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PubMed1987

Action-naming performance in four syndromes of aphasia.

This study examined the influence of two situational contexts on the action-naming performances of 44 aphasic patients: single-word confrontation naming and naming within the context of connected speech. Subjects were evenly distributed among the syndromes of Broca's. Wernicke's, anomic, and conduction aphasia. The two naming tasks employed each comprised the same 18 target verbs. Naming performance was not systematically influenced by the particular naming task in any of the aphasia groups studied. However, for some individuals, particularly in the group of anomic aphasia, there were substantial performance discrepancies between scores obtained on the two different tasks. Correlations between scores on the confrontation-naming and picture-description tasks were highest for the Wernicke's aphasics, followed by the conduction, Broca's, and anomic aphasics. The extent to which action-naming error types could discriminate between the four groups of aphasics was examined. Results obtained in the present study were compared to results obtained in an earlier study on object-naming (S. Williams & G. Canter, 1982), Brain and Language, 17, 92-106). Discussion focuses on implications for the psycholinguistic processes involved in action versus object-naming.

Adult↗
PubMed2005

Effects of atorvastatin on blood-brain barrier permeability during L-NAME hypertension followed by angiotensin-II in rats.

Recent studies suggest that 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, statins, can have direct effects on blood vessels beyond their cholesterol-lowering effects. We investigated the effects of atorvastatin on the functional and structural properties of blood-brain barrier (BBB) and the activity of astrocytes during the N(omega)-nitro-L-arginine methyl ester (L-NAME) hypertension followed by angiotensin (ANG) II. We found that decreases in concentration of serum catalase and plasma nitric oxide (NO) induced by L-NAME were significantly ameliorated by atorvastatin, whereas L-NAME-induced serum malondialdehyde and cholesterol concentration increases were significantly reduced by atorvastatin. The content of Evans blue (EB) dye significantly increased in cerebellum, left cerebral cortex and diencephalon regions but atorvastatin markedly reduced the increased BBB permeability to EB in the brain regions of animals treated with L-NAME and L-NAME plus ANG II. Brain vessels of L-NAME-treated animals showed a considerable loss of immunoreactivity of tight junction proteins, zonula occludens (ZO)-1 and occludin. Immunoreactivity for ZO-1 and occludin increased in animals treated with atorvastatin and L-NAME plus atorvastatin. Glial fibrillary acidic protein (GFAP) immunoreactivity was seen in few astrocytes in the brain sections of L-NAME, but immunoreactivity for GFAP increased in L-NAME plus atorvastatin-treated animals. We suggest that long-term L-NAME treatment may affect BBB permeability through disruption of tight junction proteins, at least partly, via decreased NO concentration and increased oxidant capacity; the improvement of BBB integrity and astrocytic activity would be more closely associated with the action of atorvastatin favoring the increase in anti-oxidant capacity and expression of tight junction proteins and GFAP.

Angiotensin II↗
PubMed2006

Hemispheric asymmetries in font-specific and abstractive priming of written personal names: Evidence from event-related brain potentials.

We assessed hemispheric differences in font-specific and abstractive repetition priming for famous persons' names. Participants performed speeded familiarity judgments for foveally presented famous and unfamiliar names. Famous target names were preceded by primes (150 ms) in the left or right visual field (LVF or RVF). Primes were either the same name as the target written in the same font (font-specific priming), the same name in a different font (abstractive priming), or a different name (unprimed condition). In reaction times, LH superiority was strong for abstractive priming across fonts, but was reduced to insignificance for font-specific priming. We observed 3 different ERP modulations of priming for target names: a small font-specific posterior N200 (160-220 ms), a left temporal N250r (220-300 ms), and an N400 modulation (300-500 ms). The left temporal N250r exhibited large and abstractive priming for RVF primes, but smaller and font-specific priming for LVF primes. N400 effects were observed in all priming conditions. With respect to previous findings that N200, N250r, and N400 reflect facilitation at the levels of font-specific encoding, lexical entries for names, and semantic processing, respectively, these findings suggest that the LH superiority for name processing is particularly pronounced for the access to abstractive lexical entries for written names, a process that may be mediated by the left fusiform cortex.

Adolescent↗
PubMed2004

Knowing letter names and learning letter sounds: a causal connection.

