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Cardiac vessel density ([beta]-actin immunolabeling) and angiogenic capacity of coronary artery explants (culture in collagen gel) was determined in hypertrophied heart obtained by exercise training (10 wk) or ANG II infusion for 10 days. A group of rats received ANG II the last 10 days of training. The heart weight index was similarly elevated after exercise, and ANG II-hypertension compared with controls (3.16 [+ or -] 0.09 and 3.11 [+ or -] 0.11 vs. 2.68 [+ or -] 0.08 mg/g, respectively), whereas tail cuff pressure (TCP) increased only in sedentary rats infused with ANG II. Vessel density was increased by 36% in trained rats and reduced by 30% in ANG II-infused rats. The number of sprouts generated by coronary rings was reduced by 50% in ANG II-infused rats and increased by 50% in exercise trained rats compared with controls (35 [+ or -] 4 and 113 [+ or -] 5 vs. 71 [+ or -] 1 sprouts per ring, respectively). Exercise-training partly prevented the hypertensive effect of ANG II (TCP of 141 [+ or -] 5 mmHg), whereas heart weight index (3.66 [+ or -] 0.06 mg/g body wt) was not lowered. Myocardial vessel density was normalized, and sprouting from coronary rings increased by 50% in trained rats infused with ANG II compared with sedentary normotensive rats. Cardiac VEGF (Western blot analysis) was higher in hypertensive rats and not affected by exercise. Facing a similar increase in cardiac mass, intense training, but not ANG II hypertension, is accompanied by an increase in vascular density of the heart. The effect of training is unlikely related to changes in resting VEGF and may represent enhanced angiogenic capacity of the coronary vascular bed. coronary artery; left ventricular vessel density; three-dimensional tissue culture; VEGF

Clinical studies suggest a strong link between tissue calcification and pressure hyperpulsatility in end stage renal disease patients. Using a Wistar rat model of arterial elastocalcinosis and hyperpulsatility [vitamin D and nicotine (VDN) treatment], we evaluated the relative importance of tissue calcification and hyperpulsatility in the etiology of renal failure. VDN rats showed significant increases in aortic wall calcium content (50 times; 992 [+ or -] 171 vs. control 19 [+ or -] 1 [micro]mol/g dry wt) and pulse pressure (1.5 times; 61 [+ or -] 4 vs. control 40 [+ or -] 2 mmHg). Significant renal calcification (16 times; 124 [+ or -] 27 vs. control 8.1 [+ or -] 0.7 [micro]mol/g dry wt) occurred mainly within the media of the preglomerular vasculature and in the areas of interstitial fibrosis in VDN. Extensive renal damages (5 times; 26 [+ or -] 5% of collapsed-atrophic or sclerotic glomeruli, or glomerular cysts vs. control 5.2 [+ or -] 0.3%; 28 times; 61 [+ or -] 12% areas of focal, cortical areas exhibiting interstitial fibrosis per section vs. control 2.2 [+ or -] 0.6%) were observed histologically. The glomerular filtration rate significantly decreased (880 [+ or -] 40 vs. control 1,058 [+ or -] 44 [micro]l x [min.sup.-1] x g kidney [wt.sup.-1]). Albuminuria increased six times (1.6 [+ or -] 0.4 vs. control 0.27 [+ or -] 0.04 mg/24 h). There were significant linear relationships between albuminuria and pulse pressure ([r.sup.2] = 0.408; n = 24) or renal calcium content ([r.sup.2] = 0.328; n = 24; P < 0.05) and between glomerular filtration rate and pulse pressure ([r.sup.2] = 0.168; n = 27). To our knowledge, this study provides the first evidence of links between both 1) hyperpulsatility and renal dysfunction, and 2) renal calcification and renal dysfunction. Given the increasing frequency of end-stage renal disease, this model could prove useful for preclinical evaluation of drugs that prevent or attenuate hyperpulsatility and/or tissue calcification. pulse pressure; renal failure; albuminuria; renal histology

Schwann cells (Sc), associated axons, and nearby vascular endothelium constitute a functional trilogy of major importance during the development and regrowth of peripheral vascular nerves. The goal of the present study is to provide a technique of triple fluorescence confocal imaging of these cell types along renal preglomerular vessels. We took advantage of a protein S100B/EGFP transgenic mouse to visualize Sc. The endothelium was labeled with an intravenous injection of fluorescently tagged lectin, and after tissue processing, adrenergic nerves were revealed with an antibody against the marker protein synaptophysin. As a validation step, we found that EGFP-positive perivascular cells with prominent cell bodies and extensive, multidirectional cell processes were protein S100B positive. They were identified as Sc and indirectly assumed to be unmyelinated Sc. By contrast, we found strong EGFP expression in proximal epithelial cells and in the epithelium lining thin limbs of Henle. This epithelial fluorescence was not associated with immunoreactive protein S100B and thus corresponded to ectopic EGFP expressions in this mouse strain. Sc were organized in bundles or as a meshwork surrounding the preglomerular vasculature from arcuate arteries to afferent arterioles. No Sc were detected in the medulla. Although most Sc were closely apposed to adrenergic varicosities, many varicosities were not associated with detectable Sc processes. The present technique, and the capacity of confocal microscopy to yield three-dimensional imaging, allow the study of the microtopology of Sc and related sympathetic axons in the renal perivascular interstitium. immunohistochemistry; triple fluorescence labeling; synaptophysin; Griffonia simplicifolia; isolectin; myelinated and unmyelinated nerves

