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)

Vasorelaxant effects of magnesium (Mg) have been described in man and in animal with arterial hypertension. Some studies have shown relationships between extracellular Mg (magnesium e.c.) and endothelial function. So, our study is designed to determine whether elevated extracellular Mg leads to an endothelium-dependent vasorelaxant effect on contractile tension developed by noradrenaline in isolated aorta from DOCA-salt hypertensive rats. Elevated extracellular Mg (4.8 mM) in the bath significantly depressed the dose-response curve to noradrenaline in aorta with endothelium. Following disruption of endothelium, the vasorelaxant effect of elevated extracellular Mg on contractile response to noradrenaline was greatly inhibited. Furthermore, in presence of L. NG nitroarginine (L-NAME) (10(-4) M), inhibitor of endothelial nitric oxide (NO) biosynthesis, the vasorelaxant effect of extracellular Mg on contractility to noradrenaline was partially inhibited. The addition of sodium nitroprussiate (5 10(-9) M), known to spontaneously release NO, caused the reappearance of Mg vasorelaxation which had disappeared in aorta without endothelium. In conclusion, vascular endothelium seems to play an important role in the Mg-induced depressed contractile response to noradrenaline in isolated aorta from DOCA-salt hypertensive rat. Endothelial NO seems to be implicated in the endothelium-dependent action of extracellular Mg.
Arch Mal Coeur Vaiss 1992 Aug
PMID:[In vitro study of the role of endothelium on the vasorelaxant effect of magnesium on the aorta from DOCA-salt hypertensive rats]. 148 62

Fourteen mongrel dogs were chronically instrumented on the circumflex coronary artery for measurement of coronary diameter (CD; Piezoelectric crystals) and coronary blood flow (CBF: Doppler flow probe). Coronary resistance (CR) was calculated as mean arterial blood pressure (MAP)/CBF. Systemic and coronary effects of three intravenous doses of NG-nitro-L-arginine (L-NAME: 0.1; 0.3; 1 mg/kg) were recorded (n = 5). Systemic and coronary effects of two vasodilators, acetylcholine (ACH) (endothelium-dependent: 0.3 micrograms/kg) and nitroglycerin (NTG) (endothelium-independent: 1 microgram/kg) were compared before and after L-NAME (1 mg/kg) (n = 6). Finally, the effects of L-NAME (1 mg/kg) were compared one week before and three days after denudation (balloon catheter) of the circumflex coronary artery (2 cm up and downstream from the crystals attachment site). All experiments were performed in conscious dogs. L-NAME induced a dose-dependent constriction of large epicardial coronary arteries [-1.5 +/- 0.5% from 3.1 +/- 0.3 mm, p < 0.05; -4.0 +/- 0.7% from 3.2 mm, p < 0.001; -5.3 +/- 1.2% from 3.0 mm, p < 0.01; respectively]. L-NAME 0.3 and 1 mg/kg induced a significant increase in MAP [+12.5 +/- 3.0% from 90 +/- 4 mmHg, p < 0.01; +11.3 +/- 3.5% from 96 +/- 7 mmHg, p < 0.05; respectively] and CR [+18.0 +/- 8.3% from 9.8 +/- 3.0 mmHg/cm.s, p < 0.01; +18.7 +/- 8.2% from 10.4 +/- 3.0 mmHg/cm.s, p < 0.01; respectively] with a significant bradycardia, but CBF was not modified. Effects of ACH were unchanged after L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1992 Aug
PMID:[Systemic and coronary hemodynamic effects of inhibition of nitrogen monoxide synthesis in conscious dogs]. 148 63

In Carney's syndrome, the association of cardiac myxomas, spotty pigmentation and endocrine over activity, the myxomas are usually multiple and have atypical locations. The authors report a case in which an accurate diagnosis of these multiple myxomas was made by transoesophageal echocardiography, although transthoracic echocardiography had missed the diagnosis.
Arch Mal Coeur Vaiss 1991 Sep
PMID:[Echocardiographic aspects of multiple myxoma in Carney's syndrome]. 195 21