Two experiments tested the common assumption that knowing the letter names helps children learn basic letter-sound (grapheme-phoneme) relation because most names contain the relevant sounds. In Experiment 1 (n=45), children in an experimental group learned English letter names for letter-like symbols. Some of these names contained the corresponding letter sounds, whereas others did not. Following training, children were taught the sounds of these same "letters." Control children learned the same six letters, but with meaningful real-word labels unrelated to the sounds learned in the criterion letter-sound phase. Differences between children in the experimental and control groups indicated that letter-name knowledge had a significant impact on letter-sound learning. Furthermore, letters with names containing the relevant sound facilitated letter-sound learning, but not letters with unrelated names. The benefit of letter-name knowledge was found to depend, in part, on skill at isolating phonemes in spoken syllables. A second experiment (n=20) replicated the name-to-sound facilitation effect with a new sample of kindergarteners who participated in a fully within-subject design in which all children learned meaningless pseudoword names for letters and with phoneme class equated across related and unrelated conditions.

Child↗
PubMed2001

Exploring the relationship between proper name anomia and word retrieval: a single case study.

We report the results of an investigation of the spoken word retrieval abilities of a patient, BG, with proper name anomia. Our investigations reveal that she is impaired in retrieving common nouns as well as proper names. Common noun retrieval was influenced by age-of-acquisition, word familiarity and name agreement. Cued retrieval of proper names was influenced by age-of-acquisition, although effects of other linguistic variables were not excluded. It is claimed that an explanation in terms of a 'continuum of word retrieval difficulty' rather than of proper names as 'pure referring expressions' can best account for the findings. However, this proposal is unlikely to be able to explain all cases of proper name anomia. Nonetheless, it is suggested that similar findings may be observed in other people with proper name anomia, and that it is necessary for future studies to investigate not only proper name but also common noun retrieval. We also provide evidence that Plausible Phonology and Specificity hypotheses of proper name anomia cannot account for BG's naming abilities.

Aged↗
PubMed1992

Cognitive components of naming in children: effects of referential uncertainty and stimulus realism.

The ease of picture naming in children was assessed as a function of two stimulus characteristics: (a) the number of available correct names for a picture (referential uncertainty) and (b) the degree to which a picture realistically represents the depicted object (stimulus realism). Two experiments employing different methods demonstrated that: (a) children named low uncertainty objects (those with a single dominant name, e.g., key, elephant) faster than high uncertainty objects (those with multiple possible correct names, e.g., lamp/light, stove/oven) and (b) this uncertainty effect arose at a stage of naming subsequent to object identification. Possible underlying mechanisms for the uncertainty effect include passive diffusion of activation over multiple object-name pathways or active inhibition among competing candidate names. Stimulus realism (colored photographs vs uncolored line drawings) did not consistently influence naming performance. Implications for understanding children's naming behavior are discussed.

Attention↗
PubMed2000

Cardiorespiratory impact of the nitric oxide synthase inhibitor L-NAME in the exercising horse.

To investigate the role of nitric oxide, NO, in facilitating cardiorespiratory function during exercise, five horses ran on a treadmill at speeds that yielded 50, 80 and 100% of peak pulmonary oxygen uptake (V(O(2)) peak) as determined on a maximal incremental test. Each horse underwent one control (C) and one (NO-synthase inhibitor; N(G)-L-nitro-arginine methyl ester (L-NAME), 20 mg/kg) trial in randomized order. Pulmonary gas exchange (open flow system), arterial and mixed-venous blood gases, cardiac output (Fick Principle), and pulmonary and systemic conductances were determined. L-NAME reduced exercise tolerance, as well as cardiac output (C, 291+/-34; L-NAME, 246+/-38 L/min), body O(2) delivery (C, 74.4+/-5. 5; L-NAME, 62.1+/-5.6 L/min), and both pulmonary (C, 3.07+/-0.26; L-NAME, 2.84+/-0.35 L/min per mmHg) and systemic (C, 1.55+/-0.24; L-NAME, 1.17+/-0.16 L/min per mmHg) effective vascular conductances at peak running speeds (all P<0.05). On the 50 and 80% trials, L-NAME increased O(2) extraction, which compensated for the reduced body O(2) delivery and prevented a fall in V(O(2)). However, at peak running speed in the L-NAME trial, an elevated O(2) extraction (P<0. 05) was not sufficient to prevent V(O(2)) from falling consequent to the reduced O(2) delivery. At the 50 and 80% running speeds (as for peak), L-NAME reduced pulmonary and systemic effective conductances. These data demonstrate that the NO synthase inhibitor, L-NAME, induces a profound hemodynamic impairment at submaximal and peak running speeds in the horse thereby unveiling a potentially crucial role for NO in mediating endothelial function during exercise.

