Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhibition of systemic endothelium-derived relaxing factor (EDRF) synthesis with L-Nw-nitroarginine (L-NAME) results in decreased RBF, which can be reversed by acute blockade of angiotensin II (AII). Because AII is particularly elevated in the renal circulation, it was hypothesized that the degree of renal vasoconstriction produced by L-NAME in Inactin-anesthetized rats is related to PRA. To test this, PRA was chronically increased or suppressed by the manipulation of dietary sodium (eating 0.03% sodium chow or deoxycorticosterone acetate plus drinking 1% NaCl, respectively). After 10 days, rats were anesthetized for determination of blood pressure (BP) and RBF before and after L-NAME (10 mg/kg body wt). In rats with high PRA (61.6 +/- 10.4 ng of angiotensin I [Al]/mL/h; N = 8), L-NAME increased BP by 29 +/- 2 mm Hg (from 110 +/- 4 to 139 +/- 5 mm Hg; P < 0.001), decreased RBF by 27% (from 7.9 +/- 0.3 to 5.8 +/- 0.3 mL/min/g kidney wt; P < 0.001), and increased renal vascular resistance (RVR) by 67% (from 14.5 +/- 0.9 to 24.2 +/- 1.1 resistance units [RU]; P < 0.001). When rats with high PRA (N = 8) were treated with 10 mg/kg body wt of DuP 753, on AII receptor antagonist, L-NAME similarly increased BP by 30 +/- 5 mm Hg (from 81 +/- 3 to 111 +/- 5; P < 0.001) but RBF did not change and RVR increased by only 31% (from 10.9 +/- 0.8 to 13.3 +/- 0.7 RU; P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma renin activity and the renal response to nitric oxide synthesis inhibition. 147 24

Inhibition of the production of the endothelium-derived relaxing factor (EDRF) nitric oxide using N omega-nitro-L-arginine methyl ester (L-NAME) increases blood pressure (BP) and decreases renal blood flow (RBF), suggesting that basal EDRF can modulate both systemic resistance and renal perfusion. We tested whether L-NAME inhibition of EDRF could also change the autoregulation of RBF. Blood pressure and RBF were measured in Inactin-anesthetized Sprague-Dawley rats. A bolus of 10 mg/kg body wt of L-NAME produced the maximum pressor response (23 +/- 3 mmHg) and blocked acetylcholine-induced renal vasodilation. In control rats, sequential changes in renal perfusion pressure showed that RBF was well autoregulated down to 95 +/- 2 mmHg. L-NAME increased BP, decreased RBF by 33% (P less than 0.005), and increased renal vascular resistance twofold. Although RBF was decreased, the kidney was still able to autoregulate RBF, although reset around the lower flow. Acute hypertension by carotid occlusion and vagotomy increased BP by 26 +/- 6 mmHg (P less than 0.005) and slightly increased RBF, while autoregulation was maintained. The pressor response to L-NAME was amplified to 38 +/- 6 mmHg (P less than 0.001), but RBF decreased by 35% (P less than 0.01). Autoregulation of RBF was maintained, although reset around the lower flow. We conclude that, although endothelial EDRF production may help maintain RBF, it does not seem to mediate the intrinsic autoregulatory responses of the renal vasculature to altered renal perfusion pressure.
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PMID:Endothelium modulates renal blood flow but not autoregulation. 162 18

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.
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PMID:Systemic and regional hemodynamics after nitric oxide synthase inhibition: role of a neurogenic mechanism. 751 12

The existence of calcitonin gene-related peptide (CGRP) nerve fibers and CGRP receptors in the kidney and the coupling of the receptors to adenylyl cyclase suggest that CGRP participates in renal regulation. This study investigates the dose-effect relationship of CGRP on renal blood flow (RBF) and arterial conductance, glomerular filtration rate (GFR) and tubular excretion in Inactin-anesthetized, Sprague-Dawley rats. The contributions of endothelium-derived relaxing factor/nitric oxide in the renal actions of CGRP also were investigated via renal arterial injection of the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 0.5 or 5 mg/kg). Renal arterial infusion of CGRP (0.3-300 pmol/kg/min) did not affect mean arterial pressure or heart rate. Low doses of CGRP increased RBF, arterial conductance and GFR, but the highest dose reduced RBF and conductance without affecting GFR. High doses of CGRP also increased urine flow and excretions of Na+ and K+. The renal vasodilator but not the constrictor effect of CGRP was inhibited by both doses of L-NAME. The increase in GFR by the lowest dose of CGRP was attenuated by the low dose and abolished by the high dose of L-NAME. L-NAME did not inhibit the diuretic, natriuretic and kaliuretic effects elicited by high doses of CGRP. The results show that a low dose of CGRP causes renal vasodilatation via the release of endothelium-derived relaxing factor/nitric acid.
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PMID:Renal vascular and tubular actions of calcitonin gene-related peptide: effect of NG-nitro-L-arginine methyl ester. 771 12

