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PubMed1999

Leakage responses to L-NAME differ with the fluorescent dye used to label albumin.

Nitric oxide synthase (NOS) inhibitors have been reported to increase as well as to decrease microvascular transport of macromolecules in a variety of models. This study was performed to determine whether the influence of NOS inhibition on albumin leakage was dependent on the fluorescent dyes used to label albumin. Albumin leakage was assessed in rat mesenteric venules during control conditions and after exposure to the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Albumin was labeled with any one of four dyes: FITC, sulforhodamine 101 [Texas Red (TR)], dichlorotriazinyl aminofluorescein (DTAF), or Oregon Green 514 (OG). Superfusion with L-NAME (10(-4) M) was accompanied by an increase in leakage of FITC-labeled albumin (n = 12) but not of albumin labeled with DTAF (n = 10), TR (n = 10), or OG (n = 4). In vessels perfused with both FITC- and TR-labeled albumin (n = 12), superfusion with L-NAME increased leakage of FITC- but not TR-labeled albumin. In conclusion, albumin leakage responses to L-NAME differ among various fluorescent dyes. Therefore, caution is advised in comparison of albumin leakage results that utilize different fluorescent dyes.

Animals↗

PubMed2005

Renal cortical and medullary blood flow responses to L-NAME and ANG II in wild-type, nNOS null mutant, and eNOS null mutant mice.

Experiments in wild-type (WT; C57BL/6J) mice, endothelial nitric oxide synthase null mutant [eNOS(-/-)] mice, and neuronal NOS null mutant [nNOS(-/-)] mice were performed to determine which NOS isoform regulates renal cortical and medullary blood flow under basal conditions and during the infusion of ANG II. Inhibition of NOS with N(omega)-nitro-l-arginine methyl ester (l-NAME; 50 mg/kg iv) in Inactin-anesthetized WT and nNOS(-/-) mice increased arterial blood pressure by 28-31 mmHg and significantly decreased blood flow in the renal cortex (18-24%) and the renal medulla (13-18%). In contrast, blood pressure and renal cortical and medullary blood flow were unaltered after l-NAME administration to eNOS(-/-) mice, indicating that NO derived from eNOS regulates baseline vascular resistance in mice. In subsequent experiments, intravenous ANG II (20 ng x kg(-1) x min(-1)) significantly decreased renal cortical blood flow (by 15-25%) in WT, eNOS(-/-), nNOS(-/-), and WT mice treated with l-NAME. The infusion of ANG II, however, led to a significant increase in medullary blood flow (12-15%) in WT and eNOS(-/-) mice. The increase in medullary blood flow following ANG II infusion was not observed in nNOS(-/-) mice, in WT or eNOS(-/-) mice pretreated with l-NAME, or in WT mice administered the nNOS inhibitor 5-(1-imino-3-butenyl)-l-ornithine (1 mg x kg(-1) x h(-1)). These data demonstrate that NO from eNOS regulates baseline blood flow in the mouse renal cortex and medulla, while NO produced by nNOS mediates an increase in medullary blood flow in response to ANG II.

Angiotensin II↗

PubMed1995

Role of renal medullary blood flow in the development of L-NAME hypertension in rats.

The effect of chronic intravenous infusion of the nitric oxide inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 8.6 mg.kg-1.day-1) on blood pressure, intrarenal blood flow distribution, and sodium and water balance was studied in conscious rats. On the 1st day of intravenous L-NAME infusion, renal medullary blood flow was reduced by 22%, renal cortical blood flow was unaltered, approximately 1 meq of sodium and 12 ml of water were retained, and blood pressure increased from 96 +/- 2 to 118 +/- 2 mmHg. Medullary blood flow was maintained at this decreased level, sodium continued to be retained, body weight continued to increase, and blood pressure remained elevated for the 5 days of L-NAME infusion. During the postcontrol period, blood flow in the renal medulla returned to levels not significantly different from control; the animals went into negative sodium balance and stopped gaining weight, and blood pressure returned to control. The present experiments indicate that decreased renal medullary blood flow and retention of sodium and water play an important role in the development of hypertension during chronic systemic L-NAME administration despite no measurable changes in renal cortical blood flow.

