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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)
...
PMID:Plasma renin activity and the renal response to nitric oxide synthesis inhibition. 147 24
NO synthase is present in magnocellular neurons of supraoptic and paraventricular nuclei as well as in the posterior pituitary gland and may participate in control of vasopressin secretion. To test this possibility, experiments were performed in conscious, chronically prepared rabbits to determine the effect of NO synthesis inhibition with NG-nitro-L-arginine methyl ester hydrochloride (L-
NAME
) on basal vasopressin secretion and vasopressin responses to increased plasma osmolality (hypertonic saline infusion; P osm) and decreased blood pressure (nitroprusside infusion). L-
NAME
infusion (0.5 mg.kg-1 x min-1 i.v.) increased mean arterial pressure [MAP; 82.6 +/- 3.4 to 93.0 +/- 3.0 mmHg (P < 0.02)], decreased heart rate [HR; 242 +/- 12 to 209 +/- 9 beats/min (P < 0.02)], decreased plasma renin activity [
PRA
; 3.1 +/- 0.6 to 2.0 +/- 0.6 ng.ml-.2 h-1 (P < 0.001)], and increased plasma vasopressin concentration [P AVP; 2.2 +/- 0.3 to 4.5 +/- 1.0 pg/ml (P < 0.05)]. P(osm) did not change. Hypertonic saline infusion did not change MAP or HR but decreased
PRA
[4.3 +/- 0.8 to 0.9 +/- 0.2 ng.ml-1 x 2 h-1 (P < 0.01)], increased P(osm) [284 +/- 1 to 305 +/- 2 mosmol/kg H2O (P < 0.001)], and increased PAVP [2.8 +/- 0.3 to 12.7 +/- 2.7 pg/ml (P < 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Effect of inhibition of nitric oxide synthesis on vasopressin secretion in conscious rabbits. 751 50
This study aimed to examine the role of local autacoids for the regulation of renin secretion and renin gene expression by the renal perfusion pressure. To this end the effects of unilateral reduction of renal perfusion by 0.2 mm clips on plasma renin activity and on renal renin mRNA levels were examined in rats treated with the cyclooxygenase inhibitor meclofenamate (8 mg/kg body wt, twice a day), with the NO-synthase inhibitor nitro-L-arginine-methylester (L-
NAME
, 40 mg/kg body wt, twice a day) or with a combination of both. L-
NAME
alone decreased basal
PRA
values from 9.9 to 5.4 ng Ang I/hr x ml, while meclofenamate alone and the combination meclofenamate/L-
NAME
had no consistent effect on basal
PRA
. Unilateral renal artery clipping increased
PRA
values from 9.9 ng Ang I/hr x ml to 34, 27, and 16 ng Ang I/hr x ml in vehicle, meclofenamate, and L-
NAME
treated animals, respectively, but did not increase
PRA
in meclofenamate/L-
NAME
treated rats (9.5 ng Ang I/hr x ml). Renal renin mRNA levels in the clipped kidneys increased 4.8-, 2.6-, 2.5- and 1.8-fold in the clipped kidneys in vehicle, meclofenamate, L-
NAME
and meclofenamate/L-
NAME
injected animals, respectively. These findings indicate that both the inhibition of prostaglandin synthesis and of the formation of endothelium-derived relaxing factor (EDRF) attenuate the increase of renin gene expression and of renin secretion in response to acute unilateral renal hypoperfusion and that the effects of both maneuvers are additive.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Renal autacoids are involved in the stimulation of renin gene expression by low perfusion pressure. 785 91
In anesthetized rats, renal perfusion is largely regulated by a balance between the vasodilator influence of endothelium-derived nitric oxide (EDNO) and angiotensin II (AII)-mediated vasoconstriction. However, in conscious rats, which are characterized by lower
PRA
, the influence of AII is largely dissipated. To determine whether chronically increasing
PRA
enhances the interaction between AII and EDNO in regulating renal perfusion, radioactive microspheres were used to assess RBF in conscious sodium-depleted rats.