The vasoconstrictor vasopressin has been reported to induce paradoxical local vasodilation in the basilar vasculature through stimulation of the endothelium-derived relaxing factor nitric oxide (NO). We investigated the possibility that at subpressor doses, exogenous arginine vasopressin (AVP) might have a similar effect in the kidney. Ten Inactin-anesthetized rats were infused with sequential doses of AVP from 25 to 6,400 microU/min in 30-min increments. Subpressor infusion resulted in progressive renal vasodilation; renal blood flow (RBF) increased significantly going from 14 +/- 6% above basal at 200 microU/min (p < 0.02) to 27 +/- 5% (p < 0.01) at 1,600 microU/min accompanied by a 24 +/- 5% decrease in renal vascular resistance (RVR). At 6,400 microU/min, blood pressure (BP) increased 29 +/- 6 mm Hg and RVR increased. A second group of 8 rats were first given 10 mg/kg b.w. of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) before infusion of AVP. L-NAME increased BP 22 +/- 3 mm Hg (p < 0.001), and decreased RBF 16 +/- 3% (p < 0.005). After L-NAME, no dose of AVP had any further effect on either BP, RBF, or RVR. Continuous infusion of a single subpressor dose of 100 microU AVP resulted in a 26% increase in RBF (from 7.52 +/- 0.68 to 9.49 +/- 0.54 ml/min/g kidney weight, p < 0.001). AVP doubled urinary cyclic guanosine monophosphate excretion, a marker for renal NO synthesis, from 8.51 +/- 1.01 to 17.48 +/- 4.26 pM/min (p < 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arginine vasopressin-induced renal vasodilation mediated by nitric oxide. 773 55

In this study, we examined whether endothelin (ET) plays a role in the short-term increase in mean arterial pressure (MAP) after nitric oxide synthase (NOS) inhibition with N(omega)-nitro-L-arginine methyl ester (L-NAME) in stroke-prone spontaneously hypertensive rats (SHRSPs). Experiments were performed by using Inactin-anesthetized male SHRSPs that were pretreated with chlorisondamine to block reflex autonomic cardiovascular effects. Injection of L-NAME (10 mg/kg, i.v.), but not D-NAME, produced rapid and marked increases (74 +/- 3 mm Hg) in MAP that were sustained for >1 h. In SHRSPs that were treated with the ET(A/B) receptor antagonist, L-754,142 (15 mg/kg + 15 mg/kg/h), L-NAME increased MAP by 45 +/- 4 mm Hg (p < 0.0001 compared with L-NAME alone). L-754,142 blocked pressor responses to big ET-1 by >90% but was without effect on pressor responses to norepinephrine. Plasma levels of ET-1 averaged 5 +/- 1 pg/ml in animals given vehicle and were slightly increased in animals given either L-NAME alone (7 +/- 2 pg/ml) or L-754,142 alone (7 +/- 2 pg/ml) but increased markedly when L-NAME and L-754,142 were given together (114 +/- 18 pg/ml). This may relate to an effect of L-754,142 to block ET-receptor-mediated clearance of ET-1. We conclude that ET plays a role in the short-term pressor response after NOS inhibition in SHRSPs.
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PMID:Contribution of endothelin to the acute pressor response of L-NAME in stroke-prone spontaneously hypertensive rats. 955 13

The present study examined the effect of renal denervation on the impairment of the pressure-diuresis response produced by nitric oxide synthesis blockade. The experiments were performed in Inactin-anesthetized Munich-Wistar rats. The animals with innervated kidneys had lower baseline values of renal blood flow, GFR, sodium excretion (UNaV), and urine flow (V) than rats with denervated kidneys. Also, renal denervation shifted pressure-diuresis and natriuresis toward lower pressures. A low dose of N(omega)-nitro-L-arginine methyl esther (NAME, 3.7 nmol/kg per min) reduced UNaV and the fractional excretion of sodium (FENa) and blunted pressure-natriuresis only in rats with innervated kidneys, whereas it had no effects in rats with denervated kidneys. A medium dose of NAME (37 nmol/kg per min) lowered FENa only in rats with innervated kidneys. The administration of NAME (37 nmol/kg per min) blunted pressure-diuresis and natriuresis in kidneys with or without the renal nerves, but the effect was more pronounced in rats with innervated kidneys. A high dose of NAME (3.7 micromol + 185 nmol/kg per min) increased UNaV and FENa only in rats with innervated kidneys, whereas it reduced GFR, V, UnaV, and FENa in rats with denervated kidneys. However, pressure-natriuresis and diuresis were blunted by this high dose of NAME independently of the presence or absence of renal nerves. These results demonstrate that renal nerves potentiate the renal effects of low doses of NAME on renal function and pressure-diuresis and natriuresis. However, high doses of NAME abolish pressure-diuresis independently of renal nerves, and the natriuretic effect of NAME in innervated kidneys may be attributed to reflex inhibition of sympathetic tone due to the rise in arterial pressure.
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PMID:Interactions between nitric oxide and renal nerves on pressure-diuresis and natriuresis. 972 66

