Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Names”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed2005

Mommy and me: familiar names help launch babies into speech-stream segmentation.

How do infants find the words in the tangle of speech that confronts them? The present study shows that by as early as 6 months of age, infants can already exploit highly familiar words-including, but not limited to, their own names-to segment and recognize adjoining, previously unfamiliar words from fluent speech. The head-turn preference procedure was used to familiarize babies with short passages in which a novel word was preceded by a familiar or a novel name. At test, babies recognized the word that followed the familiar name, but not the word that followed the novel name. This is the youngest age at which infants have been shown capable of segmenting fluent speech. Young infants have a powerful aid available to them for cracking the speech code. Their emerging familiarity with particular words, such as their own and other people's names, can provide initial anchors in the speech stream.

Attention↗
PubMed2005

L-arginine fails to protect against myocardial remodelling in L-NAME-induced hypertension.

BACKGROUND: We investigated whether the substrate for nitric oxide synthesis L-arginine is able to modify hypertension and left ventricular hypertrophy development induced by chronic blockade of nitric oxide synthase activity by NG-nitro-L-arginine-methyl ester (L-NAME). MATERIAL AND METHODS: Four groups of rats were investigated: control, L-arginine 1.5 g kg-1, L-NAME 40 mg kg-1, and L-NAME +L-arginine in corresponding doses. Systolic blood pressure was measured by non-invasive tail-cuff plethysmography each week. After 4 weeks, the animals were sacrificed and hydroxyproline and coenzyme Q9 and Q10 concentrations in the left ventricle, and nitric oxide synthase activity in the left ventricle, kidney and brain were investigated. RESULTS: In the L-NAME group, nitric oxide synthase activity was decreased in the left ventricle, kidney and brain, and hypertension, left ventricular hypertrophy and fibrosis developed. Heart remodelling was associated with the decrease of coenzyme Q9 and Q10 concentrations in the left ventricle. Simultaneous treatment with L-NAME and L-arginine prevented nitric oxide synthase activity diminution in the left ventricle but not in the kidney and brain, and completely failed to prevent hypertension, left ventricular hypertrophy and fibrosis. Nevertheless, l-arginine prevented the diminution of coenzyme Q9 and Q10 concentrations in the left ventricle. CONCLUSIONS: We conclude that L-arginine failed to prevent hypertension, left ventricular hypertrophy and fibrosis development despite restoration of nitric oxide synthase activity in the left ventricle. However, L-arginine prevented the diminution of coenzyme Q levels in the left ventricle.

Animals↗
PubMed1995

Implication of a nitric oxide synthase mechanism in the action of substance P: L-NAME blocks thermal hyperalgesia induced by endogenous and exogenous substance P in the rat.

The effects of i.p. administration of the nitric oxide synthase inhibitor NG-nitro-L-arginine methylester (L-NAME) and its inactive isomer, D-NAME, were tested in two nociceptive paradigms in the rat. In the first paradigm, rats were lightly anaesthetized with a mixture of chloral hydrate (120 mg/kg, i.p.) and sodium pentobarbital (20 mg/kg, i.p.). Tail flick reaction times were monitored and thermal hyperalgesia was induced by immersion of the tail in hot water at 55 degrees C for 1.5 min. In the groups of rats pretreated with saline (n = 5), 100 mg/kg D-NAME (n = 6), 10 (n = 5) or 25 (n = 6) mg/kg L-NAME, this thermal injury induced a transient reduction in the reaction time that was 54-59% of the baseline value. However, in the groups of rats pretreated with 50 (n = 6) or 100 (n = 7) mg/kg L-NAME the reaction times were 73.9 +/- 2.7% (P < 0.05) and 102.3 +/- 0.9% (P < 0.001) of the baseline values respectively, indicating a block of the hyperalgesic responses seen in the other groups. As this hyperalgesia has been reported to be blocked by NK-1 receptor antagonists, it is suggested that it is due to the action of endogenous substance P. In the second paradigm, tail flick responses were monitored in the awake rat and thermal hyperalgesia was induced by intrathecal administration of substance P (6.5 nmol) via a chronically implanted catheter.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Semantic constraints on word learning: proper names and adjectives.