Acetylcholine↗

PubMed2005

Superiority of combination of thiazide with angiotensin-converting enzyme inhibitor or AT1-receptor blocker over thiazide alone on renoprotection in L-NAME/SHR.

The renal and glomerular dynamic effects of combining thiazide and angiotensin antagonists have not been reported. The present study was designed to examine the effects of hydrochlorothiazide (HCTZ) alone or in combination with an angiotensin-converting enzyme inhibitor or ANG II type 1-receptor blocker on renal hemodynamics, glomerular dynamics, renal function, and renal histopathology in the N(omega)-nitro-l-arginine methyl ester-treated spontaneously hypertensive rat (l-NAME/SHR) model. HCTZ (80 mg x kg(-1) x day(-1)) alone or in combination with enalapril (30 mg x kg(-1) x day(-1)) or losartan (30 mg x kg(-1) x day(-1)) or enalapril (15 mg.kg(-1).day(-1)) plus losartan (15 mg x kg(-1) x day(-1)) was administered to l-NAME/SHR (5.0 +/- 0.10 mg x kg(-1) x day(-1)) for 3 wk. Mean arterial pressure, total peripheral resistance, renal plasma flow, glomerular filtration rate, glomerular hydrostatic pressure, afferent and efferent glomerular arteriolar resistances, single nephron plasma flow, single nephron glomerular filtration rate, serum creatinine concentration, 24-h urinary protein excretion, and glomerular and arteriolar injury scores were determined. HCTZ reduced mean arterial pressure, total peripheral resistance, glomerular hydrostatic pressure, and afferent and efferent glomerular arteriolar resistances (P < 0.05, at least) but slightly increased renal plasma flow and single nephron plasma flow associated with reduced serum creatinine concentration, urinary protein excretion, and arteriolar injury score compared with l-NAME/SHR control. However, the combination of enalapril and/or losartan with HCTZ markedly improved each of these functions. These results demonstrated minor benefits of HCTZ monotherapy and a marked superiority of its combination with enalapril and/or losartan over HCTZ monotherapy on renoprotection in l-NAME/SHR, thereby providing strong evidence of their clinical benefits for hypertensive patients with renal functional impairment.

Angiotensin II Type 1 Receptor Blockers↗

PubMed1994

Influence of sodium diet on L-NAME effects on renin release and renal vasoconstriction.

The intervention of the L-arginine-NO pathway in renal vasodilation and renin secretion was studied in an isolated perfused rat kidney model. NG-nitro-L-arginine methyl ester (L-NAME, 1-25 microM), an inhibitor of nitric oxide (NO) synthesis, caused a dose-dependent increase in perfusion pressure (PP) and a dose-dependent decrease in renal perfusate flow. Renin was inhibited independently of the rise in PP, since the effect of L-NAME on renin release was the same when PP was maintained constant. Exposure of rats to low [salt depleted (SD)] or high [salt repleted (SR)] salt intake for 1 mo influenced the renal vascular response to L-NAME (3 microM). Isolated SR rat kidney vasculature vasoconstricted to a greater extent after inhibition of NO synthase than did that of SD kidneys. A similar fall in renin release was observed after L-NAME in both groups, despite a higher renin secretion rate in SD than in SR rats. These results suggest that NO-dependent vasodilation counteracts the renal vasoconstrictor effect of sodium loading.

Analysis of Variance↗

PubMed1997

Effect of L-NAME on glomerular filtration rate in deep and superficial layers of rat kidneys.

The effect of the NO synthase blocker N(G)-nitro-L-arginine methyl ester (L-NAME) on glomerular filtration rate (GFR) in outer (OC), middle (MC), and inner cortex (IC) was studied in anesthetized male Sprague-Dawley rats by the aprotinin method. The filtered amount of 125I- and 131I-labeled aprotinin injected before and after L-NAME injection was measured in the same cortical tissue samples after excising the kidney. Arterial pressure increased on average by 43 mmHg, whereas renal blood flow fell by 26% after L-NAME, giving an increase in renal resistance of 92%. At constant renal arterial pressure, resistance rose by only 39%, revealing that autoregulation was responsible for about one-half of the resistance increase. Total and zonal GFR showed a small, statistically insignificant increase after L-NAME, regardless of whether the renal pressure was allowed to rise or not. The response varied considerably among animals, but in each animal the GFR varied proportionately in OC, MC, and IC. We conclude that the vasodilator tone of NO is predominantly located in postglomerular resistance vessels and is similar in the three cortical layers.

