OBJECTIVETo study the function of zinc in preventing human sperm from being damaged by sodium nitroprusside (SNP), an external NO donor.

METHODSAnalyses were made of the function of zinc in protecting sperm from being influenced by SNP in such aspects as sperm motility, head-tail connection and the breakage of sperm DNA chain by using phase-contrast microscope and single cell gel electrophoresis (SCGE).

RESULTSSperm motility was obviously inhibited by SNP. The percentage of comet cells increased significantly but the stability of sperm head-tail connection decreased. Zinc could promote sperm motility, protect the DNA chain and prevent the sperm head-tail connection from breaking.

CONCLUSIONZinc can protect sperm from being damaged by NO. Its mechanism may be related to the mercaptol group of sperm chromatin.

Adult ; DNA Damage ; Humans ; Male ; Nitric Oxide ; toxicity ; Nitroprusside ; toxicity ; Spermatozoa ; drug effects ; Zinc ; pharmacology

AIMTo investigate the effects of exogenous NO donors sodium nitroprusside (SNP) and 3-morpholinosydnonimine (SIN-1) on automaticity of the rabbit sino-atrial node in vitro and the action mechanism.

METHODSThe intracellular microelectrode technique is used to record the action potentials of rabbit sino-atrial node and APA (amplitude of AP), V(max) (maximal rate of depolarization), VDD (velocity of diastolic depolarization), RPF (rate of pacemaker firing) are analyzed.

RESULTSSNP(10(-5) - 10(-2) mol/L) increased its RPF and VDD dose-dependently. 10(-3) mol/L SNP increased RPF (beats/min) from 163 +/- 10.8 to 195.0 +/- 13.1 increased VDD (mV/s) from 50.3 +/- 9.6 to 70.2 +/- 12.1 (P < 0.01). SIN-1(10(-3) - 10(-2) mol/L) also increased RPF and VDD (P < 0.01).10(-4) mo/L Methylene blue (MB), a blocker of GMP cyclase, prevented the positive chronotropic effect and increasement of VDD induced by 10(-3) mol/L SNP totally (P < 0.01). 2. CsCl (2 mmol/L), a blocker of I(f) prevented the increasement of RPF and VDD in part (P < 0.05). 3. NIF (0.46 micromol/L), a blocker of I(Ca-L, had no significant effects on chronotropic effect and increasement of VDD (P < 0.01).

CONCLUSIONExogenous NO can increase the automaticity of rabbit sino-atrial node in vitro. The chronotropic effect is involved in NO-cGMP pathway and results from increasement of I(f) in the sino-atrial node at least in part; I(ca-L) is unlikely to play a major role in this effect.

Action Potentials ; Animals ; Heart Rate ; Molsidomine ; analogs & derivatives ; pharmacology ; Nitric Oxide ; metabolism ; Nitroprusside ; pharmacology ; Rabbits ; Sinoatrial Node ; drug effects ; physiology

OBJECTIVEIn our study, the function of the third-order branches of the mesentenc artery was measured by microvascular ring technique, which can be used to detect microvascular function in some disease related to microvascular dysfunction.

METHODSIsolated, fixed, standardized and then activated the third-order branches of rat mesenteric artery. Microvascular tone was measured by systolic and diastolic drags respectively, with the help of DMT tension apparatus and PowerLab data acquisition system.

RESULTSThe third-order branches of rat mesenteric artery showed excellent response to vasoactive drugs. The contraction effect of norepinephrine (NE) reached 19 in mN. When acetylcholine (Ach) or sodium nitroprusside (SNP) of 10(9)-10(5)mol/L was added, vascular tones showed gradient drop: 80% of maximal relaxation when adding ACh, while 95% of maximal relaxation when adding SNP.

CONCLUSIONThe third-order branches of the mesenteric artery function was successfully detected by using microvascular ring technique.

