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Query: UMLS:C0406810 (
NAME
)
13,345
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
1. The roles of the tissue kallikrein-kinin system and nitric oxide (NO) release in Phoneutria nigriventer venom-induced relaxations of rabbit corpus cavernosum (RbCC) smooth muscle have been investigated by use of a bioassay cascade. 2. Phoneutria nigriventer venom (10-30 micrograms), porcine pancreatic kallikrein (100 mu), rabbit urinary kallikrein (10 mu), bradykinin (BK, 0.3-3 nmol), acetylcholine (ACh, 0.3-30 nmol) and glyceryl trinitrate (GTN, 0.5-10 nmol) caused relaxations of the RbCC strips.
Captopril
(1 microM) substantially potentiated Phoneutria nigriventer venom- and BK-induced RbCC relaxations without affecting those elicited by GTN. 3. The bradykinin B2 receptor antagonist, Hoe 140 (D-Arg-[Hyp3,Thi5,D- Tic7,Oic8]-BK, 50 nM), aprotinin (10 micrograms ml-1) and the tissue kallikrein inhibitor, Pro-Phe-Aph-Ser-Val- Gln-NH2 (KIZD-06, 1.3 microM) significantly inhibited Phoneutria nigriventer venom-induced RbCC relaxations, without affecting those provoked by GTN and ACh. The B1 receptor antagonist, [Leu9]des Arg10BK (0.5 microM) and soybean trypsin inhibitor (SBTI, 10 micrograms ml-1) had no effect on Phoneutria nigriventer venom-induced RbCC relaxations. 4. The relaxations induced by Phoneutria nigriventer venom, porcine pancreas kallikrein, BK and ACh were significantly inhibited by N omega-nitro-L-arginine methyl ester (L-
NAME
, 10 microM) but not by D-
NAME
(10 microM). L-
NAME
did not affect GTN-induced relaxations. L-Arginine (300 microM), but not D-arginine (300 microM), significantly reversed the inhibitory effect of L-
NAME
. 5. Our results indicate that Phoneutria nigriventer venom activates the tissue kallikrein-kininogen-kinin system in RbCC strips leading to NO release and suggest a functional role for this system in penile erection.
...
PMID:Pharmacological characterization of rabbit corpus cavernosum relaxation mediated by the tissue kallikrein-kinin system. 752 16
This study was designed to examine if acute systemic blockade of nitric oxide (NO) production by inhibition of nitric oxide synthase (NOS) with N-omega-nitro-L-arginine methyl ester (L-
NAME
) would worsen the severity of ischemic acute renal failure (ARF). Initially three groups of rats, were studied: 45 min of bilateral renal ischemia (I) alone, Group I; L-
NAME
(L; 10 mg/kg BW, i.v.) alone, Group L; and L-
NAME
administered 15 min before renal ischemia, Group L+I. We observed, however, a 60% mortality in Group I+L during the first 4 h of reflow.
Captopril
, administered acutely 15 min before L-
NAME
in an attempt to offset any detrimental effects of increased angiotensin II generation in response to renal ischemia, failed to obviate the mortality because 67% of rats in this group (Group C+L+I) also died. Therefore, additional studies were performed in rats instrumented for cardiovascular studies to evaluate the acute hemodynamic responses during the first 90 min of reperfusion following renal ischemia in rats pretreated with L-
NAME
. As expected, L-
NAME
injection was accompanied by a 25-30 mm Hg increase in mean systemic arterial pressure (SAP) (p < 0.05), a bradycardia (p < 0.02), and a decrease in cardiac output (CO) (p < 0.02). The increase in SAP was due exclusively to an increase in systemic vascular resistance (SVR) (p < 0.01). Ischemia and reflow in the L-
NAME
-treated rats were attended by a progressive increase in SVR and a progressive decrease in CO such that by the end of 45 min of reperfusion SVR had increased 10-fold and CO had decreased to one third of its initial rate (both p < 0.02). Pulmonary artery pressure (PAP) increased promptly following L-
NAME
injection. Total pulmonary resistance (PRT) increased significantly by the end of reperfusion. L-
NAME
in combination with renal ischemia and reflow induces a large increase in both SVR and PRT, and is accompanied by a 70% reduction in CO and substantial mortality.
...
PMID:Nitric oxide synthase inhibition and acute renal ischemia: effect on systemic hemodynamics and mortality. 756 11
We investigated the effects of inhibition of both nitric oxide (NO) synthesis and angiotensin converting enzyme (ACE) on agonist-induced relaxations in the coronary system. Chronically instrumented conscious dogs (n = 4) were prepared for the measurement of coronary blood flow (CBF), coronary diameter of the left circumflex artery (LCX), mean arterial blood pressure (MAP) and heart rate (HR). Intracoronary infusions of acetylcholine, adenosine and bradykinin were performed after intracoronary pretreatment of either vehicle, L-
NAME
(6 mg.kg-1), captopril (1 mg.kg-1) or both L-NAME+captopril. Acetylcholine bradykinin and adenosine caused dose-dependent increases in CBF and LCX. HR increased concomitantly.
