Evidence for the cure of flu through nose breathing

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Breathing through nose is a healthy habit approved by researchers and it is also helpful in cure of flu. Because normal nose breathing help us to use nitric oxide generated in our sinuses. And research told us that nitric oxide has confirmed function of destruction of viruses, parasitic organisms, and malignant cells in the airways and lungs by inactivating their respiratory chain enzymes. NO inhibits the replication of influenza viruses, probably during the early steps of the viruses’ replication cycle, involving the synthesis of vRNA and mRNA encoding viral proteins. Thus NO is responsible for the cure of flu by killing influenza virus.
Internationa; Journal of Advance Research IJOAR, org
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International Journal of Advance Research, IJOAR .org
Volume 1, Issue 3, March 2013, Online: ISSN 2320-916x
Sana Jamshaid
Key words: Nose breathing, influenza, nitric oxide, flu, replication, cure, protein
Breathing through nose is a healthy habit approved by researchers and it is also helpful in cure of flu. Because
normal nose breathing help us to use nitric oxide generated in our sinuses. And research told us that nitric oxide
has confirmed function of destruction of viruses, parasitic organisms, and malignant cells in the airways and
lungs by inactivating their respiratory chain
enzymes. NO inhibits the replication of influenza viruses, probably during the early steps of the viruses’
replication cycle, involving the synthesis of vRNA and mRNA encoding viral proteins. Thus NO is responsible
for the cure of flu by killing influenza virus.
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ISSN 2320-916x 2
IJOAR© 2013
Flu season typically peaks in January or
February and can last as late as May [1].
Influenza is a virus that typically begins to
appear in the fall and then recedes as the
winter progresses (November until March).
The virus is spread from person to person by
sneezing, coughing and touching. Since the
virus can last for a short time on objects, you
can frequently become infected by touching
something contaminated with the virus and
then touching your mouth, nose or eyes [2].
During the winter, it can remain infectious
in cold fresh water for up to a month. If you
can avoid being around people sick with flu
you may delay getting ill. However, if you
are needed to provide care for a sick family
member or friend with the virus, this
strategy is not practical. Ultimately, most
people are likely to be exposed to the virus.
It’s just a matter of time [3], [4].
Influenza virus has been classified into three
types based on nucleocapsid protein:
influenza A, B, and C. Humans can be
infected by all types of influenza, although
type C results causes only mild infection and
is not associated with epidemics. All
influenza viruses undergo frequent point
mutations resulting in continuous antigenic
changes known as antigenic drift. This
allows the virus to evade immunity,
although prior exposure to the same subtype
provides partial immunity. An epidemic may
occur with antigenic drift [5], [6], [7].
Transmission of avian influenza A to
humans resulting in human infection has
been documented a number of times [8],
Antiviral Effect of Nitric Oxide
It has been demonstrated that nitric oxide
(NO) plays an important role in defense
against a wide spectrum of microbial
pathogens [11]. Nevertheless, the antiviral
activity of NO has not been observed until
recently [12], [13]
Nitric oxide is being recognized increasingly
as an important component of the host
response to infection. In addition, NO and
other reactive nitrogen intermediates have
direct microbistatic and microbicidal
activities against a variety of pathogens.
Nitric oxide had inhibitory effects on protein
and DNA synthesis as well as on cell
replication in microbial pathogens [14].
The confirmed function of the nitric oxide is
destruction of viruses, parasitic organisms,
and malignant cells in the airways and lungs
by inactivating their respiratory chain
enzymes [15], [16].
Normal nose breathing helps us to use our
own nitric oxide generated in sinuses. The
main roles of NO and its effects have been
discovered quite recently (last 20 years).
Three scientists even received a Nobel Prize
for their discovery that a common drug
nitroglycerin (used by heart patients for
almost a century) is transformed into
nitric oxide. NO dilates blood vessels of
heart patients reducing their blood pressure
and heart rate. Hence, they can survive a
heart attack. This substance or gas is
produced in various body tissues, including
nasal passages. As a gas, it is routinely
measured in exhaled air coming from nasal
passages. Therefore, we can't utilize own
nitric oxide, an important hormone, when
we start mouth breathing [17], [18], [19],
The major function of the nose is to warm
and humidify air before it reaches to the
lungs for gas exchange. Conditioning of
inspired air is achieved through evaporation
of water from the epithelial surface. The
continuous need to condition air leads to a
hyperosmolar environment on the surface of
the epithelium. As ventilation increases, the
hyperosmolar surface moves more distally,
covering a larger surface area of the
airway, and stimulates epithelial cells to
release mediators that lead to inflammation.