The chronic inhibition of NO-synthase by NG-nitro-L-arginine methyl ester (L-NAME, a L-arginine analogue) induces a dose-dependent decrease in aortic cGMP and an increase in blood pressure. We used this pharmacological approach to evaluate the release of NO in vivo in spontaneously hypertensive rats (SHR); 15 SHR and 10 Wistar-Kyoto rats (WKY) were given 25 mg L-NAME/kg/d by gavage for 15 days; 10 SHR and 10 WKY rats given water for the same period were used as control. During the trial, 10/15 SHR given L-NAME died. Systolic blood pressure (mmHg) increased from 132 +/- 6 to 170 +/- 4 in WKY given L-NAME and from 169 +/- 4 to 242 +/- 6 in SHR given L-NAME. Aortic cGMP content (fmol/mg protein) was 2,204 +/- 382 and 2,076 +/- 461 fmol/mg control WKY and SHR (NS), and was decreased to 324 +/- 44 and 641 +/- 70 in WKY and SHR given L-NAME respectively (p < 0.0001 each). L-NAME increased plasma atrial natriuretic factor only in SHR. In summary, basal aortic cGMP content, reflecting the basal release of NO, was similar in WKY and SHR. The decrease in aortic cGMP content of SHR given L-NAME, due to the blockade of NO-synthase, was accompanied by a large increase in systolic blood pressure and a tremendous mortality rate. Thus, basal release of NO is probably not impaired in SHR, but represents a major counterregulatory mechanism in this genetic model of arterial hypertension.
Arch Mal Coeur Vaiss 1993 Aug
PMID:[Vasodilator effect of nitric oxide is a necessary counter-regulation in the spontaneously hypertensive rat]. 751 Apr 67

The influence of dietary sodium restriction and angiotensin II blockade on hypertension induced by a 25-day period of administration of the inhibitor of nitric oxide synthesis NG-nitro-L-arginine methyl ester (L-NAME: 10 mg/kg twice daily by gavage) was assessed in Wistar rats fed a normal or low sodium diet. In addition, the angiotension II receptor blocker, losartan (30 mg/kg once daily by gavage) was administered prior to and during L-NAME in rats fed the normal sodium diet. Results expressed as mean +/- ESM are presented in the following table: [table: see text] At the end of studies, conscious systolic arterial pressure increased similarly in L-NAME-treated groups maintained on NS or LS intake. Moreover, a 25% reduction in cardiac output due to a decrease in stroke volume was observed in both groups. A slight but significant cardiac hypertrophic response was observed in hypertensive rats irrespective of sodium intake. Losartan totally prevented the development of hypertension as well as the decrease in cardiac output and the cardiac hypertrophy associated with L-NAME treatment in rats on normal sodium intake. In conclusion, hypertension resulting from chronic blockade of nitric oxide synthesis was not affected by dietary sodium restriction. A crucial role for the renin-angiotensin system was demonstrated in this new model of hypertension.
Arch Mal Coeur Vaiss 1993 Aug
PMID:[Sodium intake and angiotensin in hypertension induced by chronic NO synthase inhibition in the rat]. 751 Apr 68

Clinical use of the immunosuppressant cyclosporine A (CSA) is hampered by its nephrotoxicity. The renal vascular resistance is increased, may be as a consequence of a deleterious effect of the drug on the vascular endothelial cell function. The renal effects of a subchronic treatment with CSA (50 mg/kg/d, sc, 18 days), or olive oil vehicule (1 ml/kg), were studied in normotensive male Wistar rats. Creatinine clearance was measured on 24 h urine collection before the right kidney of the animals was isolated and perfused in an open circuit at 6 ml/min with Tyrode's solution. Renal vasodilator responses to acetylcholine (ACH, 10(-10) to 10(-7) M) and sodium nitroprusside (NP, 3 x 10(-9) to 3 x 10(-6) M) were studied after reestablishment of a renal vascular tone by a continuous perfusion of noradrenaline (NA, 10(-7) M). ACH was more potent than NP to induce renal vasodilation (EC50 = 0.57 +/- 0.05 x 10(-9) M, n = 8, vs 3.42 +/- 0.29 x 10(-8) M, n = 5), but both drugs reversed the NA-induced vasoconstriction by near 90%. L-NAME (3 x 10(-5) M) had no effect on NP-induced renal relaxation but suppressed responses to low concentrations of ACH and decreased by half its Emax (47 +/- 17%).(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1993 Aug
PMID:[Changing of renal endothelium-dependent vascular reactivity by cyclosporin A]. 812 33