4 experiments examined 3- and 4-year-olds' interpretations of novel words applied to familial objects in the sentence frame, "This Y is X," where X is a novel word, and Y is a familiar basic-level count noun (e.g., "dog," "cup"). These novel words are ambiguous and could be interpreted either as proper names (e.g., "Fred") or as adjectives/mass nouns (e.g., "red"/"lead"). The experiments addressed 2 questions. First, do children appreciate that the words can be construed either as proper names referring to individuals or as adjectives/mass nouns referring to salient properties/material kinds? The results showed that children could easily make either interpretation. Second, what factors affect children's tendency to make either a proper name or an adjective/mass noun interpretation? In the experiments, children learned the novel words for a range of animals and artifacts. Most children who learned the words for typical pets (e.g., a bird) made proper name interpretations, as did the majority of those who learned the words for certain non-pet animals (e.g., a caterpillar) described as possessed by someone, but only about half of those who learned the words for such non-pet animals not so described. Very few children who learned the words for either simple (e.g., a shoe) or complex (e.g., a boat) artifacts made proper name interpretations. The results provide clear evidence of the role of semantic information in constraining children's interpretation of a novel word, and they help to refine an understanding of what counts as a nameable individual for preschoolers.

Child Language↗
PubMed1995

Reduction by NG-nitro-L-arginine methyl ester (L-NAME) of antigen-induced nasal airway plasma extravasation in human subjects in vivo.

In non-allergic subjects, histamine induced a reduction of minimal nasal cross-sectional area (Amin) and an increase in albumin release into nasal lavage. The effect of histamine on albumin release was inhibited by pretreatment with NG-nitro-L-arginine methyl ester (L-NAME), 1 mumol but not by D-NAME, 1 mumol. L-NAME, 1 and 10 mumol, did not inhibit the histamine-induced reduction of Amin. In subjects allergic to grass pollen, antigen challenge induced a reduction in Amin that was not changed by pretreatment with L-NAME, and an increase in albumin release that was inhibited by L-NAME, 1 mumol. The data support a role for nitric oxide in mediating plasma extravasation in the nose induced by antigen challenge or histamine.

Adult↗
PubMed1996

The vasoconstrictor effects of L-NAME, a nitric oxide synthase inhibitor, in pregnant rabbits.

1. We have used anaesthetized, acutely instrumented non-pregnant (NP) and late pregnant (P) New Zealand white rabbits to examine the possible role of nitric oxide (NO) in the pregnancy-induced fall of vascular tone and arterial pressure. Systemic, renal and pulmonary vascular resistance, as well as plasma concentrations of cyclic GMP (PcGMP) were compared before and after the inhibition of NO synthesis by N(G)-nitro-L-arginine methyl ester (L-NAME). 2. P rabbits had lower baseline total peripheral resistance (TPR), mean arterial pressure (MAP) and higher PcGMP than NP controls (all P < 0.05 or less). L-NAME (1, 10, 50 mg kg1, i.v.) resulted in dose-dependent elevation of TPR in both groups. However, the absolute, as well as percentage increases in TPR were greater (P < 0.05) in NP than in P rabbits. 3. Cardiac output (CO) was reduced more (P < 0.01) by NO inhibition in NP than P rabbits. Therefore, despite the smaller increase in TPR, the elevation of MAP was greater (P < 0.001) in P than NP rabbits. After L-NAME, NP rabbits developed more severe bradycardia and a greater increase of pulmonary vascular resistance which might have contributed to the more pronounced reduction of CO. 4. PcGMP increased in both groups following L-NAME, but more (P < 0.01) in NP than P rabbits. 5. Infusion of acetylcholine (ACh, 0.02 micromol l-1 kg-1) reduced MAP and TPR more (both P < 0.05) in NP than P rabbits and L-NAME reduced the ACh-induced depressor response only in NP rabbits. 6. These results suggest that the low vascular tone and arterial pressure in pregnant rabbits is not mediated by NO.

Acetylcholine↗
PubMed1996

Lack of beneficial effects on the NO-donor, molsidomine, in the L-NAME-induced pre-eclamptic syndrome in pregnant rats.