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This inflammation is not identical to allergic
inflammation, but causes both short-term
and long-term changes in the epithelium. In
the short-term, it increases paracellular
water transport in an attempt to enhance
conditioning, and it stimulates sensory
nerves to initiate neural reflexes. It also
disrupts channels in the cellular membrane,
which might permit greater penetration of
foreign proteins, such as allergens, leading
to further inflammatory cascades. The
longterm inflammation induced over time by
the hyperosmolar milieu could worsen the
ability of the nose to condition air, requiring
more of the conditioning to occur in the
lower airway and leading to adverse
consequences for the respiratory system
Autoimmunization Effect
In nasal breathing the thin layer of mucus
moves as a long carpet from sinuses, bronchi
and other internal surfaces towards the
stomach. Therefore, these objects, trapped
by the mucus, are discharged into the
stomach where GI enzymes and
hydrochloric acid make bacteria, viruses and
fungi either dead or weak. Later, along the
digestive conveyor, some of these pathogens
(dead or weak) can penetrate from the small
intestine into the blood (the intestinal
permeability effect). Since these pathogens
are either dead or weakened, they could not
do much harm (no infections). Moreover,
they can provide a lesson for the immune
system. This is exactly how natural auto-
immunization can work with success.
Medical doctors and nurses inject vaccines
with dead or weakened bacteria or viruses so
that to teach and strengthen our immune
response to these pathogens. Therefore,
nasal breathing creates conditions for natural
autoimmunization. This research study
revealed that a group of healthy volunteers
had an average CO2 of about 43.7 mm Hg
for nose breathing and only around 40.6 mm
Hg for oral breathing [17], [18], [19], [20].
Further reports pointed to NO as a first line
of defense against infections in murine
systems with RNA viruses (e.g., vesicular
stomatitis virus [22], [23] Friend leukemia
virus [24] encephalomyocarditis virus [25];
Sindbis virus [SV] [26], or Japanese
encephalitis virus [27] and DNA viruses,
such as HSV-1 or vaccinia virus [28], [29].
Nitric oxide (NO) is a free radical gaseous
molecule that is a mediator of vital
physiologic functions, including host
defense. Many cell types are able to produce
NO through the enzymatic conversion of L-
arginine to L-citrulline by nitric oxide
synthetase (NOS). Neurons, endothelial
cells, and macrophages are the best
characterized sources of NO. From these
sites of production, NO modulates neuronal
function, regulates vasomotor tone, and is
involved in host responses to infection [30],
[31], [32], [33]. NO and related reactive
nitrogen intermediates exert microbistatic
and microbicidal effects against a variety of
pathogens, including protozoans, flukes,
fungi, and bacteria [33], [34], [35], [36],
[37], [38].
Nitric oxide (NO) is produced at different
sites in the human airways and may have
several physiological effects. Orally-
produced NO seems to contribute to the
levels found in exhaled air. Autoinhalation
of nasal NO increases oxygenation and
reduces pulmonary artery pressure in
The aim of this study was to measure the
concentration and output of NO during
nasal, oral and tracheal controlled exhalation
and inhalation. Ten tracheotomized patients
and seven healthy subjects were studied.
The mean+/-SEM fraction of exhaled NO
from the nose, mouth and trachea was 56+/-
8, 14+/-4 and 6+/-1 parts per billion (ppb),
respectively. During single-breath nasal, oral
and tracheal inhalation the fraction of
inhaled NO was 64+/-14, 11+/-3 and 4+/-1,
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respectively. There was a marked flow
dependency on nasal NO output in the
healthy subjects, which was four-fold
greater at the higher flow rates, during
inhalation when compared to exhalation.
There is a substantial contribution of nasal
and oral nitric oxide during both inhalation
and exhalation. Nasal nitric oxide output is
markedly higher during inhalation, reaching
levels similar to those that are found to have
clinical effects in the trachea.
These findings have implications for the
measurement of nitric oxide in exhaled air
and the physiological effects of autoinhaled
endogenous nitric oxide [39].
For millions of people each year, the flu can
bring a fever, cough, sore throat, runny or
stuffy nose, Muscle aches, fatigue, and
miserable days spent in bed instead of at
work or school. However, you may not
realize that more than 200,000 people are
hospitalized in the United States from flu
complications each year.