Acetylcholine ; pharmacology ; Animals ; In Vitro Techniques ; Male ; Mesenteric Arteries ; drug effects ; physiology ; Nitroprusside ; pharmacology ; Norepinephrine ; pharmacology ; Rats ; Vasoconstrictor Agents ; pharmacology ; Vasodilation ; physiology ; Vasodilator Agents ; pharmacology

BACKGROUND: Cytosolic Ca2+ overload and oxygen derived free radicals may contribute to stunned myocardium. The pnt study was aimed to investigate the effects of nicardipine and sodium nitroprusside (SNP) on the functional recovery of postischemic reperfused myocardium. METHODS: Fifty-seven halothane-anesthetized dogs were subjected to 15 minutes of 1eft anterior descending coronary artery (LAD) occlusion and 3 hours of reperfusion. They were randomly assigned to receive either intracoronary nicardipine (n=11) or SNP (n=10) alone or both (nicardipine plus SNP, n=10). Eleven dogs that received saline i.c. served as the controL Regional myocardial contractility was evaluated by systolic shortening (%SS), the preload recruitable stroke work slope (Mw), and intramyocardial pressure (IMPs). Diastolic function was assessed by time constant of myocardial relaxation (IMP-tau) and postsystolic shortening (%PSS), LAD blood flow was measured by a Doppler flowmeter as well. RESULTS: LAD occlusion produced a significant reduction in systolic as well as diasto1ic functions to similar degrees in all groups. However, %SS was significantly higher in the nicardipine, SNP and nicardipine-SNP groups (67%, 56%, and 68% of baseline values, respectively) than in the controls (20%) at 3 hours of reperfusion. Furthermore, Mw recovered to the baseline with the onset of reperfusian in the three experimental groups. IMP-tau was restored to the baseline during early nperfusion in the SNP-treated groups but was significantly prolonged in the control and nicardipine poups throughout the seperfusion. LAD blood flow during reperfusion was higher in the SNP-treated groups in comparison to the control group. CONCLUSIONS: Treatment with either nicardipine or SNP enhances the recovery of mgional contractile function in the canine model of myocardial stunning. SNP not nicardipine is also beneficial in attenuation of early diastolic dysfunction. Nicardipine combined with SNP improved systolic as well as early diastolic functions more significantly when compared to either nicardipine or SNP alane.
Animals ; Coronary Vessels ; Cytosol ; Dogs* ; Flowmeters ; Free Radicals ; Heart ; Myocardial Stunning* ; Myocardium ; Nicardipine* ; Nitroprusside* ; Oxygen ; Pharmacology ; Relaxation ; Reperfusion ; Sodium* ; Stroke

BACKGROUND: Since a change in venous capacitance significantly alters venous return and thus affects cardiac output, it is important to know the effects of vasodilators on venous capacitance. The purpose of this study was to examine the effects of sodium nitroprusside and nitroglycerin on venous capacitance during induced hypotension in halothane anesthetized dogs. METHODS: Fourteen mongrel dogs(SNP group: 7, NTG group: 7), weighing 10~15 kg, were anesthetized with N2O 1.5L/min-O2 1.5L/min-halothane 0.5vol%. Each dog received only one drug. In dogs anesthetized with N2O-O2-halothane, mean arterial pressure(MAP) was decreased by 15%(mild hypotension) and 30%(deep hypotension) of control value by sodium nitroprusside(SNP) and nitroglycerin (NTG), respectively. Venous capacitance was assessed before and during induced hypotension by measuring mean circulatory filling pressure(MCFP). MCFP was measured after arresting the circulation by tightening of superior vena cava and inferior vena cava snares simultaneously. RESULTS: As compared with MCFP before induced hypotension, MCFP was significantly decreased by SNP at deep hypotension and NTG at mild hypotension and deep hypotension. As compared with MCFP at mild hypotension, MCFP at deep hypotension was significantly decreased by NTG and SNP, respectively. CONCLUSIONS: These results suggest that NTG has potent venodilating effect at mild and deep induced hypotension, whereas SNP has venodilating effect only at deep induced hypotension.
Animals ; Cardiac Output ; Dogs* ; Halothane* ; Hypotension* ; Nitroglycerin* ; Nitroprusside* ; Pharmacology ; SNARE Proteins ; Sodium* ; Vasodilator Agents ; Vena Cava, Inferior ; Vena Cava, Superior

OBJECTIVETo observe the effects of nitric oxide(NO) on the DNA ploidy of germ cells and to evaluate the role of NO in modulating spermatogenesis by using SNP, a donor of NO and N-nitro-l-arginine-mythel-ester(L-NAME), an inhibitor of nitric oxide synthese(NOS) in rats physically in vivo.