PRA
of control rats on a standard diet was 2.3 +/- 0.3 ng of AI/mL per hour compared with 16.8 +/- 1.5 ng of AI/mL per hour (P < 0.001) for rats on a sodium-restricted diet. In 12 rats on a standard diet, the inhibition of EDNO synthesis with L-Nw-nitroarginine methyl ester (L-NAME) increased blood pressure (BP) from 111 +/- 2 to 135 +/- 3 (P < 0.001) and decreased RBF by 47% (from 8.0 +/- 0.6 to 4.3 +/- 0.3 mL/min per gram kidney wt; P < 0.001). Renal vascular resistance (RVR) increased by 132% (from 14.9 +/- 1.2 to 34.7 +/- 3.3 resistance units (RU); P < 0.001). Pretreatment with Losartan, an AII receptor antagonist, did not modify the changes in BP, RBF, and RVR induced by L-
NAME
.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Angiotensin II: endothelium-derived nitric oxide interaction in conscious rats. 801 77
We have reported that inhibition of nitric oxide synthesis with N(G)-nitro-L-arginine methyl ester (L-
NAME
) attenuates the renin secretory response to beta adrenoceptor stimulation. We proposed that the attenuation results from disinhibition of the cyclic GMP-inhibitable isoform of phosphodiesterase (PDE III) with a resultant increase in cyclic AMP hydrolysis in the juxtaglomerular cells. In our investigation, experiments were performed in conscious rabbits to test the effects of the specific PDE III inhibitor milrinone on resting renin secretion and on the renin responses to isoproterenol and L-
NAME
. In the first series of experiments, infusion of milrinone increased plasma renin activity from 5.4 +/- 0.6 to 10.2 +/- 1.4 ng/ml/2 hr (P < .01). Heart rate increased markedly, but arterial pressure did not change. In the second series, infusion of isoproterenol increased plasma renin activity from 6.3 +/- 1.1 to 15.0 +/- 1.0 ng/ml/2 hr (P < .01). The renin response to isoproterenol was increased (P < .01) in the presence of milrinone (15.3 +/- 3.7 to 38.4 +/- 6.2 ng/ml/2 hr, P < .01). In the third series, L-
NAME
alone decreased plasma renin activity from 5.0 +/- 1.0 to 3.3 +/- 1.0 ng/ml/2 hr (P < .01). Milrinone again increased plasma renin activity and prevented the suppression of plasma renin activity by L-
NAME
. By contrast, milrinone did not alter the suppression of plasma renin activity produced by infusion of phenylephrine. In addition, a PDE IV inhibitor failed to prevent the suppression of
PRA
by L-
NAME
. Finally, administration of milrinone completely reversed the L-
NAME
-induced suppression of the renin response to isoproterenol. These results provide evidence that PDE III participates in the regulation of renin secretion, and support the proposal that the L-
NAME
-induced reductions in renin secretion and in the renin response to beta adrenoceptor stimulation result from disinhibition of PDE III and increased hydrolysis of cyclic AMP in the juxtaglomerular cells.
...
PMID:Role of cyclic GMP-inhibitable phosphodiesterase and nitric oxide in the beta adrenoceptor control of renin secretion. 876 33
To assess the interaction of endothelin (ET) with nitric oxide (NO) and the effects on venous circulation and handling of renal water and electrolytes, ET (1.0 ng/kg/min) or saline was administered with or without three doses (0.27, 2.7 and 27 ng/kg/min for 40 min) of N omega-nitro-L-arginine methyl ester (L-
NAME
), and NO synthase inhibitor, in anesthetized dogs. ET increased total peripheral resistance (TPR), pulmonary capillary wedge pressure (PCWP), urine flow (UF), and urinary K excretion (UKV), and decreased cardiac output (CO), urinary osmolality (Uosm), renal plasma flow (RPF), and glomerular filtration rate (GFR). L-
NAME
increased blood pressure (BP), TPR, PCWP, right atrial pressure (RAP), and mean circulatory filling pressure (MCFP), and decreased CO, RPF, and GFR, ET plus L-
NAME
markedly increased TPR, resistance to venous return, and plasma atrial natriuretic peptide (ANP), but not BP and MCFP, and curtailed the ET-induced responses in UF, UKV, and Uosm. Plasma aldosterone (ALD) was decreased in all groups, but plasma vasopressin (AVP) and renin activity (
PRA
) were not altered in any group. These results indicate that ET-induced NO formation might mitigate increases in venous as well as arterial vascular resistance and changes in renal handling of water and electrolytes, and might also play an inhibitory role in ANP release but not in
PRA
or AVP and ALD release.
...
PMID:Effects of endothelin-induced nitric oxide on venous circulation and renal water-electrolyte handling. 959 20
To test the hypothesis that NO influences aldosterone production in humans, we examined the effect of N(G)-nitro-L-arginine methyl ester (L-
NAME
) on aldosterone concentrations in the presence and absence of the NO precursor L-arginine (3 g TID) and the angiotensin-converting enzyme inhibitor ramipril (10 mg QD). Ten normal subjects were given L-
NAME
(66 microg/kg per min for 30 minutes) or vehicle in random order on separate days during placebo and after randomized, double-blind treatment with L-arginine, ramipril, or L-arginine plus ramipril. Infusion of L-
NAME
significantly increased systolic blood pressure (all P<0.05) and decreased heart rate (all P< or =0.02) during all 4 treatment arms. After placebo pretreatment, serum aldosterone was significantly higher during L-
NAME
infusion than during vehicle (6.6+/-1.7 versus 3.3+/-0.5 ng/dL; P=0.045). Combined treatment with L-arginine plus ramipril abolished this effect. There was no effect of L-
NAME
on plasma renin activity (
PRA
; P=0.297) or angiotensin II concentrations (P=0.537). However, there was a significant interactive effect of L-
NAME
and time on serum potassium (P=0.039). There was a significant linear relationship between
PRA
and aldosterone concentration after vehicle infusion ([aldosterone]=3.9.PRA+1.9; r2=0.476; P=0.027) and L-
NAME
infusion ([aldosterone]=7.2.PRA+3.1; r2=0.457; P=0.032), and the intercepts of these lines were different (P=0.029). There was a significant linear relationship between serum potassium and aldosterone during L-
NAME
([aldosterone]=8.2 . [potassium]-28.9; r2=0.609; P=0.008) but not during vehicle (P=0.313). These data suggest that endogenous NO modulates aldosterone synthesis in humans.
...
PMID:NO synthase inhibition increases aldosterone in humans. 1538 75