Acid-Base Equilibrium↗
PubMed2000

Naming speed performance and stimulant effects indicate effortful, semantic processing deficits in attention-deficit/hyperactivity disorder.

This study investigated rapid automatized naming and effects of stimulant medication in school-age children with attention-deficit/hyperactivity disorder (ADHD) with and without concurrent reading disorder (RD). Two ADHD groups (67 ADHD only; 21 ADHD + RD) and a control group of 27 healthy age-matched peers were compared on four variables: color naming speed, letter naming speed, phonologic decoding, and arithmetic computation. Discriminant function analysis (DFA) was conducted to predict group membership. The four variables loaded onto two discriminant functions with good specificity: phonologic decoding, letter naming speed, and arithmetic defined the first function; color naming speed defined the second function. Both ADHD groups were significantly slower in color naming than controls, but did not differ from one another. DFA correctly classified 96% of the control group, 91% of ADHD + RD, and 82% of ADHD only. A subset of children in the ADHD groups participated subsequently in an acute, randomized, placebo-controlled, crossover trial with three single doses (10, 25, 20 mg) of methylphenidate. Methylphenidate selectively improved color-naming speed but had no effect on the speed of naming letters or digits. These findings challenge the tenet that naming speed deficits are specific to RD and implicate naming speed deficits associated with effortful semantic processing in ADHD, which are improved but not normalized by stimulant medication.

Attention Deficit Disorder with Hyperactivity↗
PubMed1999

L-NAME inhibits Mg(2+)-induced rat aortic relaxation in the absence of endothelium.

1 L-NG-nitro-arginine methyl ester (L-NAME; 100 microM), a nitric oxide synthase (NOS) inhibitor, reversed the relaxation induced by 3 microM acetylcholine (ACh) and 2-10 mM Mg2+ in endothelium-intact (+E) rat aortic rings precontracted with 1 microM phenylephrine (PE). In PE-precontracted endothelium-denuded (-E) rat aorta, 3 microM ACh did not, but Mg2+ caused relaxation which was reversed by L-NAME, but not by D-NAME. 2 The concentration response profiles of L-NAME in reversing the equipotent relaxation induced by 5 mM Mg2+ and 0.2 microM ACh were not significantly different. 3 L-NAME (100 microM) also reversed Mg(2+)-relaxation of -E aorta pre-contracted with 20 mM KCl or 10 microM prostaglandin F2alpha (PGF2alpha). L-NG-monomethyl-arginine (L-NMMA; 100 microM) was also effective in reversing the Mg(2+)-relaxation. 4 Addition of 0.2 mM Ni2+, like Mg2+, caused relaxation of PE-pre-contracted -E aorta, which was subsequently reversed by 100 microM L-NAME. 5 Reversal of the Mg(2+)-relaxation by 100 microM L-NAME in PE-precontracted -E aorta persisted following pre-incubation with 1 microM dexamethasone or 300 microM aminoguanidine (to inhibit the inducible form of NOS, iNOS). 6 Pretreatment of either +E or -E aortic rings with 100 microM L-NAME caused elevation of contractile responses to Ca2+ in the presence of 1 microM PE. 7 Our results suggest that L-NAME exerts a direct action on, as yet, unidentified vascular smooth muscle plasma membrane protein(s), thus affecting its reactivity to divalent cations leading to the reversal of relaxation. Such an effect of L-NAME is unrelated to the inhibition of endothelial NOS or the inducible NOS.

Acetylcholine↗
PubMed1997

Medical student name tags: identification or obfuscation?

OBJECTIVE: To explore how U.S. medical students doing clinical rotations are physically identified to patients via their name tags, and how patients interpret the educational status conveyed by those name tags. MEASUREMENTS AND MAIN RESULTS: A letter was sent to the dean of students at all 141 medical school campuses in the United States, requesting a photocopy of the name tag distributed to third-year students on clinical rotations. We then surveyed a convenience sample of 100 general medicine outpatients at the Hospital of the University of Pennsylvania and the Philadelphia Veterans Affairs Medical Center and presented them with examples of four ways medical students were identified on name tags we received: "medical student," "student physician," "student doctor," and "MD student." Patients were then asked to rank these, and three other identifiers ("faculty physician," "resident physician," and "house staff"), from least experienced to most experienced. Patients were told that some of the identifiers might denote the same level of experience. Fifty-three percent of the medical school name tags we received identified the medical student as "medical student," 11% as "student," 6% as "student physician," 2% as "student doctor," and 1% as "MD student." Four percent of name tags had only the student's name, and 18% had only the student's name and university affiliation. Patients thought that the four student descriptors ("medical student," "student physician," "student doctor," and "MD student") on medical student name tags indicated less experience than the other three descriptors. However, of the four student descriptors, patients thought "medical student" indicated less experience than the other three (p < .0001). CONCLUSIONS: There is great variation in how medical schools identify medical students on the name tags used during their clinical rotations. These different ways of identifying medical students are not interpreted as being identical to many patients.

