Pathophysiological implications of the vascular nitric oxide (NO)/cGMP pathway in hypertension were investigated. Sprague-Dawley rats were made deoxycorticosterone acetate (DOCA)-salt hypertensive for six weeks. The protein expression of endothelial constitutive NO synthase (ecNOS) and the tissue content of NO were determined in the thoracic aorta. The protein expression and catalytic activity of soluble guanylyl cyclase (GC) were also determined. Systolic blood pressure measured on the day of experiment was significantly higher in the experimental group than in the control. The hypertension was associated with decreases in the vascular tissue content of NO metabolites, concomitantly with the expression of ecNOS proteins. The protein expression of GC was not affected, while its catalytic activity was significantly decreased in hypertension. These results indicate that the high blood pressure is associated with a decreased activity of vascular NO/cGMP pathway in DOCA-salt hypertension.
Aorta, Thoracic ; Blood Pressure ; Desoxycorticosterone* ; Guanylate Cyclase* ; Hypertension* ; Nitric Oxide ; Nitric Oxide Synthase ; Rats, Sprague-Dawley

No abstract available.
Blood Volume* ; Hypotension* ; Nitric Oxide* ; Plasma* ; Renal Dialysis*

Acclimatization ; physiology ; Adolescent ; Altitude ; Humans ; Male ; Nitric Oxide ; blood ; Nitric Oxide Synthase ; blood ; Oxygen ; physiology ; Pulmonary Gas Exchange ; Young Adult

Nitric oxide has been implicated in many physiologic processes that influence both acute and long-term control of kidney function. Its net effect in the kidney is to promote natriuresis and diuresis, contributing to adaptation to variations of dietary salt intake and maintenance of normal blood pressure. A pretreatment with nitric oxide donors or L-arginine may prevent the ischemic acute renal injury. In chronic kidney diseases, the systolic blood pressure is correlated with the plasma level of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase. A reduced production and biological action of nitric oxide is associated with an elevation of arterial pressure, and conversely, an exaggerated activity may represent a compensatory mechanism to mitigate the hypertension.
Acute Kidney Injury ; Arginine ; Arterial Pressure ; Blood Pressure ; Diuresis ; Hypertension ; Kidney ; Natriuresis ; Nitric Oxide ; Nitric Oxide Donors ; Nitric Oxide Synthase ; Plasma ; Renal Insufficiency, Chronic

PURPOSE: Nitric oxide synthase(NOS) is an important enzyme in the production of nitric oxide(NO). The constitutive type(cNOS) is expressed in the normal physiologic state, and the inducible type(iNOS) in expressed in the active immune state. cNOS is divided into an endothelial type (eNOS) and a neuronal type(nNOS). eNOS affects blood vessels, while nNOS affects nerve fibers. In the present study, we evaluated the expression of eNOS and nNOS in rat bladders with short-term partial outlet obstructions. We presupposed that NO is responsible for prolonged micturition problems after partial outlet obstruction. MATERIALS AND METHODS: Specific pathogen-free Sprague-Dawley rats weighing 250-300g were used for the study. Individual bladders were obtained from sham-operated control rats(n=5) and from experimental rats at 12 hours and 1, 2, 3, and 7 days after partial urethral obstruction(n=25). eNOS and nNOS were detected using immunochemical staining and analyzed with confocal microscopy and an image analyzer. RESULTS: eNOS and nNOS expression were detected in both the control group and in the group with partial outlet obstruction. The expression of eNOS showed a sharp increase at 3 days after obstruction and returned to normal at 7 days. The expression of nNOS was not significantly different between the two groups. CONCLUSIONS: In this study, we showed that eNOS increases in the rat bladder after partial outlet obstruction. This finding suggests that overproduction of NO may be the result of ischemic injury sustained during partial bladder outlet obstruction.
Animals ; Blood Vessels ; Microscopy, Confocal ; Nerve Fibers ; Neurons ; Nitric Oxide ; Nitric Oxide Synthase Type I ; Nitric Oxide Synthase Type III ; Rats ; Rats, Sprague-Dawley ; Urinary Bladder ; Urination

OBJECTIVETo investigate the relationship between blood nitrogen monoxide(NO) and PaO2 or PaCO2 levels in patients with severe and moderate acute carbon monoxide poisoning.

METHODThe blood levels of NO in patients with severe and moderate acute carbon monoxide poisoning was assayed with nitrate reductase method, and its correlation with the blood levels of PaO2 and PaCO2 was analyzed.

RESULTSThe blood level of NO in patients with severe and moderate acute carbon monoxide poisoning were (36.6 +/- 9.9) and (35.7 +/- 10.7) mumol/L respectively, significantly lower than that of control group[(64.9 +/- 14.3) mumol/L, P < 0.01], but there was no significant difference between moderate and severe patients(P > 0.05). The analysis of linear correlation showed that there was significant positive correlation between NO and PaO2 but not PaCO2.

CONCLUSIONAnoxia of patients with acute carbon monoxide poisoning may be an important cause to reduce NO level in blood. This study provides the basis for low NO concentration inhalation in treatments of acute carbon monoxide poisoning.

