The present study compares cytosolic calcium concentration ([Ca2+]i) responses to angiotensin II (ANG II) of afferent (AA) and efferent arterioles (EA) by taking account of the localization and morphological differences of EA. In outer cortex, 1 nM ANG II induced smaller [Ca2+]i increases in thin EA than in AA[48 +/- 10 (n = 12) vs. 94 +/- 7 nM (n = 11); P < 0.001]. In inner cortex, two types of EA were considered, i.e., thin and muscular ones. The response to 1 nM ANG II was 35% lower in thin than in muscular EA (P < 0.05) but did not differ from that obtained with corresponding AA. In EA of the outer cortex, 1 microM nifedipine, a dihydropyridine blocker of voltage-operated channels (VOCC), did not affect calcium influx, which was suppressed by 1 mM NiCl2, a nonselective calcium entry blocker. In other arterioles, nifedipine inhibited by approximately 40% calcium entry, and remaining influx was blocked by NiCl2. These results indicate a relationship between the magnitude of [Ca2+]i responses, activation of dihydropyridine-sensitive VOCC by ANG II, and the muscular morphology in renal glomerular arterioles. They suggest that ANG II regulates differently local renal microcirculation. They do not, however, support the hypothesis of a greater sensitivity to ANG II of EA compared with the AA of a given nephron.

Background/Aims: Renal risks of nicotine exposure associated with hypercholesterolemia are still unknown. Methods: Thus, hypercholesterolemic rats (HC) and their control (C) were evaluated by inulin clearance (InCl) measured at baseline and during nicotine infusion (100 μg/kg b.w.). Five groups were studied: (i) C; (ii) DEN (C submitted to a renal denervation); (iii) C + L-arginine (0.25% in drinking water); (iv) HC, and (v) HC + L-arginine (0.25% in drinking water). Furthermore, C and HC had their renal blood flow (RBF) measured and they have also been chronically treated with nicotine (12.5 μg/ml in drinking water) to assess InCl on the 8th day. Results: Nicotine increased blood pressure in C, DEN and HC and reduced InCl only in C. L-Arginine treatment blunted nicotine effects on blood pressure and increased InCl only in C. Moreover, nicotine did not change RBF in C but elicited in HC, whereas renal vascular resistance was increased in C and unchanged in HC. Indeed, chronic nicotine exposure has also reduced InCl in C. Conclusion: Nicotine acted on the adrenergic system and nitric oxide counteracted this action in C, but the same may not be applied to HC. An impairment in renal autoregulation may explain why InCl was unchanged in HC.

1A, AT1B, and AT2 receptor mRNAs by RT-PCR in these arterioles and studied the effect of valsartan, a specific AT 1-receptor antagonist. Results indicate that muscular arterioles express AT 1A, AT1B, and AT2 receptors, whereas thin arterioles only express the AT1A and AT 2 types, and at a much lower level. Valsartan fully inhibited ANG II-induced increases in intracellular Ca 2ϩ in both arteriolar types, but with different kinetics. In muscular arterioles, inhibition was monoexponential, whereas it displayed a marked positive cooperativity in thin arterioles. Finally, the apparent affinity for valsartan was higher in muscular than in thin arterioles. In conclusion, this study further documents the differences between muscular and thin efferent arterioles with regard to ANG II signalization in the rat kidney. angiotensin II; valsartan; calcium signaling PRE-AND POSTGLOMERULAR ARTERIOLES are small resistance vessels that regulate renal microcirculation and glomerular filtration. ANG II is a major mediator of the regulation of glomerular filtration through its combined control of the vascular tone in afferent and efferent arterioles (AAs and EAs, respectively).