Animals↗

PubMed2004

Functional study of the [Ca2+]i signaling pathway in aortas of L-NAME-hypertensive rats.

A variety of mechanisms has been proposed to suggest that nitric oxide participates in the regulation of smooth muscle free [Ca(2+)](c) (the primary determinant of contractile tone), including inhibition of Ca(2+) influx across the plasma membrane and inhibition of intracellular Ca(2+) release. In view of such considerations, the aim of this study was to investigate the possible alterations in contractile responses induced by drugs that mobilize Ca(2+) from different sources in aortae from N(G)-nitro-L-arginine methyl ester (L-NAME) hypertensive rats (LHR). Treatment with L-NAME did not alter the contractile response induced by phenylephrine; however, indomethacin increased the contraction to phenylephrine only in LHR aortae (1.36 +/- 0.08 g, n = 6, vs. 1.97 +/- 0.09 g, n = 7). Both phenylephrine and caffeine evoked rapid and phasic contractions in intact or denuded aortic rings in Ca(2+)-free solution containing EGTA. Phenylephrine-elicited phasic contractions were lower in normotensive rats (NR; 0.41 +/- 0.05 g, n = 9) than in LHR (0.57 +/- 0.06 g, n = 6) and were increased by endothelium removal only in the NR group (0.64 +/- 0.05 g, n = 6). Conversely, neither with treatment with L-NAME nor endothelium removal altered the phasic contractile responses induced by caffeine. The Ca(2+) influx stimulated with phenylephrine was greater in NR (1.95 +/- 0.08 g; pD(2) 6.06 +/- 0.69; n = 8) than in the LHR denuded aorta (1.63 +/- 0.11 g; pD(2) 3.52 +/- 0.06; n = 6). Similarly, contractions stimulated with phorbol ester in denuded arteries were greater in NR (1.76 +/- 0.08 g, n = 7) than in LHR (1.11 +/- 0.11 g, n = 7). In the same manner, indomethacin failed to alter the contraction stimulated with phorbol ester in NR arteries (2.01 +/- 0.21 g, n = 7), although it completely blocked the inhibitory effect of chronic treatment with L-NAME on this contractile response (1.94 +/- 0.24 g; n = 9). Indomethacin did not change the contractile responses stimulated by increasing concentrations of extracellular Ca(2+) in either NR aortas (1.44 +/- 0.26 g; pD(2) 4.74 +/- 0.79; n = 6) or LHR aorta (1.99 +/- 0.19 g; pD(2) 4.10 +/- 0.47; n = 8). However, in the presence of indomethacin, the Ca(2+) influx was similar in NR and LHR aortae. Taken together, these results suggest that, in this model of hypertension, the increase in agonist-induced release of Ca(2+) from intracellular stores may be partly compensated by inhibition of Ca(2+) influx and that this effect is due to the increased production of the relaxant prostanoid in vascular smooth muscle cells.

6-Ketoprostaglandin F1 alpha↗

PubMed2006

Modifications produced by indomethacin and L-NAME in the effect of ultralow-dose aspirin on platelet activity in portal hypertension.

