UMLS:C0406810 - FACTA Search

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Query: UMLS:C0406810 (NAME)
13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In addition to stretch, some hormones and neurotransmitters influence atrial natriuretic factor (ANF) secretion from the mammalian heart. In the present study, we investigated the effect of specific inhibition of nitric oxide/endothelium-derived relaxing factor (NO/ EDRF) on release of ANF from the isolated spontaneously beating heart during basal conditions and in response to arginine vasopressin (AVP; 3 x 10(-8) M), acetylcholine (ACh; 10(-6) M), and angiotensin II (ANG II; 4 x 10(-7) M) to determine whether NO is involved as a mediator of basal and hormone-modulated secretion of ANF. Basal secretion from control hearts remained stable for the duration of the experiment. Intracoronary perfusion of the heart with AVP, ACh, and ANG II reduced ANF secretion significantly by 58 +/- 4, 51 +/- 6, and 26 +/- 8%, respectively, independently of concomitant changes in coronary flow and heart rate. The NO donor sodium nitroprusside (SNP, 10(-4) M) inhibited ANF secretion comparably to AVP and ACh. The effect of SNP was not affected by inhibition of NO synthase activity with NG-nitro-L-arginine methyl ester (L-NAME; 3 x 10(-5) M). Similarly, L-arginine, (3 x 10(-4) M) but not its stereoisomer D-arginine (3 x 10(-4) M), significantly reduced ANF secretion. Subsequent perfusion with AVP singly or in combination with L-arginine or D-arginine did not affect ANF secretion further. The inhibitor of NO synthase NG-monomethyl-L-arginine (L-NMMA, 3 x 10(-5) M) did not affect basal secretion, but prevented the inhibitory effect of AVP and ACh. The effect of ANG II was not changed by L-NMMA. These results indicate that AVP and ACh inhibit ANF secretion in the isolated heart indirectly by stimulating NO/EDRF and suggest a novel function of NO/EDRF as a negative modulator of ANF secretion.
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PMID:Effect of nitric oxide inhibition on secretion of atrial natriuretic factor in isolated rat heart. 876 65

Previous studies have demonstrated that the nitric oxide (NO) synthase inhibitor L-NAME exerts positive effects on the arginine vasopressin (AVP) and oxytocin (OT) responses to insulin-induced hypoglycemia, suggesting inhibitory actions of NO. The present study was designed to determine whether a gamma-aminobutyric acid (GABA)ergic pathway is involved in regulation of NO action. AVP and OT secretory patterns during insulin (0.15 IU/kg, i.v.)-tolerance tests (ITT) were examined in seven normal male subjects with (experimental tests) and without (control test) concomitant treatment with L-NAME (40 micrograms/kg injected plus 50 micrograms/kg infused, i.v.), the GABAergic agent sodium valproate (600 mg in three divided doses orally) or the combination of L-NAME and sodium valproate. Insulin-induced hypoglycemia increased by 2-fold (peak vs. baseline) plasma AVP and OT levels. In the presence of L-NAME, plasma AVP and OT levels rose 3-fold in response to hypoglycemia and were significantly higher than those in the control test. Administration of sodium valproate alone changed neither AVP nor OT secretory patterns during ITT. In contrast, sodium valproate abolished the facilitating effect of L-NAME on both AVP and OT responses to hypoglycemia. In the ITT plus L-NAME plus sodium valproate test, plasma AVP and OT levels were not significantly different at any time point from those observed during the control ITT. These data indicate a GABAergic mediation of the inhibitory modulation by NO of the AVP and OT responses to insulin-induced hypoglycemia.
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PMID:Gamma-aminobutyric acid mediation of the inhibitory effect of nitric oxide on the arginine vasopressin and oxytocin responses to insulin-induced hypoglycemia. 895 1

In view of the fact of the high concentration of neuronal nitric oxide synthase (NOS) in the supraoptic and paraventricular nuclei as well as the posterior pituitary, it has been supposed that nitric oxide (NO) may be involved in the regulation of hormone secretion from these sites. In the present study, L-arginine, the precursor of NO, and N(omega)-nitro-L-arginine methyl ester (L-NAME), the NOS inhibitor, were intracerebroventricularly (i.c.v.) administered into the pentobarbital anesthetized rats. The results showed that plasma arginine vasopressin (AVP) concentration increased after the injection of L-arginine (1.0 mg in microliters, i.c.v.) and decreased after the L-NAME (270 micrograms in 5 microliters, i.c.v.). The elevated plasma AVP level in response to short-term hypotension induced by intravenous infusion of sodium nitroprusside was also significantly reduced by i.c.v. administration of L-NAME. The results indicate that NO acts as a stimulating factor to both the basal and reflex release of AVP, opposing the view that NO plays an inhibitory role in the regulation of AVP secretion.
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PMID:Nitric oxide stimulates both the basal and reflex release of vasopressin in anesthetized rats. 901 78