Captopril
potentiated the vasodilating effects of bradykinin and acetylcholine on LCX and CBF significantly (P < or = 0.05) and those of adenosine slightly. L-
NAME
caused vasoconstriction, hypertension and bradycardia. The effects of acetylcholine on CBF were abolished during L-
NAME
treatment while bradykinin and adenosine responses were markedly reduced. When captopril and L-
NAME
were given simultaneously, the vasodilator responses to bradykinin but not to acetylcholine or adenosine were partially restored (P < or = 0.05). We conclude that in vivo, (a) adenosine possibly elicits endothelium-dependent dilation; (b) adenosine and bradykinin act in part independently of the L-arginine/NO pathway; (c) vasodilation to acetylcholine is potentiated by acute ACE inhibition via NO-dependent mechanisms.
...
PMID:Coronary vasodilation to acetylcholine, adenosine and bradykinin in dogs: effects of inhibition of NO-synthesis and captopril. 829 69
The effect of chronic inhibition of nitric oxide (NO) biosynthesis has been investigated in two models of acute inflammation induced by carrageenin, i.e., paw oedema and pleurisy. Chronic inhibition of NO biosynthesis was achieved by including N omega-nitro-L-arginine methyl ester (L-
NAME
) in the drinking water to give a dose of approximately 75 mumol/rat/day for 2 and 4 weeks. Control animals received either tap water alone or the inactive enantiomer D-
NAME
. Since chronic NO inhibition increases blood pressure, rats made hypertensive (2 kidney-1 clip model; 2K-1C) were used to evaluate the effect of hypertension on the carrageenin-induced paw oedema. In a separate set of experiments, L-
NAME
-treated animals concomitantly received captopril (140 mumol/rat/day) to prevent hypertension. Animals chronically treated with L-
NAME
(but not D-
NAME
) for 2 and 4 weeks developed hypertension to the same extent as 2K-1C rats. Carrageenin-induced paw oedema was significantly reduced in animals chronically treated with L-
NAME
, but not with D-
NAME
or in 2K-1C rats. Subplantar injection of iloprost completely reversed the inhibition of paw oedema caused by L-
NAME
.
Captopril
(140 mumol/rat/day) significantly lowered the high blood pressure levels induced by L-
NAME
but did not significantly affect the inhibition of paw oedema caused by L-
NAME
. No changes in vascular permeability, as assessed by Evans blue extravasation, were observed in L-
NAME
-treated animals. The chronic treatment with L-
NAME
for 2 and 4 weeks did not inhibit carrageenin-induced leucocyte migration and fluid exudation into the pleural cavity. Although carrageenin-induced paw oedema is reduced in L-
NAME
-treated rats, this response reflects a decrease in local blood flow rather than an effect on vascular permeability.
...
PMID:Effect of chronic nitric oxide synthesis inhibition on the inflammatory responses induced by carrageenin in rats. 856 27
Short-term infusions of angiotensin II (Ang II) increase renal vascular resistance and thereby endothelial shear stress and nitric oxide (NO) release. Prolonged stimulation of Ang II can decrease the expression of NO synthase isoforms in the macula densa, but prolonged increases in shear stress can increase transcription of endothelial NO synthase. Therefore, we designed these studies to test the hypothesis that Ang II exerts time-dependent effects on renal NO generation as assessed from renal excretion of nitrate and nitrite, percent increases in renal vascular resistance during inhibition of NO synthase with intravenous NG -nitro-L-arginine methyl ester (L-
NAME
), or decreases in renal vascular resistance during stimulation of endothelial NO synthase with intravenous acetylcholine. Rats were tested during graded short-term (30 to 90 minutes intravenous) or prolonged (5 to 6 days subcutaneous) Ang II infusions that led to dose-dependent increases in blood pressure and renal vascular resistance and reductions in renal blood flow.