In our previous study, we demonstrated the effect of ultralow-dose aspirin (ULDA) on platelet activity and bleeding in rats with portal hypertension (PHT) produced by portal vein ligation (PVL). This paper reports modifications in this effect caused by blocking NO production by nitro arginine methyl ester (NAME) and cyclooxygenase (COX) activity with indomethacin. PVL rats and sham-operated controls were treated with placebo, indomethacin or NAME and 30 min thereafter with placebo or ULDA treatment. Platelet activity was studied by a model of in vivo laser-induced thrombus production in the mesenteric circulation, induced hemorrhage time (IHT) and platelet aggregation ex vivo induced by adenosine diphosphate in an aggregometer. The PVL group receiving placebo showed a decreased platelet activity with prolonged IHT, an effect that was reversed by ULDA. Indomethacin induced a decreased platelet activity in the control rats and a prolonged IHT. In PHT with ULDA, in vivo platelet activity was enhanced but the normalization of IHT observed in rats without indomethacin was blunted. The addition of NAME normalized the diminished in vivo platelet aggregation and increased the IHT observed in PVL animals. These changes decreased the effect of ULDA in both sham-operated and PVL animals. The effect of indomethacin was more clearly modified by ULDA than the effect of NAME, thus suggesting that modifications in the COX pathway might alter the effect of ULDA. The simultaneous administration of indomethacin and ULDA could inhibit its beneficial effect on bleeding in rats with PHT.

Animals↗

PubMedDate not supplied

Changes of the relative severity of naming, fluency and recall impairment in the course of dementia of the Alzheimer type.

In a longitudinal study of 90 patients with mild to moderate dementia of the Alzheimer type (DAT) we investigated the relative severity of impairment in a confrontation naming, a categorical word fluency and a word list recall task. Severity of impairment was assessed in comparison to a healthy age-matched control group. At baseline, confrontation naming and fluency deficits were about equally often the most severe deficit. The number of patients with most severe naming deficits increased from mild to moderate dementia and from baseline to 1-year follow-up. Word recall was the most severe deficit only in a minority of patients. An addition of lexical-semantic and visual-perceptive dysfunctions is discussed as a possible cause for the shift towards naming deficits in the course of the disease.

Aged↗

PubMed1996

Preglomerular sudanophilia in L-NAME hypertensive rats: involvement of endothelin.

To characterize alterations of renal vessels occurring during systemic hypertension elicited in rats by 5, 10, and 25 days of treatment by the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME)(20 mg/kg daily), preglomerular vasculatures, consisting of arcuate arteries and their branches, interlobular arteries, and afferent arterioles, were isolated by HCl maceration. Blockade of nitric oxide synthase significantly increased tail-cuff systolic blood pressure by 21 +/- 2% and 42 +/- 3% after 5 and 25 days, respectively. Medias of hypertensive arcuate arterial branches and interlobular arteries but not of afferent arterioles had focal deposits of Sudan black-positive lipid droplets. At 25 days, vessel wall thickness increased by 72 +/- 6% along the sudanophilic areas. Immunostaining of sudanophilic lesions with a panel of antibodies unveiled medial cell proliferation, macrophage invasion, immunoreactive vascular cell adhesion molecule-1, and low-density lipoprotein. The frequency of sudanophilic lesions increased with time to affect 26 +/- 2% and 36 +/- 3% of arcuate arterial branches and interlobular arteries, respectively, at 25 days. Hypertensive L-NAME-treated rats developed glomerular injury probed by albuminuria and glomerular immunostaining for alpha-smooth muscle actin. Administration of the nonselective endothelin antagonist bosentan (30 mg/kg daily) blunted the development of sudanophilic lesions during L-NAME treatment without affecting arterial hypertension or degree of glomerular injury. Therefore, L-NAME hypertension leads to rapid development of focal, inflammatory, proliferative, and sudanophilic lesions along preglomerular vessels, suggesting atherosclerosis-like processes. Furthermore, endothelin is a likely mediator in the development of these lesions.

Animals↗

PubMed1997

Angiotensin II blockade does not prevent renal effects of L-NAME in sodium-repleted humans.