METHODSForty adult male, Sprague-Dawley rats (60-70 days) were divided into four groups, and injected ultraperitoneally with one of the following agents (once a day, for 12 days): SNP, L-NAME and SNP + L-NAME with normal saline. Two hours after the last injection the rats were sacrificed. The sera were collected and stored at -70 degrees C for subsequent hormone assay. The concentration of serum testosterone was measured by radioimmunoassay. Serum NOx- (nitrite/nitrate) concentration was measured by Greiss method. DNA of spermatogenic cells was detected by flow cytometry(FCM), and the percentage of 1c, 2c and 4c germ cells calculated.

RESULTSIn the SNP treatment group, the serum concentration of NOx- was higher, testosterone concentration was lower and the number of 1c cells was smaller compared with the control group. However, in rats treated with L-NAME, the concentration of NOx- was significantly lower, testosterone concentration was higher and the number of 1c cells was larger compared with the control group(P < 0.01). No changes were observed in the SNP + L-NAME group.

CONCLUSIONEnhancing ectogenous NO will suppress spermatogenesis while inhibiting NO productive pathway will promote it.

Animals ; DNA ; analysis ; Flow Cytometry ; Male ; NG-Nitroarginine Methyl Ester ; pharmacology ; Nitric Oxide ; physiology ; Nitroprusside ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Spermatogenesis ; drug effects

AIMTo observe the role of nitric oxide in dorsal root ganglion (DRG) neurons and its related ionic mechanisms, and explore the function of NO in pain transmission process.

METHODSIn freshly isolated rat DRG samples, using intracellular recording technique, we perfused sodium nitroprusside (NO donor) to observe the role of NO in DRG neurons.

RESULTSIn 77.45% of the bath cells, application of sodium nitroprusside (10 -100 mmol/L) induced concentration-dependent membrane hyperpolarization (79/102), and remaining neurons had no response. The membrane conductance increased from control value of (21.06 +/- 1.94) nS to (23.08 +/- 0.92) nS during sodium nitroprusside induced hyperpolarization. L-NAME (1 mmol/L), CdCl2 (0.1 mmol/L) and non-sodium BSS failed to change the amplitude of sodium nitroprusside induced hyperpolarization. When BSS containing 10 mmol/L TEA was used, sodium nitroprusside induced hyperpolarization was obviously inhibited.

CONCLUSIONSodium nitroprusside could cause concentration-dependent hyperpolarization in DRG neurons by activating K+ channels.

Animals ; Female ; Ganglia, Spinal ; physiology ; Male ; Membrane Potentials ; physiology ; Neurons ; physiology ; Nitric Oxide ; pharmacology ; Nitroprusside ; pharmacology ; Pain ; physiopathology ; Rats ; Rats, Sprague-Dawley

BACKGROUNDThe balance between vasodilation and vasoconstriction plays a major role in maintaining vascular homeostasis. However, the underlying mechanisms are unclear. More and more evidence suggested that there was an interaction in the regulation of vasorelaxation between nitric oxide (NO) and hydrogen sulfide (H(2)S). We explored the interaction between and effects of NO and H(2)S on the relaxation of pulmonary arteries in rats.

METHODSSeven male Sprague-Dawley rats were anaesthetized with chloral hydrate and the pulmonary arteries of each rat separated for the study of vascular activities. The vasorelaxing activities of pulmonary artery rings in response to different doses of a NO donor, sodium nitroprusside (SNP), or a H(2)S donor, sodium hydrogen sulfide (NaHS), were measured in vitro. When pulmonary artery rings were treated with a cystathionine-gamma-lyase inhibitor, DL-propargylglycine, in the presence of SNP or a nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine methyl ester, in the presence of NaHS, the changes in relaxing activities were analyzed.