Adult↗
PubMed2006

Will Julia Roberts harm Nicole Kidman? Semantic priming effects during face naming.

Three experiments are reported, which examine whether face naming is vulnerable to semantic competition in a similar way to object naming. Previous experiments with object naming have shown that a related prime picture presented 3 trials before a target picture results in an increase in error rate and naming latencies when compared to unrelated prime conditions. The experiments here use the same paradigm, with errors as the main dependent variable. In Experiment 1, the prime and target faces were from the same occupational category (e.g., politicians, actors), and in Experiment 2, the primes and target faces were also associated to each other. In Experiment 3, the prime was presented as a name to be read aloud. Unrelated filler stimuli intervened between prime and target. In all experiments, there was a reduction in target-naming errors in the related conditions, and in Experiment 3 this was shown to be largely a reduction in naming failures. The results suggest that related name representations for famous people are not activated in parallel and in competition, and that there is some evidence for a relatively long lasting facilitatory effect. These results require some modification to any serial account of face naming to differentiate it from the generally well-established serial account of object naming.

Adolescent↗
PubMed1988

The problem of naming in SDAT: a relative deficit.

Research relating to language disorder in senile dementia of the Alzheimer type (SDAT) has focused primarily on naming impairment, formally termed anomia or nominal aphasia/dysphasia. Data resulting from this research have been insufficiently informed by a comparative linguistic framework in which performance on naming tasks is contrasted with performance on other forms of language tasks. The present study involves the comparison of 21 adults with SDAT and 18 demographically controlled normal elderly adults on the Test for Syntactic Complexity and fifteen subtests of the Western Aphasia Battery. Performance on naming is compared with performance on oral language variables of repetition, yes/no response, auditory word recognition, sequential commands, syntactic processing, as well as with performance on reading tasks and non-verbal tasks. Findings relating to oral language tasks show that structured syntactic processing requiring explicit interpretation and sequential commands are significantly more difficult for the SDAT sample than are three of four naming tasks. Further, significant SDAT performance variability is found across naming tasks. The generative categorical naming task is found to be significantly more difficult for the SDAT patient than are the other three naming tasks. It is concluded that the generative categorical naming task should be regarded as a meta-naming task. In sum, it is found that although language dysfunction in SDAT has anomic components, the essential character of the language disorder is not best conceptualized as a problem of naming.

Aged↗
PubMed1999

Species names in phylogenetic nomenclature.

Linnaean binomial nomenclature is logically incompatible with the phylogenetic nomenclature of de Queiroz and Gauthier (1992, Annu. Rev. Ecol. Syst. 23:449-480): The former is based on the concept of genus, thus making this rank mandatory, while the latter is based on phylogenetic definitions and requires the abandonment of mandatory ranks. Thus, if species are to receive names under phylogenetic nomenclature, a different method must be devised to name them. Here, 13 methods for naming species in the context of phylogenetic nomenclature are contrasted with each other and with Linnaean binomials. A fundamental dichotomy among the proposed methods distinguishes those that retain the entire binomial of a preexisting species name from those that retain only the specific epithet. Other relevant issues include the stability, uniqueness, and ease of pronunciation of species names; their capacity to convey phylogenetic information; and the distinguishability of species names that are governed by a code of phylogenetic nomenclature both from clade names and from species names governed by the current codes. No method is ideal. Each has advantages and drawbacks, and preference for one option over another will be influenced by one's evaluation of the relative importance of the pros and cons for each. Moreover, sometimes the same feature is viewed as an advantage by some and a drawback by others. Nevertheless, all of the proposed methods for naming species in the context of phylogenetic nomenclature provide names that are more stable than Linnaean binomials.

Phylogeny↗
PubMed1991

The nature of the naming deficit in Alzheimer's and Huntington's disease.