Reversal by the mineralocorticoid receptor antagonist spironolactone on cardiac eand renal abnormalities, associated with long-term (since weaning) administration of a high (2 and 8% NaCl chow, HS2 and HS8) sodium diet, was assessed in Sprague-Dawley rats. At the age of 5 mo, spironolactone (20 or 100 mg/kg, gavage) or placebo were given for 14 days to HS2 and HS8 rats. A group fed a regular diet (0.8% NaCl, NS) remained untreated. High sodium intake had no detectable effect on blood pressure; however, cardiac mass index and cross-sectional area of the carotid artery, as well as albuminuria, were increased only in the HS8 group compared with the control group on NS diet. In addition, a marked reduction in glomerular filtration rate (by 40%), associated with a nonproportional fall in renal plasma flow (thus resulting in a decrease in filtration fraction), was observed only in the HS8 group. No change in cardiac and renal fibrosis was detected. Production of the reactive oxygen species (ROS) by aortic tissue was increased in HS8 rats, whereas ROS production by the heart was unaffected. Only the high dose of spironolactone was effective, as it markedly reversed the cardiac hypertrophy and renal hypofiltration associated with the HS8 feeding. The changes were observed in the absence of any effect on systemic blood pressure and production of ROS. These observations favor aldosterone's role in the deleterious effects of marked and prolonged increases in sodium intake. spironolactone; renal function; reactive oxygen species; cardiac hypertrophy

The effects of branching topologies on the autoregulatory responses of individual afferent arterioles (AAs) were analyzed in blood-perfused juxtamedullary nephron (JMN) preparations. Analysis of JMN preparations indicated the similar heterogeneity of autoregulatory responses in paired AAs compared to proximal AAs. Furthermore, the spatial organization of pressure-induced autoregulatory responses along the AA indicated the association between autonomic pairing and functional nephron coupling.

Selective loss of pressure responsiveness along different segments of juxtamedullary preglomerular vasculature is caused by chronic N(super G)-nitro-L-arginine methyl ester (L-NAME) hypertension. Intraglomerular expression of alpha-smooth muscle actin is enhanced by chronic L-NAME hypertension. Basal tone is generated by vessels even after alteration of preglomerular vascular function. The study is conducted on rats.

Videomicroscopic studies of blood-perfused juxtamedullary preglomerular vasculature confirm that guanosine 3',5'-cyclic monophosphate (cGMP)-dependent dilators influence autoregulatory responses of arcuate arteries (AR) and afferent arterioles at initial and juxtaglomerular sites. Perivascular treatment of 8-bromo-cGMP, sodium nitroprusside and atrial natriuretic factor causes dose- and pressure-dependent dilation of preglomerular vessels and attenuates their AR.

Studies to quantitatively assess the degree of afferent arteriolar (AA) connectivity using an HCl maceration-microdissection method in rat, rabbit, mouse and human renal vasculatures reveals the arrangement of 51 to 60% of the total AA populations into vascular units, with the origin and joining arterial unit being shared by two AAs in all the species studies. The non-random pattern of recin distribution and correlation between arteriolar lengths within anatomic pairs indicates an association between the endocrine functions of paired arterioles.

Three new methods enable the distribution of granulated renin-positive cells in preglomerular vessel in settings where the vascular architecture is significantly preserved to be directly visualized. The variations in the optical characteristics of granulated and smooth muscle cells enable the convenient location of granulated cells in standard transillumination. Quinacrine, a fluroescent intravital strain, can be utilized to strain intracellular granules. A polyclonal anti rat renin antibody in vascular trees after cell permeabilization can be asked to achieve specific * of renin.

In vitro measurements of the intravascular pressure in the different arterial segments from the arcuate to the afferent arterioles and the glomerular capillaries were undertaken to investigate the intravascular pressure autoregulation existing inthe pre-glomerular vascular bed. Results indicate that a large proportion, 65%,of the autoregulatory function is mediated by the distal afferent arterioles. The interlobular arteries also contribute significantly to pressure autoregulation.