1. In pregnant rats, chronic NO-synthase inhibition induces the development of a pre-eclamptic syndrome, characterized by an increase in maternal blood pressure, a loss of vascular refractoriness to pressor stimuli, a reduction in litter size and a decrease in pups (and maternal) weight. We investigated whether a NO-donor, molsidomine, administered during NO synthase inhibition, could restore a normal pregnancy. 2. Pregnant rats were given daily, starting from day 14 of gestation, saline (controls), or L-NAME (50 mg kg-1 d-1), or molsidomine (15 or 30 mg kg-1 d-1), or the L-NAME + molsidomine combinations. Maternal blood pressure and body weight, litter size, pups weight and vascular reactivity to pressor stimuli (angiotensin II, noradrenaline, electrical stimulation of the spinal cord) were investigated. 3. L-NAME alone, as compared to controls, increased maternal blood pressure, reduced litter size (-59%), increased foetal reabsorptions (+ 625%) and decreased foetal weight (-10%). Vascular reactivity to pressor stimuli was enhanced. 4. Molsidomine alone, as compared to controls, dose-dependently decreased maternal blood pressure but had no effect vascular reactivity and, whatever the dose, on foetal outcome. 5. The L-NAME-molsidomine combinations dose (of molsidomine)-dependently limited the rise in maternal blood pressure induced by L-NAME alone but unexpectedly, dose-dependently and significantly worsened pregnancy evolution, e.g., at 30 mg kg-1 d-1: litter size (-80%), foetal reabsorptions (+ 1025%), foetal weight (-24%). Vascular reactivity to pressor stimuli was paradoxically further enhanced. 6. Thus, in a chronic NO deprivation-induced model of pre-eclampsia in rats, molsidomine, possibly because of its hypotensive action, worsens the foetal outcome, which questions the usefulness of NO-donors in pre-eclamptic women.

Animals↗
PubMed1996

Naming deficit in herpes simplex encephalitis.

OBJECTIVES: The preferential involvement of living categories in naming impairment is well recognised in Herpes Simplex Encephalitis (HSE). In this paper we describe naming, neuropsychological and neuroradiological findings with seven fresh HSE cases. MATERIAL & METHODS: Patients were given a picture naming task that included 60 items belonging to 6 different categories (three living, i.e. fruits, vegetables and animals and three non-living, i.e. furniture, vehicles and tools). In the statistical analysis several possible sources of bias as the frequency of the target word, the familiarity with the objects to name, the image complexity and other parameters were taken into account. RESULTS: Four out of seven patients were significantly more impaired with living things. We describe their general cognitive profile and discuss the anatomo-functional aspects of category dissociation. CONCLUSION: Language impairment, disproportionately severe for the naming of living exemplars, is frequently observed in HSE, is clinically relevant and should be specifically investigated.

Adolescent↗
PubMed1995

Regional difference in the distribution of L-NAME-sensitive and -insensitive NANC relaxations in cat airway.

1. To investigate the distribution profile of functional inhibitory non-adrenergic non-cholinergic (i-NANC) nerves and the contribution of NO to the NANC relaxation in the cat, we studied the effects of N omega-nitro-L-arginine methyl ester (L-NAME) on NANC relaxation elicited by electrical field stimulation (EFS) in the trachea, bronchus and bronchiole. 2. EFS applied to the tracheal smooth muscle during contraction induced by 5-HT (10(-5) M) in the presence of atropine (10(-6) M) and guanethidine (10(-6) M) elicited a monophasic NANC relaxation. By contrast, NANC relaxation elicited in the peripheral airway was biphasic, comprising an initial fast followed by a second slow component and L-NAME (10(-5) M) selectively abolished the first component without affecting the second one. In the trachea, L-NAME (10(-5) M) completely suppressed the monophasic NANC relaxation when single or short repetitive stimuli (< 5) with 1 ms pulse duration were applied. However, at higher repetitive stimuli (> 10) with 1 or 4 ms pulse duration, suppression of NANC relaxation was incomplete. 3. In the small bronchi obtained from L-NAME-pretreated cats, EFS applied during contraction induced by 5-HT (10(-5) M) elicited only the slow component of NANC relaxation which is sensitive to tetrodotoxin. 4. In the peripheral airway, a newly synthesized VIP antagonist (10(-6) M) or alpha-chymotrypsin (1 U ml-1) considerably attenuated the amplitude of L-NAME-insensitive relaxation. 5. Single or repetitive EFS consistently evoked excitatory junction potentials (EJPs) in the central and peripheral airways. When tissues were exposed to atropine (10(-6) M) and guanethidine (10(-6) M), single or repetitive EFS did not alter the resting membrane potential. 6. These results indicate that at least two neurotransmitters, possibly NO or NO-containing compounds and VIP, are involved in i-NANC neurotransmission and the distribution profile of the two components differs in the central and peripheral airway of the cat.