In seven healthy, young subjects on a 240 mmol sodium diet, mean arterial pressure (MAP), renal hemodynamics, and renal handling of Na and exogenous Li were measured at baseline and during short-term nitric oxide (NO) blockade with a 90-minute infusion of 3.0 microg x kg(-1) x min(-1) of N(G)-L-arginine methyl ester (L-NAME). The infusion was performed twice: after a 3-day pretreatment with either placebo or 50 mg losartan to block Ang II receptors. With placebo, L-NAME produced no change in MAP from 0 to 45 minutes (period 1) and only a 5% increase at 45 to 90 minutes (period 2) of infusion. Effective renal plasma flow (ERPF, PAH clearance) and glomerular filtration rate (GFR, inulin clearance) declined by 11.7% and 8.0%, respectively in period 1 and by 14.6% and 11.6%, respectively, in period 2. Calculated renal vascular resistance (RVR) increased by 13.0% to 20.6%. Fractional excretion of Na (FE(Na)) and Li (FE(Li)) fell by 30.0% and 21.0%, respectively, in period 1 and by 44.2% and 31.1% in period 2. All these variations were significant versus baseline. With losartan, the rise in MAP at 45 to 90 minutes was completely abolished, whereas all changes in ERPF, GFR, RVR, FE(Na), and FE(Li) in response to L-NAME were the same as those observed with placebo. The present data show that NO blockade with low-dose systemic infusion of L-NAME produces renal vasoconstriction, reduced GFR, and increased tubular Na reabsorption independent of changes in MAP. Reduced FE(Li) indicates an effect of NO on the proximal tubule. Since these changes are not prevented by losartan, we conclude that in Na-repleted humans, renal vasoconstriction and Na-retaining effects of inhibition of basal NO production are not due to the unopposed action of endogenous Ang II.

Adult↗

PubMed2005

Naming the same entities from visual or from auditory stimulation engages similar regions of left inferotemporal cortices.

We have proposed that the left inferotemporal (IT) region contains structures that mediate between conceptual knowledge retrieval and word-form retrieval, and we have hypothesized that these structures are utilized for word retrieval irrespective of the sensory modality through which an entity is apprehended, thus being "modality neutral." We tested this idea in two sensory modalities, visual and auditory, and for two categories of concrete entities, tools and animals. In a PET experiment, 10 normal participants named tools and animals either from pictures or from characteristic sounds (e.g., "scissors" from a picture of a scissors or from the sound of a scissors cutting; "rooster" from a picture of a rooster or from the sound of a rooster crowing). Visual and auditory naming of tools activated the left posterior/lateral IT; visual and auditory naming of animals activated the left anterior/ventral IT. For both tools and animals, the left IT activations were similar in location and magnitude regardless of whether participants were naming entities from pictures or from sounds. The results provide novel evidence to support the notion that left IT structures contain "modality-neutral" systems for mediating between conceptual knowledge and word retrieval.

Acoustic Stimulation↗

PubMed1998

An MEG study of picture naming.

The purpose of this study was to relate a psycholinguistic processing model of picture naming to the dynamics of cortical activation during picture naming. The activation was recorded from eight Dutch subjects with a whole-head neuromagnetometer. The processing model, based on extensive naming latency studies, is a stage model. In preparing a picture"s name, the speaker performs a chain of specific operations. They are, in this order, computing the visual percept, activating an appropriate lexical concept, selecting the target word from the mental lexicon, phonological encoding, phonetic encoding, and initiation of articulation. The time windows for each of these operations are reasonably well known and could be related to the peak activity of dipole sources in the individual magnetic response patterns. The analyses showed a clear progression over these time windows from early occipital activation, via parietal and temporal to frontal activation. The major specific findings were that (1) a region in the left posterior temporal lobe, agreeing with the location of Wernicke"s area, showed prominent activation starting about 200 msec after picture onset and peaking at about 350 msec (i.e., within the stage of phonological encoding), and (2) a consistent activation was found in the right parietal cortex, peaking at about 230 msec after picture onset, thus preceding and partly overlapping with the left temporal response. An interpretation in terms of the management of visual attention is proposed.

Adult↗

PubMed2006

The anatomy of category-specific object naming in neurodegenerative diseases.