RESULTSThe relaxation of pulmonary artery rings was in a dose dependent manner in response to either SNP or NaHS. The relaxation rates of pulmonary artery rings increased from (30.90+/-4.62)% to (60.50+/-8.08)% when the concentration of SNP increased from 1 micromol/L to 3 micromol/L and from (26.13+/-4.12)% to (53.09+/-14.01)% when the concentration of NaHS increased from 25 micromol/L to 100 micromol/L. However, when appropriate inhibitor was added, the relaxation responses to SNP and NaHS decreased.

CONCLUSIONSThe results suggested that similarly to NO, H(2)S acted as a vasorelaxant either independently of, or synergistically with NO in the regulation of vasorelaxation. The interaction between NO and H(2)S played an important role in regulating relaxing activities of pulmonary arteries.

Animals ; Hydrogen Sulfide ; pharmacology ; In Vitro Techniques ; Male ; Nitric Oxide ; physiology ; Nitroprusside ; pharmacology ; Pulmonary Artery ; drug effects ; physiology ; Rats ; Rats, Sprague-Dawley ; Vasodilation ; drug effects

OBJECTIVETo study the effects of Geniposide on SNP(sodium nitroprusside)-induced apoptosis of chondrocyte in vitro and cell cycle.

METHODSThe chondrocyte of three-week-old SD rats were separated and cultivated. The second generation of chondrocyte cells were involved in experiment. Chondrocyte proliferation was measured by assay; flow cytometer were adopted to observe cell cycle and apoptosis rate; NO examination adopted nitrate reductase method.

RESULTSGeniposide could significantly decrease the percentage of SNP-induced chondrocytes in G0/G1 phase and increased percentage in S phase and G2/M phase. The apoptosis of chondrocyte and the concentration of NO in the culture supernatants was reduced significantly (r=0.917, P<0.01).

CONCLUSIONGeniposide could impact SNP-induced apoptosis of chondrocyte by reducing the concentration of NO in the culture supernatants, promoting proliferation of chondrocytes, which is a probable and important mechanism of Geniposide preventing osteoarthritis.

Animals ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Chondrocytes ; drug effects ; physiology ; Female ; Iridoids ; pharmacology ; therapeutic use ; Male ; Nitroprusside ; pharmacology ; Osteoarthritis ; drug therapy ; Rats ; Rats, Sprague-Dawley

In this study, we used a rat model of pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT) to investigate the role and mechanism of angiotensin (Ang)-(1-7) in regulating pulmonary artery diastolic function. Three weeks after subcutaneous injection of MCT or normal saline, the right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVHI) of rats were detected using a right heart catheter. Vascular endothelium-dependent relaxation was evaluated by acetylcholine (ACh)-induced vasodilation. The relaxation function of vascular smooth muscle was evaluated by sodium nitroprusside (SNP)-induced vasodilation. Human pulmonary artery endothelial cells (HPAECs) were incubated with Ang-(1-7) to measure nitric oxide (NO) release levels. The results showed that compared with control rats, RVSP and RVHI were significantly increased in the MCT-PAH rats, and both ACh or SNP-induced vasodilation were worsened. Incubation of pulmonary artery of MCT-PAH rats with Ang-(1-7) (1 × 10^-9-1 × 10^-4 mol/L) caused significant vaso-relaxation. Pre-incubation of Ang-(1-7) in the pulmonary artery of MCT-PAH rats significantly improved ACh-induced endothelium-dependent relaxation, but had no significant effect on SNP-induced endothelium-independent relaxation. In addition, Ang-(1-7) treatment significantly increased NO levels in HPAECs. The Mas receptor antagonist A-779 inhibited the effects of Ang-(1-7) on endothelium-dependent relaxation and NO release from endothelial cells. The above results demonstrate that Ang-(1-7) promotes the release of NO from endothelial cells by activating Mas receptor, thereby improving the endothelium-dependent relaxation function of PAH pulmonary arteries.
Rats ; Humans ; Animals ; Vasodilation ; Pulmonary Arterial Hypertension ; Monocrotaline/toxicity* ; Rats, Sprague-Dawley ; Hypertension, Pulmonary/chemically induced* ; Endothelial Cells ; Pulmonary Artery ; Endothelium ; Acetylcholine/pharmacology* ; Nitroprusside/pharmacology*