Nitric oxide is an important regulator of vascular tone, as evidenced by the marked increase in blood pressure produced by the inhibition of its synthesis. Furthermore, nitric oxide may be implicated in the modulation of vascular growth, although in vitro and in vivo studies have provided conflicting results. The aim of this study is to determine the effects of chronic nitric oxide synthase inhibition, with or without antihypertensive treatment, on the structure of the basilar artery in the rat. Rats were treated for 6 weeks with N omega-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day) alone or in combination with verapamil (100 mg/kg/day) or with trandolapril (1 mg/kg/day). Untreated rats served as controls. The structure of perfused and pressurized basilar arteries were analyzed in vitro using a video dimension analyzer. Chronic L-NAME treatment increased systolic arterial pressure (229 +/- 5 vs 147 +/- 3 for controls; p < 0.05) and the media to lumen ratio of the basilar artery (0.22 +/- 0.02 vs 0.15 +/- 0.01 for controls; p < 0.05). This structural alteration was mainly due to remodeling (remodeling index: 76%), but not to growth (growth index: 8%, NS). The concomitant administration of verapamil and trandolapril prevented the increase in blood pressure (154 +/- 6 and 146 +/- 5 mmHg, respectively) and the structural changes produced by L-NAME (Media/lumen ratio: 0.15 +/- 0.01 and 0.14 +/- 0.01 mmHg, respectively). In fact, a positive correlation was observed between the media to lumen ratio and the systolic arterial pressure (r = 0.6; p < 0.001). The effect of the two antihypertensive treatments, as well as the correlation between the wall to lumen ratio and the arterial pressure, suggest that the remodeling of the basilar artery depends mainly on the elevation of arterial pressure with little contribution of the L-arginine pathway. Furthermore, the very small and non significant increase in the cross-sectional area of the basilar arteries from L-NAME-treated rats (growth index of 8%), suggest that nitric oxide does not play an important role in the modulation of normal cerebral vascular growth in vivo.
Arch Mal Coeur Vaiss 1995 Aug
PMID:[Effect of chronic inhibition of nitric oxide synthesis on vascular structure: remodeling or growth?]. 857 61

Although it is clear that vascular endothelial cells synthesize and release endothelin (ET), the contribution of this vasconstrictor peptide to the regulation of vascular tone appears limited in normal conditions. One possibility to explain this moderate effect is that continuous production of nitric oxide (NO) may permanently inhibit the release and the vasoconstrictor effects of ET. In these conditions, inhibition of NO synthesis might unmask a vasopressor response to ET. Thus, we tested whether bosentan (3 mg/kg i.v.), a non-peptide antagonist of ETA and ETB receptors, or BQ-123 (3 mg/kg), an antagonist of ETA receptors, affected the hypertensive response induced by the NO synthase inhibitors NG-nitro-L-arginine methyl ester (L-NAME 3 mg/kg) or NG-nitro L-arginine (3 mg/kg) in anesthetized, normotensive rats. Bosentan or BQ-123 did not affect blood pressure. L-NAME significantly increased mean arterial pressure (% increase from baseline: 25 +/- 5%), and this was reduced by bosentan (13 +/- 3%; p < 0.05) or by BQ-123 (14 +/- 5%; p < 0.01). In contrast, bosentan did not affect the pressor response to phenylephrine. The response to L-NAME (3 mg/kg) was also reduced by bosentan in ganglion-blocked (chlorisondamine: 2.5 mg/kg; controls 89 +/- 10; bosentan: 45 +/- 7%) or pithed rats (controls: 165 +/- 9; bosentan 85 +/- 12%; p < 0.01). Bosentan also inhibited the pressor response to NG-nitro L-arginine (3 mg/kg-1) in normal (controls 24 +/- 5, bosentan 10 +/- 3%; p < 0.01) or ganglion-blocked rats (controls 86 +/- 13; bosentan 25 +/- 8; p < 0.01). Finally, L-NAME induced a modest increase in plasma levels of ET-1 (controls: 26.8 +/- 4.1; L-NAME: 38.5 +/- 3.3 pg/ml; p < 0.05). Thus, acute inhibition of NO synthesis unmasks a tonic vasopressor influence of ET.
Arch Mal Coeur Vaiss 1995 Aug
PMID:[Demonstration of a vasopressor role of endogenous endothelin after inhibition of nitric oxide synthesis in rats]. 857 76

