Disease relevance of Sodium nitroprusside

• Sodium nitroprusside in acute myocardial infarction [1].
• Sodium nitroprusside in the treatment of extreme pyrexia [2].
• Afterload reduction with sodium nitroprusside was performed in a patient with idiopathic lactic acidosis in whom sodium bicarbonate therapy had precipitated pulmonary edema [3].
• Sodium nitroprusside and epidural blockade in the treatment of ergotism [4].
• Rings from both the controls and the patients with chronic lung disease relaxed similarly in response to the endothelium-independent vasodilator sodium nitroprusside (10(-4) M) [5].

Psychiatry related information on Sodium nitroprusside

• RESULTS: Responses to acetylcholine, sodium nitroprusside or reactive hyperaemia (area under the time-response curve: pre-maxEPA 14,850 +/- 3502, post-maxEPA 17,118 +/- 4576 units) were unaffected by maxEPA [6].
• PURPOSE: We propose an alternative technique for intracavernous self-injection of sodium nitroprusside for erectile dysfunction by inserting a Medtronic ImPort* catheter with a valved tip [7].
• The N-Arg-induced (15 microg i.c.v.) impairment could be attenuated when the nitric oxide donor, sodium nitroprusside (1 mg/kg), was administered intraperitoneally 1 min prior to maze learning [8].
• Most phasic-type neurons showed excitation in response to i.v. administration of sodium nitroprusside (20 microg/kg, 66.7%; 18/27) and water deprivation (15 h, 77.8%; 7/9) when compared to non-phasic-type neurons [9].
• A sodium nitroprusside depressor challenge increased VMS activity more in REM sleep than in quiet sleep, with the increase being even less in waking [10].

High impact information on Sodium nitroprusside

• In contrast, the vasodilation in response to sodium nitroprusside was similar at all three times of day [11].
• However, there were no significant differences between groups in the responses of blood flow and vascular resistance to sodium nitroprusside [12].
• Contraction was induced in isolated strips of corporal smooth muscle by norepinephrine; then relaxation was assessed with electrical stimulation of autonomic nerves and with the administration of three agents: acetylcholine, which is known to be mediated by endothelium-derived relaxing factor; papaverine; and sodium nitroprusside [13].
• Methemoglobinemia after sodium nitroprusside therapy [14].
• Removal of the endothelium abolished the changes in phosphorylation with the endothelium-dependent vasodilator (acetylcholine), but not those with the nitrovasodilator (sodium nitroprusside) [15].

Chemical compound and disease context of Sodium nitroprusside

• The decrease in Na(+)-K+ ATPase activity induced by hyperglycemia was totally reversed upon adding to the medium either L-arginine, a precursor of EDNO biosynthesis or sodium nitroprusside, which bypasses endothelium and directly activates the soluble guanylate cyclase in vascular smooth muscle [16].
• Glyburide also induced vasoconstriction and restoration of blood pressure in the vasodilatory hypotension caused by hypoxic lactic acidosis, while it was ineffective in the hypotension induced by sodium nitroprusside [17].
• Parenteral therapy is generally preferred, and strategies include use of sodium nitroprusside, beta-blockers, labetelol, or calcium-channel antagonists, magnesium for pre-eclampsia and eclampsia; and short-term parenteral anticonvulsants for seizures associated with encephalopathy [18].
• Sodium nitroprusside (SNP), an NO donor, elevated caspase activity and induced death in human SH-SY5Y neuroblastoma cells and primary cultures of cortical neurons [19].
• METHODS AND RESULTS: In 14 patients with coronary atherosclerosis and 5 with risk factors, we tested femoral vascular endothelial function with acetylcholine and substance P and endothelium-independent function with sodium nitroprusside before and after intravenous aspirin [20].

Biological context of Sodium nitroprusside

• Drugs useful in acutely lowering blood pressure include diazoxide, sodium nitroprusside, methyldopa intravenously, reserpine intramuscularly, and trimethaphan camsylate intravenously [21].
• The effect of sodium nitroprusside on the relationship between left ventricular pressure and volume during diastole was studied in 11 patients with congestive heart failure [22].
• We studied renal plasma flow and glomerular filtration rate during graded blood pressure reduction induced with sodium nitroprusside infusion in 16 hypertensive patients with atherosclerotic renovascular disease [23].
• Addition of sodium nitroprusside (10(-5) mol/L) to the medium caused a time-dependent increase in apoptosis of vascular cells (largely macrophages) in the intimal lesion [24].
• Baroreflex sensitivity was assessed on the basis of the ratio of the change in heart rate or muscle sympathetic activity to the change in mean arterial pressure during intravenous infusion of sodium nitroprusside or phenylephrine [25].