Animals↗
PubMed2005

Effects of nitric oxide synthase inhibition by L-NAME on oxygen uptake kinetics in isolated canine muscle in situ.

Nitric oxide (NO) has an inhibitory action on O2 uptake (VO2) at the level of the mitochondrial respiratory chain. The aim of this study was to evaluate the effects of NO synthase (NOS) inhibition on muscle (VO2) kinetics. Isolated canine gastrocnemius muscles in situ (n = 6) were studied during transitions from rest to 4-min of electrically stimulated contractions corresponding to approximately 60% of the muscle peak . Two conditions were compared: (i) Control (CTRL) and (ii) L-NAME, in which the NOS inhibitor L-NAME (20 mg kg(-1)) was administered. In both conditions the muscle was pump-perfused with constantly elevated blood flow (Q), at a level measured during a preliminary contraction trial with spontaneous self-perfused (Q). A vasodilatory drug was also infused. Arterial and venous O2 concentrations were determined at rest and at 5-7 s intervals during the transition. VO2 was calculated by Fick's principle. Muscle biopsies were obtained at rest and during contractions. Muscle force was measured continuously. Phosphocreatine hydrolysis and the calculated substrate level phosphorylation were slightly (but not significantly) lower in L-NAME than in CTRL. Significantly (P < 0.05) less fatigue was found in L-NAME versus CTRL. The time delay (TD(f)) and the time constant (tau(f)) of the 'fundamental' component of VO2 kinetics were not significantly different between CTRL (TD(f) 7.2 +/- 1.2 s; and tau(f) 10.6 +/- 1.3, +/- s.e.m.) and L-NAME (TD(f) 9.3 +/- 0.6; and tau(f) 10.4 +/- 1.0). Contrary to our hypothesis, NOS inhibition did not accelerate muscle VO2 kinetics. The down-regulation of mitochondrial respiration by NO does not limit the kinetics of adjustment of oxidative metabolism at exercise onset.

Animals↗
PubMedDate not supplied

Product names, proper claims? More ethical issues in the marketing of drugs.

OBJECTIVES: To analyse the explicit or implicit claims embodied in the proprietary names of pharmaceutical products. DESIGN: Linguistic and ethical analysis of proprietary names of pharmaceutical products marketed in the UK and in Denmark. RESULTS AND CONCLUSIONS: A number of drugs have names that allude to their indication or actions. Such names may be problematic, however, because they often promise more than the drug can deliver. Taking into account, firstly, the type of allusion and its degree of sophistication, and, secondly, the seriousness of the indication may help in identifying the most problematic drug names.

Denmark↗
PubMed2002

What's in a name? A systematic review of the nomenclature of Chinese medical formulae.

Traditional Chinese Medicine (TCM) has been modified to some extent in other Far Eastern countries such as Korea and Japan. Researchers of each of the three countries seem to use different English names for the same Chinese medicinal formulae. Lack of knowledge of the Chinese characters is destined to increase this confusion. In order to investigate this matter systematically, all investigations of Chinese medicine formulae published in the American Journal of Chinese Medicine (AJCM, 1997-March 2001) were evaluated. Moreover, PubMed (1966-June 2001) was searched using keywords differentiated by language, location and number of hyphens, and upper-or lower-case of the first letter of the English equivalent of each Chinese character. Fifty-four formulae of TCM were identified in 45 reports published in AJCM. Thirty-two were named in Chinese only (23 reports); six in Japanese (six reports); and five in Korean (five reports). Ten formulae were named in Japanese with the Chinese name in brackets (ten reports); and one in Chinese with the Japanese name in brackets (one report). By computerized literature search, different numbers of research papers were retrieved by using keywords differentiated by language, location and number of hyphens. Such confusion may prevent progress in the evaluation of TCM. To increase the efficiency of studies on Chinese medical formulae, standardization of terminology is required.

Chemistry, Pharmaceutical↗
PubMed1996

Nitric oxide inhibitor L-NAME suppresses mechanically induced bone formation in rats.