A comparison of naming performance, on the Boston Naming Test, of 52 patients with dementia of Alzheimer's type (DAT), 16 patients with Huntington's disease (HD) and 52 normal control subjects was performed using a comprehensive classification of error types. Spontaneous and cued naming scores were significantly impaired both in the DAT and HD groups, but performance in the DAT patients was significantly worse than that of the HD patients. Normal controls made predominantly semantic-category and circumlocutory errors. The HD group differed from normal only in the proportion of visually based errors, which was greater in the patient group. By contrast, the DAT patients made a significantly greater proportion of semantic-superordinate and semantic-associative errors. The same pattern of naming errors was found when a group of DAT and HD patients matched for overall naming ability was compared. A subgroup of 22 DAT patients was followed longitudinally over 3 y. Their deterioration in overall naming performance was accompanied by a consistent change in the profile of naming errors: the proportion of semantic-associative errors increased significantly as did the proportion of visual errors. These results are considered in the light of current cognitive models of naming. They suggest that in HD, naming deficits initially involve disruption of perceptual analysis, whereas in DAT such impairments in the early stages reflect a breakdown in semantic processes. However, as DAT progresses, perceptual problems also begin to contribute to the patients' naming difficulties. Postlexical (phonemic) processes remain relatively intact throughout in both diseases.

Aged↗
PubMed2005

Nomega-nitro-L-arginine methyl ester (L-NAME) amplifies the pulmonary hypertensive response to microparticle injections in broilers.

We tested the hypothesis that microparticles entrapped within the pulmonary vasculature elicit the production of nitric oxide (NO) in quantities sufficient to modulate the combined impact of physical occlusion plus contemporaneously released vasoconstrictors. In experiment 1, male broilers were given an injection of the NO synthase (NOS) inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME), followed by an intravenous injection of cellulose microparticles while the pulmonary arterial pressure (PAP) and cardiac output (CO) were recorded. When L-NAME was used to block NO synthesis induced by the microparticles, an early peak of pulmonary hypertension was revealed that rarely developed in the absence of L-NAME. The subsequent more prolonged increases in PAP and pulmonary vascular resistance (PVR) were greater in amplitude and duration in broilers pretreated with L-NAME than in broilers in the control group. These amplified responses occurred in spite of a simultaneous reduction in CO, thereby conclusively demonstrating that inhibiting NOS permitted the development of a much more profound increase in the PVR. In experiment 2 the mortality triggered within 48 h after injecting microparticles was evaluated in the presence and absence of L-NAME. The 48 h postinjection mortality more than doubled when L-NAME was combined with microparticle injection doses that otherwise caused relatively low mortality in the absence of L-NAME. Experiment 3 was conducted to determine whether NO contributes to the systemic hypoxemia that develops after microparticles are injected. L-NAME administration had no impact on the magnitude and duration of the microparticle induced decline in the percentage saturation of hemoglobin with oxygen (%HbO2). Evidently hypoxemia per se contributes relatively little to the amplified pulmonary vasoconstriction and 48 h postinjection mortality triggered by microparticle injections in broilers pretreated with L-NAME. These observations indicate that NO modulates the responses to vasoconstrictors released when microparticles become entrapped in the pulmonary vasculature. Inhibition of NOS by L-NAME exposed a more dramatic increase in PVR and pulmonary hypertension leading to enhanced mortality in response to microparticle injections.

Animals↗
PubMed2000

Enhanced expression of Gi proteins in non-hypertrophic hearts from rats with hypertension-induced by L-NAME treatment.