The flu also can be deadly. Between 1976
and 2007, CDC estimates that annual flu
associated deaths in the United States ranged
from a low of about 3,000 people to a high
of about 49,000 people [1].
The World Health Organization (WHO) has
approximately 110 laboratories worldwide
that monitor and tract viral mutation rates,
and look for potential pandemics. The WHO
looks for "antigenic shifts". When these
occur the population is susceptible to major
epidemics or pandemics.. Historically, a
strong immune system has not been enough
to fend off these mutations. Remember
approximately 20 40 million healthy adults
died in the 1918 influenza pandemic [40].
The antiviral activity associated with NO
also could be secondary to its well-
recognized cytotoxic properties [41].
Several approaches were taken to evaluate
the effects of NO on cellular metabolism
and viability. Nitric oxide (NO) has been
shown to contribute to the pathogenesis of
influenza virus-induced pneumonia in
mouse models. Here we show that
replication of influenza A and B viruses in
Mabin Darby canine kidney cells
is severely impaired by the NO donor,S-
Reduction of productively infected cells and
virus production proved to correlate with
inhibition of viral RNA synthesis, indicating
that NO affects an early step in the
replication cycle of influenza viruses [42],
[43], [44], [45], [46].
Nitric oxide (NO) has multiple biological
functions. NO is catalytically generated by
one of the three isoforms of NO synthase
(NOS) from l-arginine. eNOS and nNOS,
which are produced in endothelial cells and
neuronal cells, have been shown to play a
role in vasodilatation and neurotransmission,
respectively, where as NO generated by
iNOS (NOS2), the inducible form of NOS,
has been shown to play a role in the defense
against a variety of microbial pathogens,
including bacteria, parasites [47] and
viruses, including herpes simplex virus type
1 (HSV-1), vesicular stomatitis virus,
Japanese encephalitis virus, poliovirus,
murine hepatitis virus, murine leukemia
virus, coxsackievirus, ectromelia virus,
rhinovirus, and vaccinia virus. Taken
together, the data presented demonstrate that
NO inhibits the replication of influenza
viruses, probably during the early steps of
the virus replication cycle, involving the
synthesis of vRNA and mRNA encoding
viral proteins. Therefore we hypothesize that
the production of NO by iNOS in airway
epithelial cells, induced by cytokines which
are known to be synthesized shortly after
infection with influenza viruses by NK cells
and macrophages [48], [49], provides an
antiviral effect in these cells.
This mechanism would reduce primary
replication of influenza viruses before other
effector mechanisms of the immune system,
such as those mediated by B and T
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lymphocytes, are activated to control the
infection. To be beneficial for the host, the
production of NO must be tightly regulated
to exert antiviral rather than harmful
effects, such as cell death and tissue
Nitric oxide is being recognized increasingly
as an important component of the host
response to infection [33], [34], [35], [36],
[37], [38]. NO modulates immune responses
by mediating the regulation of lymphocyte
proliferation by suppressor macrophages
[50]. Furthermore, it influences local
inflammatory reactions by altering
adherence of neutrophils to endothelial
surfaces [51], [52].
Antiviral Drugs used commonly for
treatment of Flu
Most common antiviral drugs recommended
by doctors for the treatment of flu are
aspirin, iodized lime, opiates and quinine.
There are two other antiviral drugs
recommended by CDC are Tamiflu® and
Relenza® (The generic names for
these drugs are oseltamivir and zanamivir).
Tamiflu® is available as a pill or liquid
and Relenza® is a powder that is inhaled
Side Effects of Antiviral Drugs Used for
the Treatment of Flu
According to the Dewey article the use of
aspirin either directly or indirectly was the
cause of more loss of lives than the
influenza illness itself. Frank Newton, M.D
and many of the other physicians indicated
that its indirect action came through the fact
that aspirin was taken until it caused
prostration and then the patient developed
pneumonia. A principle druggist from
Montreal declared that 900 patients died
from influenza. They were directed to take a
5 – grain aspirin tablet every three hours, but
more took than ten grains every three hours.
Many of the physicians who practiced the
conventional medicine of the day were using
aspirin, iodized lime, opiates and quinine
and they commonly spoke about losing 60%
of their pneumonia cases. The homeopathic
physicians avoided the use of aspirin and
other drugs prescribed in material doses and
subsequently had a very low death rate.
Arthur Grimmer M.D declared that the
development of pneumonia was a rare
occurrence if a good homeopathic physician
was called during the first 24 hours of an
attack of influenza [54].
