereas efferent arteriolar diameter decreased by only 12 +/- 4% (i.e., from 15.8 +/- 1.6 to 13.8 +/- 1.4 microns, P = 0.05). Nifedipine completely returned afferent arteriolar diameter to control levels with a mean effective dose of 41 +/- 2 nM. These findings indicate that the afferent arteriole is more responsive to depolarization-induced vasoconstrictor stimuli than is the efferent arteriole and suggest a greater prevalence of potential-dependent calcium channels in this vessel

Direct visualization of effects of endothelin on the renal microvasculature

The renal microvascular and hemodynamic actions of endothelin were assessed directly in isolated perfused hydronephrotic (HYD) and normal kidneys, respectively. In HYD kidneys endothelin was a potent vasoconstrictor of the afferent arteriole (AA), eliciting a threshold vasoconstrictor response at 0.01 nM (P less than 0.05). At 0.1 and 0.3 nM, endothelin reduced AA diameter by 22 +/- 6 (P less than 0.025) and 41 +/- 4% (P less than 0.001), respectively. Furthermore, endothelin provoked oscillatory vasomotion in the AA. In contrast, endothelin had less effect on the efferent arteriole (EA), reducing EA diameter by only 7 +/- 4 (P greater than 0.20) and 13 +/- 4% (P less than 0.05), at 0.1 and 0.3 nM, respectively. In normal kidneys endothelin elicited a long-lasting vasoconstriction with a dose dependency similar to that observed in the AA of HYD kidneys. Furthermore, endothelin reduced glomerular filtration rate (GFR) from 0.58 +/- 0.04 to 0.09 +/- 0.05 ml.min-1.g-1 (P less than 0.001) in this model. Both the AA vasoconstriction and reduction in GFR were completely reversed by nifedipine. These findings indicate that endothelin is a potent renal vasoconstrictor that decreases GFR by a predominant vasoconstriction of the AA. Our observations are consistent with the postulate that endothelin elicits renal vasoconstriction via a mechanism involving dihydropyridine-sensitive calcium channels and that such calcium channels play a prominent role in the activation of the AA

Impaired myogenic responsiveness of the afferent arteriole in streptozotocin-induced diabetic rats: role of eicosanoid derangements

Evidence suggests that diabetes is associated with an impairment of renal autoregulation. It has previously been demonstrated that pressure-induced (myogenic) afferent arteriolar vasoconstriction is well preserved in the isolated perfused hydronephrotic kidney. In this study, pressure-induced afferent arteriolar vasoconstriction was examined in kidneys from streptozotocin-induced diabetic rats. Vessel diameters were measured by videomicroscopy as renal arterial pressure was elevated from 80 to 180 mm Hg. In normal kidneys, the afferent arteriole vasoconstricted progressively as renal arterial pressure was increased (-24 +/- 2% decrement in diameter at 180 mm Hg; N = 35; P less than 0.001). In contrast, afferent arterioles of diabetic kidneys exhibited a greatly attenuated response to pressure (i.e., -3 +/- 2% change at 180 mm Hg; N = 60). In vitro treatment with 100 microM ibuprofen completely restored myogenic vasoconstriction (-21 +/- 2% change at 180 mm Hg), but did not alter myogenic responses of control (i.e., nondiabetic) kidneys. The control of hyperglycemia by insulin treatment resulted in a partial preservation of myogenic vasoconstriction (i.e., -11 +/- 3% change at 180 mm Hg), which was further restored by the administration of a low dose (10 microM) of ibuprofen (-21 +/- 1% change at 180 mm Hg). These observations indicate that diabetes is associated with an impaired responsiveness of the afferent arteriole to pressure that is mediated by an alteration in eicosanoid metabolism. This deranged renal microcirculatory response to pressure may represent a functional impairment of the diabetic kidney that may contribute to the progression of diabetic nephropathy