Close afferent arteriolar (AA) connectivity is a prerequisite for hemodynamic interaction between superficial rat nephrons. Studies were conducted in rat, mouse, rabbit, and human renal vasculatures obtained by an HCl maceration-microdissection technique to document the extent of AA connectivity. In rat kidneys, we assessed the possibility for a slow component of internephron coupling, as reflected by arteriolar renin cell distribution after specific immunostaining for renin. In the four species examined, 51% (human) to 60% (mouse) of total AA populations were organized as vascular units consisting of mostly two AA sharing a common origin and a connecting arterial segment. In rat AA pairs, branch lengths were significantly correlated, suggesting coordinated arteriolar growth. The sum of AA branch lengths averaged 278 +/- 6 microns. Rat arteriolar renin status, ranging from no renin cells to renin-recruited midafferent arterioles, distributed in a significantly nonrandom fashion within AA pairs, and 52% of the pairs had equal renin status. Hence, AA pairing is a consistent anatomic characteristic of mammalian kidneys and may constitute an optimal vascular design for hemodynamic as well as endocrine interactions.
Darlot F, Artuso A, Lautredou-Audouy N, Casellas D. Topology of Schwann cells and sympathetic innervation along preglomerular vessels: a confocal microscopic study in protein S100B/EGFP transgenic mice. Am J Physiol Renal Physiol 295: F1142-F1148, 2008. First published August 20, 2008 doi:10.1152/ajprenal.00599.2007, 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 EGFPpositive 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 RECENT STUDIES UNDERLINE THE crucial role played by Schwann cells (Sc) in the development and maturation of peripheral sympathetic nerves (5, 21). Functional interactions between Sc and axons are also present during posttraumatic axonal regrowth (5, 7). In this respect, the addition and/or migration of Sc within artificial nerve guides appears as an essential determinant of axonal regrowth (13,26,43). In addition, recent studies establish the existence of common molecular mechanisms that link axonal and vascular guidance during early development (1,31,33,34,38), during posttraumatic axonal regrowth (20), and during tumoral angiogenesis (4, 34). The existence of such a "functional trilogy" among Sc, axons, and vascular endothelial cells gives relevance and importance to the possibility of specifically, and simultaneously, imaging these three cell types in normal and pathological animal models.Transmission electron microscopy (TEM) and immunohistochemist...
Our goal was to assess the cardiovascular and renal protection afforded by angiotensin II type 1-receptor blockade against NG-nitro-L-arginine methyl ester (L-NAME)-exacerbated hypertension in young spontaneously hypertensive rats (SHR), in comparison with the antihypertensive drug, hydralazine. Male SHR were assigned to four groups (n=8 per group): no treatment (controls); L-NAME-treated group (20 mg/kg/day, 10 days, orally); co-treatment with L-NAME and hydralazine (15 mg/kg/day, by gavage); co-treatment with L-NAME and candesartan cilexetil (10 mg/kg/day, by gavage), i.e. at a dose that inhibited acute pressor responses to 5-20 ng angiotensin II. One animal died in the L-NAME group, and tail-cuff systolic blood pressure (SBP) increased significantly compared with controls to 201±5 mmHg. Albumin excretion increased 235-fold in L-NAME-treated rats. Heart weight index averaged 3.5±0.1 and 3.8±0.1 mg/g body weight (p<0.05) in control and L-NAME rats, respectively, indicating moderate cardiac hypertrophy induced by L-NAME. Preglomerular vascular lesions affected 63±6% of interlobular arteries and 10±2% of afferent arterioles (vs. 8±3 and 0.8±0.4% in controls, respectively). Hydralazine and candesartan cilexetil treatment similarly reduced SBP to 153±7, and 165±6 mmHg, respectively. However, candesartan provided more protection, in terms of no significant change in albuminuria (vs. 25-fold increase with hydralazine), regression of cardiac hypertrophy, frequency of vascular lesions and histological indices of renal injury maintained within control values. In conclusion, candesartan cilexetil prevented L-NAME-exacerbated hypertension and associated cardio-renal injury in young SHR, the beneficial effects exceeding those of hydralazine.
Objective: To develop a new method for viewing adrenergic innervation along renal preglomerular vessels; to assess nerve densities and vascular lesions along arcuate arteries (ArcA), arcuate arterial branches (ArcB), and interlobular arteries (ILA) in spontaneously hypertensive rats (SHR) and in angiotensin II (AngII) and in N G -nitro-L-arginine methyl ester (L-NAME) hypertensive rats. Methods: Preglomerular vasculatures were isolated after HCl maceration and were immunostained against synaptophysin, a membrane protein of synaptic vesicles. Lesions were stained with Sudan black. Longitudinal nerve densities and relative frequencies of ArcA, ArcB, and ILA endowed with sudanophilic lesions were assessed separately. Results: Synaptophysin immunostaining revealed the vascular neural plexus. Nerves were adrenergic, as the plexus was destroyed by treatment with 6-hydroxy dopamine. Vascular lesions were not seen in SHR, and increased nerve density was observed along ArcA and ILA. In L-NAME-and AngIIhypertensive rats, vascular lesions affected predominantly ArcB and ILA, and nerve density was reduced by 12% and 28% (ArcA), 37% and 31% (ArcB), and by 55% and 34% (ILA), respectively, versus normotensive controls. Endothelin-1 receptor blockade did not affect AngII-induced hypertension but prevented both lesion development and reduction of density of the vascular neural plexus. Conclusions: The method we have devised provides a direct en face view of the vascular adrenergic innervation of isolated preglomerular vasculature. Measurements in hypertensive rat models suggest a link between vascular lesions and reduction in nerve density in hypertension. Endothelin-1 likely plays a key role in mediating both vascular injury and altered vascular nerve density in hypertension. Microcirculation (2000) 7, 429-437.
Accumulation of Sudan black-stainable (SB+) lipids is a hallmark of the focal inflammato-proliferative lesions that develop along preglomerular vessels in N G-nitro-L-arginine methyl ester (L-NAME) and angiotensin II hypertensive rats. We extended our findings to genetically hypertensive Lyon (LH) rats aged 14 and 30 weeks and to age-matched normotensive (LN) rats. Vessels were isolated by HCl maceration. Despite high systolic blood pressure (SBP), hypercholesterolaemia, albuminuria and increased interlobular and afferent arteriolar media thickness, SB+ lesions were rarely found in LH rats, regardless of age. To probe nitric oxide as a potential source of vascular protection, 14-week-old LN and LH rats received L-NAME for 10 days (20 mg kg-1 day-1, per os), which increased SBP to 174 +/- 5 and to >200 mmHg, respectively. It induced formation of focal SB+ lesions less frequently in LN than LH rats, in which they affected 39 +/- 7, 44 +/- 5 and 15 +/- 5% of arcuate arterial branches, interlobular arteries and afferent arterioles, respectively. Immunoreactive endothelin-1 was found to accumulate at the level of SB+ lesions. Co-administered with L-NAME, hydralazine (15 mg kg-1 day-1, per os) limited SBP rise to approximately 10 mmHg in both LN and LH rats. As a result, SB+ lesions were rare in LN rats, but were frequent in LH rats. In conclusion, preglomerular SB+ lesions are spontaneously lacking in LH rats. Endogenous nitric oxide production provides protection against vascular barotrauma. Endothelin-1 likely plays an autocrine/paracrine role in vascular lesion formation.
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