OBJECTIVE: The objective of the present studies is to investigate if the enhanced expression of Gs alpha protein and their mRNA observed in various models of hypertensive rats is due to the expressed hypertrophy or hypertension. METHODS: Hypertension, in Sprague-Dawley rats was induced by the oral administration of the arginine analog N(omega)-nitro-L-arginine methyl ester (L-NAME) in their drinking tap water for a period of 4 weeks. The control rats were given plain tap water only. The levels of inhibitory guanine nucleotide regulatory proteins (Gi alpha-2, Gi alpha-3), stimulatory guanine nucleotide proteins (Gs alpha) and G beta proteins were determined by immunoblotting, whereas the levels of Gi alpha-2, Gi alpha-3, Gs alpha and adenylyl cyclase type V enzyme mRNA were determined by Northern-blotting techniques. Adenylyl cyclase activity was determined by measuring [32P]cAMP formation from [alpha32P]ATP. RESULTS: The systolic blood pressure was enhanced in L-NAME-treated rats compared to control rats (190 +/- 9.2 mmHg versus 121 +/- 6.3 mmHg); however, heart-to-body-weight ratio was not different in two groups. The levels of Gi alpha-2 and Gi alpha-3 proteins and their mRNA were significantly augmented in hearts from L-NAME-treated rats, however, the levels of Gs alpha and G beta were unaltered. In addition, the effect of low concentrations of GTPgammaS on forskolin (FSK)-stimulated adenylyl cyclase activity (receptor-independent functions of Gi alpha) was significantly enhanced in L-NAME-treated rats. However, the inhibitions of adenylyl cyclase exerted by oxotremorine, C-ANP(4-23) and angiotensin II (AII) (receptor-dependent function of Gi alpha) were completely attenuated in L-NAME-treated rats. On the other hand, cholera toxin stimulated GTP or GTPgammaS-sensitive adenylyl cyclase activity (Gs alpha function) to similar extent in control and L-NAME-treated rats, suggesting that Gs alpha functions were not altered by L-NAME treatment. However, the stimulatory effects of isoproterenol, glucagon, NaF on adenylyl cyclase were diminished in L-NAME-treated rats. In addition, FSK-stimulated enzyme activity was also diminished in L-NAME-treated rats without any changes in the mRNA levels of type V enzyme. CONCLUSIONS: These results suggest that L-NAME hypertensive rats that do not express cardiac hypertrophy exhibit enhanced expression of Gi alpha protein and associated adenylyl cyclase activity.

Adenylyl Cyclases↗
PubMed2004

Vasoactive systems in L-NAME hypertension: the role of inducible nitric oxide synthase.

OBJECTIVES: The contribution of the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) to blood pressure (BP) maintenance was evaluated in rats with N(omega)-nitro-L-arginine methyl ester (L-NAME) hypertension. Furthermore, we studied the extent of nitric oxide (NO) synthesis inhibition and the participation of remaining NO in the counterbalance of pressor systems, with a special reference to inducible nitric oxide synthase (iNOS). METHODS: Wistar rats subjected to chronic L-NAME treatment (40 mg/kg per day for 4 weeks) were used. A consecutive blockade of RAS (captopril) and SNS (pentolinium) was followed by acute L-NAME injection. Dimethylguanidine or aminoguanidine were used to affect NO synthesis by iNOS. RESULTS: L-NAME hypertensive rats had borderline augmentation of depressor response to captopril injection, but their BP fall after pentolinium was considerably enhanced compared with controls. Residual BP (recorded after simultaneous blockade of the RAS and the SNS) was elevated by 20-40% in hypertensive rats. Pronounced inhibition of NO synthase activity (50% reduction in the aorta and myocardium) was detected in L-NAME hypertensive rats in which the BP rise elicited by acute L-NAME injection was considerably attenuated (by 60-80%). In contrast, acute administration of dimethylguanidine [mixed endothelial NO synthase (eNOS)/iNOS inhibitor] to hypertensive rats induced a major BP rise similar to that caused by L-NAME injection in controls. Aminoguanidine (a selective iNOS inhibitor) caused a substantial BP rise in L-NAME hypertensive rats only. CONCLUSION: The contribution of SNS to BP maintenance in L-NAME hypertension is more important than that of RAS. In L-NAME hypertensive rats the iNOS becomes a major source of hemodynamically important NO production, which is still insufficient to compensate prevailing vasoconstriction.

Animals↗
PubMed2003

Role of central and sympathetic nervous systems in pressor effect of L-NAME.

The pressor effect of N -nitric-l-arginine methyl ester (l-NAME) in rats has been attributed to the inhibition of the endothelial nitric oxide synthase; however, recent findings suggest that the central and sympathetic nervous systems may be also involved. In the present work, the authors attempted to study the possible central and sympathetic mechanisms involved in the pressor effect of l-NAME. They compared mean arterial pressure response during 1 h of continuous infusion of normal saline or l-NAME (0.031 mg. kg. min ) in Wistar rats treated with reserpine, adrenal medullectomy, pithing, and pithing + medullectomy. After 15-20 min infusion, a significantly greater increase of mean arterial pressure was observed in anesthetized rats with l-NAME and l-NAME + medullectomy versus rats with l-NAME + reserpine and l-NAME + pithing, and the magnitude of the difference increased further during the continuous 1-h l-NAME infusion. Adrenal medullectomy totally abolished the pressor effect of l-NAME in pithed group. The present findings suggest that the central and sympathetic nervous systems play important roles in the maintenance of the pressor effect of l-NAME, while the adrenal medulla becomes important only when the sympathetic nervous system has been suppressed.

Adrenal Medulla↗