Tamiflu® has been in use since 1999. The
most common side effects are nausea or
vomiting which usually happen in the first 2
days of treatment. Taking Tamiflu® with
food can reduce the chance of having these
side effects.
Relenza® has been in use since 1999. The
most common side effects are dizziness,
runny or stuffy nose, cough, diarrhea,
nausea, or headache. Relenza® may also
cause wheezing and trouble breathing in
people with lung disease, which is why
those people should not take this drug.
Confusion and abnormal behavior leading to
injury has been observed rarely in people
with the flu, mostly children, who were
treated with Tamiflu® or Relenza®. Flu
can also cause these behaviors. But people
taking these drugs should be watched for
signs of unusual behavior. This behavior
should be immediately reported to a health
care provider [53].
Our nasal passages are created to humidify, clean and warm the incoming flow of air due to the
layers of protective mucus. This thin layer of mucus can trap about 98-99 percent of bacteria,
viruses, dust particles, and other airborne objects. In this regard the nitric oxide prepared in
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sinuses of nose utilizes and influenza virus killed to cure us from flu. But use of Antiviral drugs
for the treatment of flu leads less to cure but more to side effects.
Obviously, during mouth breathing it is not possible to utilize one's own nitric oxide which is
produced in the sinuses. The mouth is created by Nature for eating, drinking, and speaking. At
other times it should be closed. Still breathing through mouth in flu allowing these pathogens to
gain access, settle and reproduce themselves in various parts of the body causing the infection.
There is an easy tip to keep nasal passage open while breathing during flu, is to fill the mouth
with air, the pressure creates causes the nasal passage to open and thus nose can breathe easily.
The author is thankful to Allah Almighty and his family for inspiration and supporting.
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Sana Jamshaid
M.Sc Chemistry
University of Sargodha, Pakistan
The Author can be contacted on sanajamshaid41@gmail.com
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    Nitric oxide (NO) exerts microbicidal effects on a broad spectrum of pathogens, including viruses, but its antiretrovirus properties have not yet been described. The purpose of this study was to determine whether NO inhibits murine Friend leukemia virus (FV) replication in vitro and to what extent NO may play a role in defenses against FV infection in mice, Three NO-generating compounds were studied: 3-morpholino-sydononimine (SIN-1), sodium nitroprusside (SNP), and S-nitroso-N-acetylpenicillamine (SNAP). The effects of these three compounds were compared with those of their controls (SIN-1C, potassium ferricyanide, and N-acetylpenicillamine, respectively), which do not generate NO and with that of sodium nitrite (NaNO2). SIN-1, SNP, and SNAP inhibited FV replication in dunni cells in a concentration-dependent manner. In contrast, no significant inhibitory effect was observed with the three controls or NaNO2. Furthermore, the addition of superoxide dismutase did not alter the inhibitory effect of SIN-1, which is also known to generate superoxide anions, No dunni cell toxicity was observed in the range of concentrations tested. We also assessed the effect of NO produced by activated macrophages on FV replication, Macrophages activated by gamma interferon and lipopolysaccharide inhibited FV replication in a concentration-dependent manner. This inhibition was due in part to NO production, since it was reversed by N-G-monomethyl L-arginine, a competitive inhibitor of NO synthase, In vivo administration of N-G-nitro-L-arginine methyl ester, a competitive inhibitor of NO synthase, significantly increased the viral load in spleen cells of FV-infected mice, These results suggested that NO may play a role in defenses against the murine Friend leukemia retrovirus.
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    THERE is general recognition of the fact that infective agents may pass from the respiratory tract of one host to that of another throutgh the air. There has, however, been but little study of the precise mechanism of this transmission under experimental conditions. The term " droplet infection " is in common use; this includes infection caused by the scattering of fairly large drops from the mouth or nose. Wells and Wells (1936) have lately emphasized the importance of droplet nuclei: droplets which are fairly large as they leave the mouth are expelled with such speed that they rapidly lose fluid by evapora-tion until they become so small that they can float in the air for many hours. Wells and Wells have urged that for this reason " droplet nuclei " form a greater source of danger than the coarse particles. Infection may be carried in the air in yet a third way, on particles of dust. The relative importance of the various potential vehicles of infection is hard to determine under field conditions. We have therefore attempted to study the problem experimen-tally, deliberately avoiding the somewhat artificial conditions produced by spraying suspensions of organisms into the air. We began by investigating aerial transmission of influenza A virus in the ferret, as we know of no other infection more suitable for our purpose.