We hypothesized that nitric oxide may act as an intermediary in the transduction of mechanical loading of bone into a bone formation response. In the present study, 48 rats were divided into the following three treatment groups: control, treatment with N omega-nitro-L-arginine methyl ester (L-NAME; an inhibitor of nitric oxide synthase), and treatment with D-NAME (the less active enantiomer of L-NAME). The rats were subdivided into groups subjected to four-point bending or sham loading of their right tibiae. Bone formation was measured at the midshaft of the loaded and nonloaded (left) tibiae of each rat using histomorphometric methods. The application of four-point bending, but not sham loading, resulted in new bone formation. Treatment with L-NAME reduced the rate of mechanically induced bone formation by 66% compared with the control group. Bone formation rates in nonloaded or sham-loaded limbs were not affected by L-NAME treatment. The results suggest that nitric oxide may play a role in the transduction of a mechanical stimulus into a biological response in bone.

Animals↗
PubMed1996

Nitric oxide synthase inhibition by L-NAME during repetitive focal cerebral ischemia in rabbits.

The effects of nitric oxide synthase inhibition on brain acidosis, regional cortical blood flow (rCBF), and NADH redox state were examined using in vivo fluorescence imaging during four 15-min periods of moderate focal cerebral ischemia, each separated by three 5-min reperfusion periods followed by a final 3-h reperfusion period. Fasted rabbits under 1.5% halothane were divided into six groups of seven animals each: nonischemic controls, ischemic controls, and the following drug groups receiving NG-nitro-L-arginine methyl ester (L-NAME) intravenously 20 min before repetitive ischemia (as follows: 0.1 mg/kg, 1 mg/kg, 10 mg/kg, and 1 mg/kg + 5 mg/kg L-arginine). L-NAME at 0.1 and 1 mg/kg prevented the development of significant brain acidosis throughout the four ischemic insults. L-NAME at 10 mg/kg reduced preischemic rCBF by 21% (P < 0.05) and did not mitigate brain acidosis after the third and fourth ischemic insults. Brain intracellular pH returned toward baseline after the 3-h final reperfusion in all groups. NADH redox state was significantly (P < 0.05) elevated from baseline controls in all groups during the last three ischemic insults. During the final reperfusion period, NADH redox state returned toward baseline values only in the 0.1 mg/kg L-NAME and ischemic control group. In conclusion, low-dose L-NAME attenuated brain acidosis independent from rCBF changes during intermittent, moderate focal cerebral ischemia.

Animals↗
PubMed1998

Local L-NAME decreases blood flow and increases leukocyte adhesion via CD18.

Local inhibition of nitric oxide (NO) synthesis with L-arginine analogs such as NG-nitro-L-arginine methyl ester (L-NAME) decreased red blood cell velocity (VRBC) in capillaries and increased leukocyte adhesion in postcapillary venules in rat skeletal muscle. The goal of the present study was to determine the mechanism of this response to L-NAME. Using intravital videomicroscopy, we examined blood flow in the surface microvasculature of rat extensor digitorum longus muscle. L-NAME (30 mM in the pipette) locally applied to capillaries (300 microns from feeding arteriole) reduced VRBC [control VRBC = 244 +/- 53 (SE) microns/s; delta VRBC = -52 +/- 8%] and increased leukocyte adhesion (from 0.2 +/- 0.01 to 1.3 +/- 0.3 cells/100 microns) in control animals. Systemic pretreatment with fucoidan (selectin binder), superoxide dismutase and catalase (extracellular antioxidants), dimethylthiourea (intracellular antioxidant), or ketotifen (mast cell stabilizer) did not alter this response. Pretreatment with CL26, an anti-CD18 antibody, abolished the L-NAME response. Our results suggest that L-NAME increased leukocyte-endothelial interactions via an effect on CD11/CD18 or its ligand, intercellular adhesion molecule.

Animals↗
PubMed2002

Hypertension in L-NAME-treated diabetic rats depends on an intact sympathetic nervous system.

We demonstrated previously that induction of diabetes in rats that were treated chronically with the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) causes a severe, progressive increase in mean arterial pressure. This study tested the role of the sympathetic nervous system in that response. Rats were instrumented with chronic artery and vein catheters and assigned randomly to four diabetic groups pretreated with vehicle (D), L-NAME (D+L), the alpha(1)- and beta-adrenergic receptor antagonists terazosin and propranolol (D+B), or L-NAME, terazosin, and propranolol (D+LB). After baseline measurements were taken, rats were pretreated; 6 days later, streptozotocin was administered and 3 wk of diabetes ensued. D+L rats had a marked, progressive increase in arterial pressure that by day 20 was approximately 60 mmHg greater than in D rats. The pressor response to L-NAME was significantly attenuated in diabetic rats cotreated with adrenergic blockers. During week 1 of diabetes, plasma renin activity (PRA) increased and then returned to control levels in D rats. PRA increased progressively in D+L rats, and chronic adrenergic receptor blockade restored the biphasic renin response in D+LB rats. These results suggest that the sympathetic nervous system may be involved in the hypertensive response to onset of diabetes in L-NAME-treated rats, possibly through control of renin secretion.