Acute Disease ; Carbon Dioxide ; blood ; Carbon Monoxide Poisoning ; blood ; Humans ; Nitric Oxide ; blood ; Oxygen ; blood

OBJECTIVETo investigate the roles of nitric oxide (NO) and eNOS in the pathogenesis of vasovagal syncope (VVS).

METHODSFourteen children with VVS (group A), 10 children with syncope other than vasovagal (group B) and 20 healthy volunteers (group C) were enrolled. Plasma NO levels in groups A and B were determined before and at the termination of the head-up tilt table test (HUT). The G894T polymorphism within the eNOS gene was determined in the three groups.

RESULTSPlasma NO levels in group A increased significantly when syncope attacked from 76.7+/-9.6 micromol/L (before HUT) to 90.0+/-11.4 micromol/L (P<0.05). After the syncope attack was improved, plasma NO level in group A was significantly reduced. There were no statistical differences in plasma NO levels before and after the HUT in group B. Determining the G894T polymorphism within the eNOS gene showed that group A was associated with a higher incidence of the GT gene type as compared to groups B and C (42.9% vs 10%; P<0.05).

CONCLUSIONSPlasma NO may be involved in the pathogenesis of VVS. The increased plasma NO level may be associated with the G894T polymorphism of the eNOS gene.

Child ; Humans ; Nitric Oxide ; blood ; physiology ; Nitric Oxide Synthase Type III ; genetics ; physiology ; Polymorphism, Genetic ; Syncope, Vasovagal ; etiology

Nitric oxide (NO) signaling has been one of the most rapidly growing areas of study in biology. We know today that NO acts as a signal molecule in the nervous system, a weapon against infection, a regulator of blood pressure, and a gatekeeper of blood flow to different organs. However, much remains to be determined about the physiological and pathophysiological role of NO in the airways. NO appears to be co-localized to cholinergic innervation and involved in vasomotor and secretomotor control of the nasal mucosa. NO is present in exhaled air and appears to originate mainly from paranasal sinus epithelium. Moreover, immunohistochemical and in situ hybridization studies identify all three known isoforms of NO synthase in nasal mucosa. Inhaled endogenous NO in the airways is suggested as playing a role in host defense, and involved in the regulation of pulmonary function as an 'aerocrine.' However, the role of NO in airway inflammation is complicated and clearly has to be determined. The physiological role of NO in the nasal mucosa and its possible pathophysiological role in rhinitis are to be discussed.
Biology ; Blood Pressure ; Epithelium ; In Situ Hybridization ; Inflammation ; Nasal Mucosa* ; Nervous System ; Nitric Oxide Synthase ; Nitric Oxide* ; Protein Isoforms ; Rhinitis*

There are several aspects of blood pressure. Clinically, how to best assess blood pressure average and variability is still a matter of the ongoing debate. Besides office blood pressure, we must pay more careful attention focused on hypertension with blood pressure fluctuation. Impaired endothelial function is intimately associated with the development of hypertension and atherosclerosis. In this review, we describe the relation between endothelial dysfunction and hypertension, the effect of gene polymorphism on endothelial dysfunction, the effects of antihypertensive agents and dietary supplementation on impaired endothelial function in hypertension. In order to predict the future atherosclerosis and cardiovascular events in subjects with hypertension, the adequate assessment of endothelial function is one of the most reliable markers. Furthermore, we discuss the close relationship between blood pressure variability and endothelial function. Blood pressure variability during a day or a week is an important, new risk factor for cardiovascular disease and restoring impaired endothelial function might be a target to prevent blood pressure variation and future cardiovascular events.
Antihypertensive Agents ; Atherosclerosis ; Blood Pressure ; Cardiovascular Diseases ; Dietary Supplements ; Hypertension ; Nitric Oxide ; Nitric Oxide Synthase Type III ; Risk Factors

The present study was aimed at investigating whether there are changes in the expression of nitric oxide synthase (NOS) in relation with the unclipping-induced fall of blood pressure in two-kidney, one clip (2K1C) hypertension. Male Sprague-Dawley rats were made 2K1C hypertensive by clipping the left renal artery for four weeks. Sham-clipped rats served as control. The expression of endothelial constitutive (ec) NOS proteins and tissue levels of NO metabolites were determined in the kidney. Systolic blood pressure was significantly increased in clipped rats compared with that in the control. The development of hypertension was associated with decreases in the expression of ecNOS proteins and tissue levels of NO metabolites in the clipped kidney. The blood pressure at twenty-four hours after removal of the renal arterial clip fell to the control level. Accordingly, in the unclipped kidney, the expression of ecNOS proteins and tissue contents of NO metabolites were increased to the control level. The contralateral kidney was not affected by the development or reversal of hypertension. It is suggested that an enhanced expression of ecNOS in the unclipped kidney is an important component in the reversal of renovascular hypertension.
Animals ; Blood Pressure ; Humans ; Hypertension ; Hypertension, Renovascular* ; Kidney ; Male ; Nitric Oxide Synthase* ; Nitric Oxide* ; Rats ; Rats, Sprague-Dawley ; Renal Artery