Captopril
was administered for 3 to 4 days to suppress Ang II generation. The renal excretion of nitrate and nitrite was increased during short-term Ang II infusions (from 205 +/- 22 to 331 +/- 58 pmol.min-1, P < .05) but was unchanged during prolonged Ang II infusion (control group, 197 +/- 33 versus Ang II, 245 +/- 42 pmol.min-1, P=NS). The percent increase in renal vascular resistance with L-
NAME
was potentiated dose dependently by short-term but not long-term Ang II infusions. The increase in renal vascular resistance with L-
NAME
in control rats without Ang II infusions was +150 +/- 13%. At an Ang II infusion of 200 ng.kg-1.min-1, the L-
NAME
-induced percent increase in renal vascular resistance was significantly (P < .01) increased compared with controls in short-term Ang II-infused rats (+369 +/- 70%) but was not significantly different in prolonged infused rats (+190 +/- 33%). Intravenous acetylcholine caused dose-dependent renal vasodilation that was not significantly changed in rats receiving short-term intravenous Ang II but was significantly (P < .005) potentiated in those receiving prolonged Ang II infusions (change in renal vascular resistance with acetylcholine at 10 micrograms.kg-1.min-1 versus control, -21.5 +/- 5.0%; with short-term Ang II, -24.9 +/- 4.5%; with long-term Ang II, -52.1 +/- 7.2%). In conclusion, short- and long-term Ang II infusions caused equivalent changes in blood pressure and renal blood flow and hence presumably equivalent increases in endothelial shear stress. However, only short-term Ang II infusions increased NO generation and the dependence of the renal circulation on NO, whereas acetylcholine-induced NO release was enhanced selectively during long-term Ang II infusions. This suggests that during long-term Ang II, renal NO release may become uncoupled from shear stress yet remains highly responsive to receptor-mediated stimulation.
...
PMID:Role of nitric oxide in short-term and prolonged effects of angiotensin II on renal hemodynamics. 862 Dec 13
The role of nitric oxide (NO) in renal function was evaluated under conditions of elevated peripheral and renal sympathetic nerve activity (RSNA), achieved by bilateral carotid occlusion (CO) in anesthetized dogs. Renal function was monitored during CO with the NO system intact and with it blocked by the administration of L-
NAME
. With NO intact, CO increased arterial pressure and heart rate. With renal perfusion pressure held constant, CO also significantly decreased renal blood flow (RBF) and glomerular filtration rate (GFR) by 46% and 43%, respectively. CO, after L-
NAME
administration, resulted in a significantly exaggerated renal vasoconstriction. RBF and GFR decreased by 82% and 80%, respectively. Changes in water and sodium excretion were not different between the NO-intact and NO-blocked states during CO. These studies were also performed with the converting enzyme inhibitor,
Captopril
. The exaggerated renal hemodynamic responses to CO with NO synthesis inhibition were identical with or without
Captopril
. These findings indicate that under conditions of elevated peripheral and RSNA, NO plays an important role in modulating renal hemodynamics, but not sodium excretion. This effect does not appear to involve angiotensin II.
...
PMID:Nitric oxide attenuates the renal hemodynamic responses to increased peripheral and renal sympathetic nerve activity. 867 72
The aim of the study was to assess whether angiotensin converting enzyme (ACE) inhibition with captopril prevents the development of hypertension and myocardial hypertrophy and affects nitric oxide synthase (NOS) activity in rats. Animals were divided into five groups: control, two groups receiving NG-nitro-L-arginine methyl ester (L-
NAME
) 20 or 40 mg/kg/day, a group receiving captopril 100 mg/kg/day and a group concomitantly treated with 40 mg/kg/day L-
NAME
plus 100 mg/kg/day captopril. After four weeks, systolic blood pressure (SBP) significantly increased in both L-
NAME
groups by 30% and 34%, respectively. In the captopril group, SBP significantly decreased by 30% and in the captopril plus L-
NAME
group SBP was not changed as compared to the control. Although left ventricular weight/body weight (LVW/BW) ratio in both L-
NAME
groups was significantly elevated by 19% and 29%, respectively, no alterations in LVW/BW ratio were found in the captopril group and captopril plus L-
NAME
group. In both groups receiving L-
NAME
, NOS activity significantly decreased by 17% and 69% in the heart, by 14% and 26% in the aorta, by 60% and 73% in the brain and by 13% and 30% in the kidney, respectively.
Captopril
did not influence NO synthase activity in any of the studied tissues. We conclude that captopril prevents the development of hypertension and LV hypertrophy without affecting NO formation.
...
PMID:Captopril prevents NO-deficient hypertension and left ventricular hypertrophy without affecting nitric oxide synthase activity in rats. 908 55
1. We investigated the effects of losartan and captopril on noradrenaline (NA) release and vascular reactivity to NA in the pithed rat. 2. The pressor responses to sympathetic nerve stimulation (SNS) before and after i.v. administration of captopril (1 mg/kg), losartan (1 and 10 mg/kg), sodium nitroprusside (SNP: 5 micrograms/kg per min), losartan (1 mg/kg)+captopril (1 mg/kg), captopril (1 mg/kg) + losartan (1 mg/kg) or the bradykinin B2 receptor antagonist HOE 140 (1 mg/kg)+captopril (1 mg/kg) were measured. Plasma NA concentrations were measured during 60 s SNS before and after losartan (1 mg/kg), captopril (1 mg/kg), SNP (5 micrograms/kg per min) or HOE 140 (1 mg/kg)+captopril (1 mg/kg). Pressor responses to exogenous NA were measured before and after administration of losartan (1 mg/kg), captopril (1 mg/kg), HOE 140 (1 mg/kg) + captopril (1 mg/kg) or the nitric oxide synthase (NO) inhibitor, NG-nitro-L-arginine methyl ester (L-
NAME
; 10 mg/kg) + captopril (1 mg/kg). 3.