Adrenergic alpha-Antagonists↗
PubMed1998

Human renal and systemic hemodynamic, natriuretic, and neurohumoral responses to different doses of L-NAME.

Experimental evidence indicates that the renal circulation is more sensitive to the effects of nitric oxide (NO) synthesis inhibition than other vascular beds. To explore whether in men the NO-mediated vasodilator tone is greater in the renal than in the systemic circulation, the effects of three different intravenous infusions of NG-nitro-L-arginine methyl ester (L-NAME; 1, 5, and 25 microg. kg-1. min-1 for 30 min) or placebo on mean arterial pressure (MAP), systemic vascular resistance (SVR), renal blood flow (RBF), renal vascular resistance (RVR), glomerular filtration rate (GFR), and fractional sodium and lithium excretion (FENa and FELi) were studied in 12 healthy subjects, each receiving randomly two of the four treatments on two different occasions. MAP was measured continuously by means of the Finapres device, and stroke volume was calculated by a model flow method. GFR and RBF were estimated from the clearances of radiolabeled thalamate and hippuran. Systemic and renal hemodynamics were followed for 2 h after start of infusions. During placebo, renal and systemic hemodynamics and FENa and FELi remained stable. With the low and intermediate L-NAME doses, maximal increments in SVR and RVR were similar: 20.4 +/- 19.6 and 23.5 +/- 16.0%, respectively, with the low dose and 31.4 +/- 26.7 and 31.2 +/- 14.4%, respectively, with the intermediate dose (means +/- SD). With the high L-NAME dose, the increment in RVR was greater than the increment in SVR. Despite a decrease in RBF, FENa and FELi did not change with the low L-NAME dose, but they decreased by 31.2 +/- 11.0 and 20.2 +/- 6.3%, respectively, with the intermediate dose and by 70.8 +/- 8.1 and 31.5 +/- 15.9% with the high L-NAME dose, respectively. It is concluded that in men the renal circulation is not more sensitive to the effects of NO synthesis inhibition than the systemic circulation and that the threshold for NO synthesis inhibition to produce antinatriuresis is higher than the threshold level to cause renal vasoconstriction.

Adult↗
PubMed2001

Mechanism underlying diuretic effect of L-NAME at a subpressor dose.

The diuretic effects of nitric oxide (NO) synthase inhibitors administered at subpressor dose in rats are controversial, and the tubular segments involved are not known. In the present study, we examined the effect of N(omega)-nitro-L-arginine methyl ester (L-NAME) at a subpressor dose on renal interstitial NO and cGMP activity and on renal tubular segmental reabsorption of fluid in the rat. Intravenous infusion of L-NAME at 1 microg. kg(-1). min(-1) in Sprague-Dawley rats (N = 8), which did not alter mean arterial pressure or glomerular filtration rate, significantly increased urine flow rate (U(v); from 78.2 +/- 12.7 to 117.1 +/- 14.9 microl/min, P < 0.05). Paradoxically, this effect of L-NAME was concomitant with significant increases in nitrite/nitrate (from 10.79 +/- 1.20 to 16.50 +/- 2.60 microM, P < 0.05) and cGMP (from 0.65 +/- 0.09 to 0.98 +/- 0.18 nM, P < 0.05) concentrations in renal cortical microdialysate as well as the nitrite/nitrate concentration in the medullary microdialysate. Micropuncture studies in the superficial nephron revealed that L-NAME significantly increased the flow rate (from 8.3 +/- 0.9 to 12.2 +/- 1.2 nl/min, P < 0.05) and fractional delivery of fluid to the distal tubule, but not those in the late proximal tubule. In conclusion, L-NAME, at the subpressor dose used in this study, increased renal nitrate/nitrite and cGMP and inhibited fluid reabsorption in tubular segments between the late proximal tubule and the distal tubule of superficial nephrons.

Animals↗