The goals of this study were to determine whether long-term nitric oxide (NO) synthesis inhibition in dogs results in an increase in the sodium sensitivity of arterial pressure and whether changes in plasma renin activity or the plasma concentrations of arginine vasopressin (AVP) and aldosterone play an important role in this hypertension. Studies were conducted in a control group and groups that received NO inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) at 10 or 25 microg x kg(-1) x min(-1). Each group was challenged with normal, low, and high sodium intake for periods of 5 days each. Urinary nitrate + nitrite excretion (UNOx) more than doubled in the control group during high sodium intake. In both L-NAME groups, UNOx decreased significantly, there was a hypertensive shift in the relation between urinary sodium excretion and arterial pressure, and urinary sodium excretion remained normal even in the high-sodium intake period. L-NAME infusion did not change the sodium sensitivity of arterial pressure or plasma renin activity, plasma aldosterone, and plasma AVP. In conclusion, the data suggest that, in dogs, increases in NO synthesis are not necessary to excrete a chronic sodium load, and decreases in NO do not increase the sodium sensitivity of arterial pressure.
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PMID:Role of nitric oxide in the arterial pressure and renal adaptations to long-term changes in sodium intake. 914 16

1. Increased production of nitric oxide (NO) has been suggested to underlie both the vascular hyporeactivity to vasoconstrictors and the splanchnic vasodilatation seen in portal hypertension. This study assessed the role of NO in the vasoconstrictor hyporeactivity of portal vein-ligated (PVL) rats in isolated and in situ perfused mesenteric arterial beds. 2. Isolated perfused mesenteric arteries of PVL rats were significantly less reactive to noradrenaline (NA), methoxamine (METH), arginine vasopressin (AVP) and endothelin-1 (ET-1) than those from sham-operated (Sham) rats. 3. Blockade of NO synthesis with NG-nitro-L-arginine methyl ester (L-NAME, 100 microM) in isolated perfused mesenteric arteries from PVL rats restored the reactivity to bolus injections of AVP and ET-1, but had little effect on the hyporeactivity to NA or METH. Cyclo-oxygenase inhibition with indomethacin (5 microM) likewise did not restore reactivity to METH of isolated perfused mesenteric arteries of PVL rats. 4. The hyporeactivity to METH seen in isolated perfused mesenteric arteries from PVL rats was reduced by low concentrations of AVP (20 nM) or ET-1 (1 nM) which per se caused only a slight increase in perfusion pressure. When L-NAME (100 microM) was combined with AVP (20 nM) or ET-1 (1 nM), respectively, reactivity to METH of isolated perfused mesenteric arteries of PVL rats was restored to the level seen in Sham rats. These effects of AVP and ET-1 were not mimicked by precontracting the vessels with 5-hydroxytryptamine (5 microM). 5. The differential effects of L-NAME and AVP on the hyporesponsiveness to methoxamine and AVP were corroborated by experiments performed with the in situ perfused mesenteric vascular bed preparation. 6. These data indicate that both NO-dependent and NO-dependent mechanisms are involved in the vasoconstrictor hyporesponsiveness of mesenteric arteries from portal hypertensive rats. The hyporeactivity to AVP and ET-1 is mediated by NO whereas the reduced responsiveness to adrenoceptor agonists appears to be predominantly NO-independent AVP and ET-1, in addition, seem to inhibit the NO-independent mechanism of vascular hyporeactivity, since the hyporesponsiveness to METH was reduced in the presence of AVP or ET-1 and abolished by the combination of these peptides with L-NAME.
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PMID:Nitric oxide-dependent and -independent vascular hyporeactivity in mesenteric arteries of portal hypertensive rats. 922 64

Nitric oxide (NO) has been shown to down regulate its own synthesis in vitro. We tested the hypothesis that NO inhalation (30 ppm under normoxic conditions) could decrease the release of endogenous endothelial NO, and thus alter pulmonary vasoreactivity. Pulmonary vasoreactivity was assessed in isolated perfused rat lungs immediately or 6 h after a 48 h NO inhalation period, and compared with a control group. NO inhalation resulted in an increase in pulmonary vasoconstrictor reactivity to angiotensine II and U-46619, a reduction in the potentiation by the eNOS inhibitor L-NAME of the angiotensine II response, a decrease in endothelium-dependent vasodilation to arginine vasopressin, whereas non-endothelium-dependent vasodilation to sodium nitroprusside remained unaltered. These alterations returned to control values in the group studied 6 h after the end of NO inhalation, and were not prevented by inhibition of the prostanoid synthesis, or by pretreatment with the endothelin receptors antagonist Bosentan. These results indicate that NO inhalation over 2 d induces a reversible alteration of pulmonary vasoreactivity in relationship with a decrease in endogenous NO release. Inhibition of eNOS could be involved.
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PMID:Effect of 48 hours of nitric oxide inhalation on pulmonary vasoreactivity in rats. 927 26