Captopril
, losartan and SNP decreased frequency-response curves to a similar extent. The captopril-induced decrease in pressor responses to SNS was restored by pretreatment with HOE140. Adding captopril to losartan decreased the curve more than did adding losartan to captoprill. Both losartan, captopril and HOE 140 + captopril significantly decreased the plasma NA concentration after SNS (34.1 +/- 5.0, 27.4 +/- 2.6 and 41.4 +/- 8.1%, respectively). Sodium nitroprusside did not change the plasma NA concentration after SNS (3.8 +/- 28.2%). The dose-response curves to i.v. NA were not affected by losartan, but were significantly decreased by captopril. However, responses to NA that were reduced by captopril were restored to control values by pretreatment with HOE 140 or L-
NAME
. 4. We suggest that both losartan and captopril decrease pressor responses to SNS by inhibiting NA release from sympathetic nerve endings; however, captopril also decreases 'vascular reactivity' to NA, which is mediated by nitric oxide produced by activation of the bradykinin B2 receptors.
...
PMID:Losartan and captopril follow different mechanisms to decrease pressor responses in the pithed rat. 931 72
Long-term administration of NG-nitro-L-arginine methyl ester (L-NAME) induces development of NO-deficient hypertension. The aim of the present study was to determine whether treatment with the angiotensin-converting enzyme (ACE) inhibitor captopril can prevent hypertension, left ventricular (LV) hypertrophy, changes in nucleic acid concentration, protein synthesis and protein profile of the left ventricle. Four groups of rats were investigated: control, L-
NAME
40 mg/kg/day, captopril 100 mg/kg/day, L-
NAME
40 mg/kg/day along with captopril 100 mg/kg/day. NO-synthase activity in the left ventricle was found to be decreased by 69% in the L-
NAME
group.
Captopril
did not influence this inhibition of NO-synthase activity. However, it completely prevented hypertension and left ventricular hypertrophy development. The increase in left ventricular RNA and DNA concentration and -14C-leucine incorporation observed in the L-
NAME
group was completely prevented by simultaneous captopril treatment. The protein profile of the left ventricle in the L-
NAME
group was characterized by higher concentration of metabolic proteins (MP), soluble collagenous proteins (SCP) and of hydroxyproline in insoluble collagenous proteins (ICP). The concentration of hydroxyproline in ICP was significantly decreased by simultaneous captopril treatment. We conclude that captopril prevented the development of hypertension, left ventricular hypertrophy, increase in nucleic acid concentration and diminished collagen concentration by mechanisms different from affecting NO-synthase activity.
...
PMID:Protein remodelling of the heart in NO-deficient hypertension: the effect of captopril. 944 42
The sensitivity (EC50) of the ring segment of the mesenteric artery to serotonin (4.84 +/- 0.53 x 10(-7) mol.l-1) was 17x greater than that of the aortic ring segment (5.29 +/- 0.46 x 10(-6) mol.l-1). Incubation of the ring segments in physiological salt solution (PSS) containing methylene blue greatly potentiated the sensitivity of both the aorta and mesenteric artery to serotonin. The degree of potentiation was higher in the aorta than mesenteric artery. L-
NAME
also increased the sensitivity of both the aorta and mesenteric artery to serotonin and there was no difference in the degree of potentiation of the responses between the aorta and the mesenteric artery. Indomethacin inhibited the contractile responses of the aorta and the mesenteric artery to serotonin. Phenoxybenzamine reduced the contractile responses of both the aorta and the mesenteric artery by the same magnitude.
Captopril
(10(-4) mol.l-1) significantly attenuated the responses of the mesenteric artery more than the aorta, while methysergide (10(-8) mol.l-1) completely abolished the difference in the responses (EC50 for aorta = 3.50 +/- 0.55 x 10(-5) mol.l-1 vs 5.00 +/- 0.49 x 10(-5) mol.l-1 for mesenteric artery). This study demonstrates that rat aorta and mesenteric artery respond differently to serotonin and the differential response is due to a methylene blue sensitive factor and differences in either the receptor population or sensitivity.
...
PMID:Rat aorta and mesenteric artery respond differently to serotonin. 965 98
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