Neuropsychological studies suggest that knowledge about living and nonliving objects is processed in separate brain regions. However, lesion and functional neuroimaging studies have implicated different areas. To address this issue, we used voxel-based morphometry to correlate accuracy in naming line drawings of living and nonliving objects with gray matter volumes in 152 patients with various neurodegenerative diseases. The results showed a significant positive correlation between gray matter volumes in bilateral temporal cortices and total naming accuracy regardless of category. Naming scores for living stimuli correlated with gray matter volume in the medial portion of the right anterior temporal pole, whereas naming accuracy for familiarity-matched nonliving items correlated with the volume of the left posterior middle temporal gyrus. A previous behavioral study showed that the living stimuli used here also had in common the characteristic that they were defined by shared sensory semantic features, whereas items in the nonliving group were defined by their action-related semantic features. We propose that the anatomical segregation of living and nonliving categories is the result of their defining semantic features and the distinct neural subsystems used to process them.

Adult↗

PubMed1994

Odor identification by name and by edibility: life-span development and safety.

The study explored how subjects from childhood (8-14 years old) to elderly adulthood could identify the odors of 17 everyday products. Performance at naming followed an inverted U-shaped course over age, best in young adults and poorest in children and elderly. A discrimination task given to the adults revealed parallel age-related declines in ability to name and to discriminate odors. Correct identification by edibility exceeded that by name considerably. For dangerous household products, children achieved only 15% correct naming but 79% correct edibility/inedibility. Scenting of dangerous household products, however, may compromise the discriminability of these products from less harmful ones. "Fresh"-scented hypochlorite bleach yielded significantly more errors regarding its possible causticity than did unscented bleach. Such modifications of products would seem to necessitate other compensatory changes to enhance discriminability and thereby maintain safety.

Adolescent↗

PubMedDate not supplied

The role of speed of processing, rapid naming, and phonological awareness in reading achievement.

This study investigated the role of speed of processing, rapid naming, and phonological awareness in reading achievement. Measures of response time in motor, visual, lexical, grammatical, and phonological tasks were administered to 279 children in third grade. Measures of rapid object naming, phonological awareness, and reading achievement were given in second and fourth grades. Reading group comparisons indicated that poor readers were proportionally slower than good readers across response time measures and on the rapid object naming task. These results suggest that some poor readers have a general deficit in speed of processing and that their problems in rapid object naming are in part a reflection of this deficit. Hierarchical regression analyses further showed that when considered along with IQ and phonological awareness, speed of processing explained unique variance in reading achievement. This finding suggests that a speed of processing deficit may be an "extraphonological" factor in some reading disabilities.

Child↗

PubMedDate not supplied

Naming difficulties in children with dyslexia: application of the tip-of-the-tongue paradigm.

The present study used the tip-of-the-tongue (TOT) experimental paradigm in a picture naming task to explore the source of the naming deficits of children with dyslexia. Compared with a control group of typically developing readers, the children with dyslexia showed fewer correct responses and spontaneous recalls, more don't know (DK) and TOT responses, and less accurate feeling of knowing (FOK) judgments. When they failed to retrieve a target word, the children with dyslexia did not differ from the control group in the partial semantic information they provided, but they gave less valid and more invalid partial phonological information. The children with dyslexia also benefited less from phonological cues. The phonologically related responses of the children with dyslexia elicited during the administration of the TOT procedure were related to their performance on a phonological awareness test. These findings suggest that the naming problems of children with dyslexia arise because of their difficulty in accessing the phonological word forms after the corresponding abstract lexical representation has been successfully accessed. The results are discussed in relation to the claim that two-stage models of naming can be profitably used in the early identification and treatment of reading disabilities.

Anomia↗

PubMedDate not supplied

Naming speed deficits in adults with reading disabilities: a test of the double-deficit hypothesis.

The present study investigated the persistent nature of naming speed deficits within the context of the double-deficit hypothesis in a university sample of adults with reading disabilities (RD). Twenty-five university students with RD were compared to 28 typically achieving readers on measures of reading skill, phonological processing, and naming speed. The results indicated that both naming speed and phonological processing deficits characterized the RD group. In a regression analysis, neither naming speed nor phonological processing were important variables in explaining comprehension when reading rate was in the model. The results of the present study are mixed at best and are consistent with earlier conclusions that support for the double-deficit hypothesis of dyslexia remains limited.

Adult↗