Anatomical context of Sodium nitroprusside

• NG-monomethyl-L-arginine, an inhibitor of nitric oxide (NO) synthase, prevents IL-1beta-induced Fas expression, whereas the NO donors sodium nitroprusside and nitric oxide releasing compound (NOC)-18, induce functional Fas expression in normal pancreatic beta cells [26].
• Rat mesenteric artery resistance vessels (MARV, n = 9) were incubated for 48 h with either L, M, L + M, or vehicle (V) and tested for reactivity to NE, serotonin, acetylcholine, atrial natriuretic peptide, and sodium nitroprusside (SNP) [27].
• In these systems, the nitric oxide (NO) donors sodium nitroprusside (SNP) and NONOate and the NO synthase substrate L-arginine mimicked the effect of VP, stimulating relocation of AQP2 from cytoplasmic vesicles to the plasma membrane [28].
• All smooth muscle strips from normal and Ls/Ls mice produced relaxation in response to sodium nitroprusside and vasoactive intestinal polypeptide [29].
• Third, mitochondria were exposed to sodium nitroprusside in vitro, washed, mixed with blood, and recovered [30].

Associations of Sodium nitroprusside with other chemical compounds

• Furthermore, incubation of Møs with sodium nitroprusside mimicked the L-arginine-dependent inhibition of H+ ATPase activity [31].
• Both insulin and L-NMMA were unable to alter the phenylephrine-induced vasoconstriction and the sodium nitroprusside vasodilation [32].
• The NO donors, sodium nitroprusside and S-nitroso-N-acetylpenicillamine, alone did not increase basal PGE2 formation [33].
• METHODS AND RESULTS: IV injections of nitroglycerin or sodium nitroprusside produced dose-dependent and sustained increases in the exhaled levels of nitric oxide measured by chemiluminescence in awake lambs with tracheostomies [34].
• Coronary resistance arteries 64 to 157 microns in diameter were isolated for in vitro evaluation of relaxation responses to the endothelium-independent dilators sodium nitroprusside (1 x 10(-10) to 1 x 10(-4) mol/L) and adenosine (1 x 10(-10) to 1 x 10(-5) mol/L) and to bradykinin (1 x 10(-13) to 3 x 10(-7) mol/L), an endothelium-dependent agent [35].

Gene context of Sodium nitroprusside

• Furthermore, sodium nitroprusside (0.25-1 mM) increased arachidonic acid-stimulated PGE2 production by murine recombinant COX-1 and COX-2 [36].
• This effect was not due to actions of nitric oxide on the smooth muscle, because sodium nitroprusside-mediated relaxation in either denuded or endothelium-intact aortas was unaffected by PLB ablation [37].
• Both IGF-1 and bFGF prevented apoptosis induced by NO donors, sodium nitroprusside (SNP) or 3-morpholinosydnonimin (SIN-1) in hippocampal neuronal cultures [38].
• In addition, sodium nitroprusside evoked a sequential increase in nuclear Ca2+ transients, activation of p42 MAPK, NF-kappaB binding to DNA consensus sequence, and dependent iNOS RNA [39].
• The specific MAPK kinase inhibitor PD 98059 abolished ERK1/2 activation and endothelial cell proliferation in a concentration-dependent manner in response to VEGF and sodium nitroprusside [40].

Analytical, diagnostic and therapeutic context of Sodium nitroprusside

• Intravenous infusion of sodium nitroprusside can be used in the truly emergent situation and is effective, reliable, and safe [41].
• Sodium nitroprusside has proved to be the most effective and best-tolerated vasodilator drug available for the management of acute hypertension, heart failure, and other vasoconstricted states as well as for the induction of controlled hypotension during surgery [42].
• METHODS AND RESULTS: Forearm blood flow responses to the endothelium-dependent vasodilator acetylcholine (7.5, 15, 30, and 60 micrograms/min) and the endothelium-independent vasodilator sodium nitroprusside (1, 3, and 10 micrograms/min) were measured by venous occlusion plethysmography in 10 control subjects and 10 chronic smokers [43].
• Skin blood flow responses after iontophoresis of acetylcholine and sodium nitroprusside were evaluated by laser Doppler flowmetry [44].
• Intra-arterial infusions of ACh or sodium nitroprusside (SNP) at graded doses progressively decreased FVR in HF as well as in C [45].

References