In Inactin-anesthetized Wistar rats with an intact renal innervation, intratubular nitro-L-arginine methyl ester (L-NAME, 10(-4) M) increased proximal fluid uptake (J(va), at 2.47 +/- 0.61 x 10(-4) mm(3). mm(-2). s(-1)) by 17% (P < 0.05), whereas coadministration with sodium nitroprusside (SNP, 10(-4) M) decreased J(va) by 18% (P < 0.01). Similar manipulation of NO generation was without effect in groups of Wistar rats subjected to acute renal denervation. Intratubular aminoguanidine (10(-4) M), a selective inducible nitric oxide synthase (NOS) blocker, had no effect on J(va) in intact kidneys of Wistar rats, but the neuronal NOS (nNOS) blocker, 7-nitroindazole (10(-4) M and 10(-6) M) increased J(va) by 19-23% (both P < 0.001). In stroke-prone spontaneously hypertensive rats (SHRSP), J(va) values in the innervated kidneys were lower (P < 0.05) than in the corresponding Wistar groups and were unchanged by intratubular L-NAME or L-NAME plus SNP. The tonic attenuation of proximal epithelial transport by NO was dependent on the renal sympathetic nerves and appeared to be generated by the nNOS isoform of the enzyme. This role of NO was not evident in the SHRSP.
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PMID:Nitric oxide and renal nerve-mediated proximal tubular reabsorption in normotensive and hypertensive rats. 1051 80

The pathogenesis of radiocontrast nephropathy is poorly understood. In an animal model, inhibition of the synthesis of nitric oxide and prostaglandins appears to predispose rats to severe renal injury following the administration of radiocontrast. Here we have investigated whether administration of radiocontrast, as well as changes in renal medullary oxygenation following pharmacologic inhibition of nitric oxide and prostaglandin synthesis, might be evaluated by blood oxygenation level-dependent (BOLD) MRI. Nineteen anesthetized (Inactin 100 mg/kg) rats were studied. BOLD MRI measurements were performed following administration of L-NAME (N-nitro-L-arginine methyl ester, 10 mg/kg), Indomethacin (10 mg/kg), and a radiocontrast agent (sodium iothalamate 60%, 6 mL/kg). Marked sequential changes in medullary R(*)(2), presumably reflecting decline in medullary pO(2), were noted after each of the pharmacological interventions employed. These results, obtained by noninvasive MRI, are consistent with prior direct recordings of pO(2) and doppler flow in the rat renal medulla after administration of L-NAME, Indomethacin and iothalamate. Medullary oxygenation in rats was reduced by inhibition of the synthesis of prostaglandins and nitric oxide, as well as by intravenous injection of radiocontrast agents. BOLD MRI can noninvasively evaluate changes in medullary oxygenation in rats that appear to predispose acute renal failure. J. Magn. Reson. Imaging 2001;13:744-747.
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PMID:Changes in intrarenal oxygenation as evaluated by BOLD MRI in a rat kidney model for radiocontrast nephropathy. 1132 96

The role of endothelium-derived nitric oxide (NO) in renal baroreceptor stimulation of renin was tested comparing endothelial nitric oxide synthase (eNOS)-deficient mice with C57BL/6J (C57) controls. We measured blood pressure, renal blood flow (RBF), and plasma renin concentration (PRC) in Inactin-anesthetized mice. Blood pressure in eNOS knockout mice was higher than in controls (100 +/- 3 vs. 86 +/- 1 mmHg, respectively; P < 0.001), but RBF was similar (1.71 +/- 0.06 vs. 1.66 +/- 0.09 ml. min(-1). 100 mg kidney wt(-1), respectively), so that renal vascular resistance was also higher in the knockouts (59.81 +/- 2.07 vs. 51.81 +/- 2.66 resistance units, respectively; P < 0.025). PRC was similar (8.24 +/- 1.57 in eNOS knockouts vs. 7.10 +/- 1.19 ng ANG I. ml(-1). h(-1) in C57). NOS inhibition with nitro-L-arginine methyl ester (L-NAME) in C57 controls increased blood pressure (from 85 +/- 2 to 106 +/- 1 mmHg, P < 0.001) and decreased RBF (from 1.66 +/- 0.09 to 1.08 +/- 0.02; P < 0.005), but L-NAME had no effect in eNOS knockout mice. When renal perfusion pressure was reduced in C57 controls to 55 mmHg, PRC increased from 6.6 +/- 0.9 to 14.5 +/- 1.9 microg. ml(-1). h(-1) (P < 0.025), but this response was blocked by L-NAME. However, in eNOS knockouts, reduced renal perfusion pressure increased PRC from 7.6 +/- 1.4 to 15.0 +/- 2.8 microg. ml(-1). h(-1) (P < 0.001). Thus in the chronic absence of eNOS, blood pressure was elevated, but RBF was normal. Additionally, the absence of eNOS did not modify baroreceptor-stimulated renin, suggesting that eNOS-derived NO does not directly mediate this renin-regulating pathway.
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PMID:Renal baroreceptor-stimulated renin in the eNOS knockout mouse. 1173 13


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