This study was conducted to determine the effect of stevioside (SVS) on glucose metabolism. The experiments were performed in male Wistar rats treated with SVS either by intravenous infusion or feeding. SVS infusion (150 mg/mL) was carried out in doses of 0.67, 1.00, and 1.33 mL.kg-1 body weight.h-1. The plasma glucose level significantly increased both during and after SVS infusion, whereas it was not affected by SVS feeding (13.3 mL.kg-1 body weight). The glucose turnover rate (GTR) of [14C(U)]glucose and [3(-3)H]glucose was not significantly different between control and SVS infusion animals. Percent glucose carbon recycling and glucose clearance were reduced from 28.7 +/- 1.3 to 23.0 +/- 1.6% (p < 0.05) and from 6.46 +/- 0.34 to 4.99 +/- 0.20 mL.min-1.kg-1 body weight (p < 0.01), respectively. The plasma insulin level did not change, whereas the plasma glucose level significantly increased from 120.3 +/- 5.9 to 176.8 +/- 10.8 mg% (p < 0.01) during SVS infusion. Animals pretreated with angiotensin II and arginine vasopressin showed no significant effect, while animals pretreated with prazosin had an attenuated hyperglycemic effect of SVS infusion. Pretreatment with indomethacin or N omega-nitro-L-arginine methyl ester (L-NAME) alleviated the plasma glucose level during the second period of SVS infusion. Pretreatment with the combination infusion of indomethacin and L-NAME reduced the plasma glucose level from 117.0 +/- 1.8 to 109.0 +/- 1.7 mg% (p < 0.001), and normalized the plasma glucose level in the second period of SVS infusion. Insulin infusion inhibited the hyperglycemic effect of SVS infusion. The present results show that the elevation of the plasma glucose level during SVS infusion is not due to the reduction of the insulin level. It is probably the effect of SVS on glucose transport across the cell. Insulin response to a high plasma glucose level is suppressed during SVS infusion. Several interactions among norepinephrine, prostaglandin, and nitric oxide are involved in modulating the hyperglycemia during SVS infusion.
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PMID:The effect of stevioside on glucose metabolism in rat. 936 11

1. The haemodynamic effects of angiotensin II (AII) and, for comparison, arginine vasopressin (AVP) in the femoral and superior mesenteric artery of urethane-anaesthetized rats were analysed with the ultrasonic transit time shift technique. 2. I.v. bolus injection of AII (0.1-3 nmol kg-1) and AVP (0.03-1 nmol kg-1) increased blood pressure which was accompanied by a decrease in blood flow through the superior mesenteric artery and an increase in femoral blood flow. The femoral hyperaemia was in part due to vasodilatation as indicated by a rise of femoral vascular conductance up to 200% relative to baseline. The femoral vasodilatation caused by AVP, but not AII, was followed by vasoconstriction. 3. Blockade of angiotensin AT1 receptors by telmisartan (0.2-20 mumol kg-1) prevented all haemodynamic responses to AII. 4. The femoral dilator responses to AII and AVP depended on the increase in vascular perfusion pressure since vasodilatation was reversed to vasoconstriction when blood pressure was maintained constant by means of a gravity reservoir. However, the AII-evoked femoral vasodilatation was not due to an autonomic or neuroendocrine reflex because it was not depressed by hexamethonium (75 mumol kg-1), prazosin (0.25 mumol kg-1) or propranolol (3 mumol kg-1). 5. The AII-induced femoral vasodilatation was suppressed by blockade of nitric oxide (NO) synthesis with NG-nitro-L-arginine methyl ester (L-NAME, 40 mumol kg-1) and reversed to vasoconstriction when L-NAME was combined with indomethacin (30 mumol kg-1), but was left unaltered by antagonism of endothelin ETA/B receptors with bosentan (37 mumol kg-1). 6. These results demonstrate that the effect of AII to increase systemic blood pressure and the resulting rise of perfusion pressure in the femoral artery stimulates the formation of NO and prostaglandins and thereby dilates the femoral arterial bed. This local vasodilator mechanism is sufficient to mask the direct vasoconstrictor response to AII.
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PMID:Dilatation by angiotensin II of the rat femoral arterial bed in vivo via pressure/flow-induced release of nitric oxide and prostaglandins. 940 58