The aim of this study was to investigate, using spectral analysis, 1) the blood pressure (BP) variability changes in the conscious rat during blockade of nitric oxide (NO) synthesis by the L-arginine analogue L-NAME; 2) the involvement of the renin-angiotensin system in these modifications, using the angiotensin II AT1-receptor antagonist losartan. The blockade of the NO synthesis was made by infusion for 1 hour of a low dose (10 micrograms/kg/min, i.v.; n = 10) and a high dose (100 micrograms/kg/min, i.v.; n = 10) of L-NAME. The same treatment was applied in two further groups (n = 2 x 10) after a bolus of losartan (10 mg/kg, i.v.). The low dose of L-NAME increased systolic BP (SBP) on and after thirty min of infusion (+10 +/- 3 mmHg; p < 0.01). BP reached a maximum value 5 min after stopping L-NAME administration (+20 +/- 4 mmHg; p < 0.001). With the high dose of L-NAME, SBP increased immediately (5 min: +8 +/- 2 mmHg; p < 0.05) and reached a maximum at 40 min (+53 +/- 4 mmHg; p < 0.001); a bradycardia was observed (60 min: -44 +/- 13 batt/min; p < 0.01). The low dose of L-NAME increased the low-frequency component (LF: 0.02-0.2 Hz) of SBP variability (50 min: 6.7 +/- 1.7 mmHg2 vs 3.4 +/- 0.5 mmHg2; p < 0.05). The high dose of L-NAME increased the LF component (40 min: 11.7 +/- 2 mmHg2 vs 2.7 +/- 0.5 mmHg2; p < 0.001) and decreased the mid frequency (MF: 0.2-0.6 Hz) component (60 min: 1.14 +/- 0.3 mmHg2 vs 1.7 +/- 0.1 mmHg2, p < 0.05) of SBP. Losartan did not modify BP levels but had a tachycardic effect (+33 +/- 10 batt/min; n = 27). Moreover, losartan increased MF oscillations of SBP (4.26 +/- 0.49 mmHg2 vs 2.43 +/- 0.25 mmHg2; p < 0.001; n = 27). Losartan prevented the BP rise provoked by the low-dose of L-NAME and delayed the BP rise provoked by the high-dose. Losartan prevented the amplification of the LF oscillations of SBP induced by the L-NAME; the decrease of the MF oscillations of SBP induced by the L-NAME was reinforced after losartan). We concluded that the renin-angiotensin system is involved in the increase of variability of SBP in the LF range which resulted from the withdrawal of the vasodilatating influence of NO. We proposed that NO could counterbalance LF oscillations provoked by the activity of the renin-angiotensin system.
Arch Mal Coeur Vaiss 1996 Aug
PMID:[Contribution of the renin-angiotensin system to the variability of blood pressure in hypertensive rat after blockade of nitric oxide synthesis]. 894 70

One hundred patients operated for left atrial myxoma in the same surgical department underwent clinical and anatomical assessment at long-term from 1959 to July 1995 (66 women and 34 men, average age 52.2 years). The clinical presentation was related to mitral valve obstruction in half the cases (dyspnoea, cough, pulmonary oedema), the presentation in the other half of cases being very variable. The widespread use of echocardiography has relegated other investigations to a subsidiary role: auscultation, radiology, ECG (9 cases diagnosed by echocardiography performed for another indication). Serious complications of left atrial myxoma include systemic embolism : 37 cases out of the 100 in this series, including 10 plurifocal but mainly cerebral (19 cases including 11 isolated cerebral emboli). Surgical treatment is well established, should not be deferred and gives excellent results (2 early postoperative deaths out of 100 cases in the early years of the study). There were 6 cases of recurrences including 3 cases of Carney's syndrome. Clinico-pathological correlations showed that mitral stenotic effects occurred when the tumour diameter exceeded 5 cm and embolism was associated with tumours having multiple villositi. Histopathological analysis distinguished between active and inactive tumours, differentiated or not, and enabled the elaboration of hypotheses on the rate of growth of the tumour and on the absence of true metastases. Histopathological techniques also show the presence of lymphoplasmocytic infiltration, the sign of secretion of interleukin 6 by the myxoma, a cytokine involved in the general inflammatory process and which explains the unusual clinical presentation sometimes observed.
Arch Mal Coeur Vaiss 1996 Sep
PMID:[Myxoma of the left atrium, Clinical outcome of 100 operated patients]. 895 35


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