Normalization of the increased vascular nitric oxide (NO) generation with low doses of NG-nitro-L-arginine methyl ester (L-NAME) corrects the hemodynamic abnormalities of cirrhotic rats with ascites. We have undertaken this study to investigate the effect of the normalization of vascular NO production, as estimated by aortic cyclic guanosine monophosphate (cGMP) concentration and endothelial nitric oxide synthase (eNOS) protein expression in the aorta and mesenteric artery, on sodium and water excretion. Rats with carbon tetrachloride-induced cirrhosis and ascites were investigated using balance studies. The cirrhotic rats were separated into two groups, one receiving 0.5 mg/kg per day of L-NAME (CIR-NAME) during 7 d, whereas the other group (CIR) was administrated the same volume of vehicle. Two other groups of rats were used as controls, one group treated with L-NAME and another group receiving the same volume of vehicle. Sodium and water excretion was measured on days 0 and 7. On day 8, blood samples were collected for electrolyte and hormone measurements, and aorta and mesenteric arteries were harvested for cGMP determination and nitric oxide synthase (NOS) immunoblotting. Aortic cGMP and eNOS protein expression in the aorta and mesenteric artery were increased in CIR as compared with CIR-NAME. Both cirrhotic groups had a similar decrease in sodium excretion on day 0 (0.7 versus 0.6 mmol per day, NS) and a positive sodium balance (+0.9 versus +1.2 mmol per day, NS). On day 7, CIR-NAME rats had an increase in sodium excretion as compared with the CIR rats (sodium excretion: 2.4 versus 0.7 mmol per day, P < 0.001) and a negative sodium balance (-0.5 versus +0.8 mmol per day, P < 0.001). The excretion of a water load was also increased after L-NAME administration (from 28+/-5% to 65+/-7, P < 0.05). Plasma renin activity, aldosterone and arginine vasopressin were also significantly decreased in the CIR-NAME, as compared with the CIR rats. The results thus indicate that normalization of aortic cGMP and eNOS protein expression in vascular tissue is associated with increased sodium and water excretion in cirrhotic rats with ascites.
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PMID:Nitric oxide synthase (NOS) inhibition for one week improves renal sodium and water excretion in cirrhotic rats with ascites. 942 86

To examine the role of vasopressin V1 and V2 receptors, nitric oxide and prostanoids in the coronary vascular effects of [Arg8]vasopressin, coronary blood flow was measured with an electromagnetic flow transducer placed around the left circumflex (23 goats) or anterior descending (11 goats) coronary artery and vasopressin (0.03-1 microg) was intracoronarily injected in 34 anesthetized, open-chest goats. Basal mean values for coronary blood flow, mean systemic arterial pressure and heart rate, were 34 +/- 2.38 ml/min, 89 +/- 3.34 mmHg and 80 +/- 3.06 beats/min, respectively. Vasopressin produced dose-dependent decreases in coronary blood flow and the maximal reduction of this flow, attained with 1 microg of vasopressin, was 14 +/- 1.49 ml/min (42 +/- 2.64% of basal flow) (P < 0.01). Desmopressin (0.03-1 microg; 8 goats) did not affect significantly coronary blood flow. The intracoronary infusion of the antagonist for vasopressin V1 receptors d(CH2)5Tyr (Me) arginine vasopressin (2 microg/min per kg, 6 animals) significantly diminished the effects of vasopressin on coronary blood flow (the effects of 1 microg of vasopressin were reduced by 28%, P < 0.05). The mixed antagonist for vasopressin V1 and V2 receptors desGly-d(CH2)5-D-Tyr(Et)Val arginine vasopressin (0.2, 0.7 and 2 microg/min per kg, 9 animals) decreased in a dose-dependent manner the effects of vasopressin on coronary blood flow (the effects of 1 microg of vasopressin were decreased by 61% with 2 microg/min per kg, P < 0.01). Intracoronary infusion of saline (vehicle, 3 goats) did not change the effects of vasopressin on coronary blood flow. Intravenous administration of the inhibitor of nitric oxide synthesis N-omega-nitro-L-arginine methyl ester (L-NAME, 47 mg/kg, 9 animals) decreased resting coronary blood flow by 10% (P < 0.01) and augmented mean systemic arterial pressure by 20% (P < 0.01), without changing heart rate. During this treatment the reduction in coronary blood flow produced by vasopressin was higher than under control (the effects of 1 microg of vasopressin were increased by 28%, P < 0.01). Intravenous administration of the inhibitor of cyclooxygenase, meclofenamate (5 mg/kg, 7 animals), neither modified resting coronary blood flow, arterial pressure and heart rate nor the effects of vasopressin on this flow. These data indicate that vasopressin produces marked coronary vasoconstriction and suggest that: (a) it may be mediated by vasopressin V1 receptors, without involvement of vasopressin V2 receptors, (b) it is probably inhibited by nitric oxide under normal conditions and (c) it may be not modulated by prostanoids.
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PMID:Coronary vasoconstriction produced by vasopressin in anesthetized goats. Role of vasopressin V1 and V2 receptors and nitric oxide. 954 90

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