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    The objective of the present study was to assess the craniocervical posture and the positioning of the hyoid bone in children with asthma who are mouth breathers compared to non-asthma controls. The study was conducted on 56 children, 28 of them with mild (n=15) and moderate (n=13) asthma (14 girls aged 10.79+/-1.31 years and 14 boys aged 9.79+/-1.12 years), matched for sex, height, weight and age with 28 non-asthma children who are not mouth breathers. The sample size was calculated considering a confidence interval of 95% and a prevalence of 4% of asthma in Latin America. Eighteen variables were analyzed in two radiographs (latero-lateral teleradiography and lateral cervical spine radiography), both obtained with the head in a natural position. The independent t-test was used to compare means values and the chi-square test to compare percentage values (p<0.05). Intraclass correlation coefficient (ICC) was used to verify reliability. The Craniovertebral Angle (CVA) was found to be significantly smaller in asthma than in control children (106.38+/-7.66 vs. 111.21+/-7.40, p=0.02) and the frequency of asthma children with an absent or inverted hyoid triangle was found to be significantly higher compared to non-asthma children (36% vs. 7%, p=0.0001). The values of the inclination angles of the superior cervical spine in relation to the horizontal plane were significantly higher in moderate than in mild asthma children (CVT/Hor: 85.10+/-7.25 vs. 90.92+/-6.69, p=0.04 and C1/Hor: 80.93+/-5.56 vs. 85.00+/-4.20, p=0.04). These findings revealed that asthma children presented higher head extension and a higher frequency of changes in hyoid bone position compared to non-asthma children and that greater the asthma severity greater the extension of the upper cervical spine.
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    Children with adenotonsillar hypertrophy and those with an abnormal craniofacial morphology are predisposed to having sleep disordered breathing; many of these children are mouth breathers. The aim of this study was to determine whether an association exists between polysomnographic findings and cephalometric measures in mouth-breathing children. Twenty-seven children (15 mouth-breathing children and 12 nose-breathing children [control subjects]), aged 7 to 14 years, took part in the study. Polysomnographic variables included sleep efficiency, sleep latency, apnea-hypopnea index, oxygen saturation, arousal index, number of periodic limb movements in sleep, and snoring. Cephalometric measures included maxilla and mandible position, occlusal and mandibular plane inclination, incisor position, pharyngeal airway space width, and hyoid bone position. As compared with nose-breathing children, mouth breathers were more likely to snore (p < 0.001) and to have an apnea-hypopnea index greater than 1 (p = 0.02). Mouth-breathing children were also more likely to have a retruded mandible, more inclined occlusal and mandibular planes, a smaller airway space, and a smaller superior pharyngeal airway space (p < 0.01). The apnea-hypopnea index increased as the posterior airway space decreased (p = 0.05). Our study showed an association between polysomnographic data and cephalometric measures in mouth-breathing children. Snoring was the most important variable associated with abnormal craniofacial morphology. Orthodontists should send any mouth-breathing child for an evaluation of sleep if they find that the child has a small superior pharyngeal airway space or an increased ANB (the relationship between the maxilla and mandible), NS.PIO (occlusal plane inclination in relationship to the skull base), or NS.GoGn (the mandibular plane inclination in relation to the skull base), indicating that the child has a steeper mandibular plane.
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    The vast majority of health care professionals are unaware of the negative impact of upper airway obstruction (mouth breathing) on normal facial growth and physiologic health. Children whose mouth breathing is untreated may develop long, narrow faces, narrow mouths, high palatal vaults, dental malocclusion, gummy smiles, and many other unattractive facial features, such as skeletal Class II or Class III facial profiles. These children do not sleep well at night due to obstructed airways; this lack of sleep can adversely affect their growth and academic performance. Many of these children are misdiagnosed with attention deficit disorder (ADD) and hyperactivity. It is important for the entire health care community (including general and pediatric dentists) to screen and diagnose for mouth breathing in adults and in children as young as 5 years of age. If mouth breathing is treated early, its negative effect on facial and dental development and the medical and social problems associated with it can be reduced or averted.
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    We investigated a broad spectrum of immunoactive mediators in a mouse model of influenza. ICR mice (4-5 wk old) that were infected with a 10 LD50 dose of influenza A/PR8/34 virus died after 6 days without evidence of bacterial superinfection. Maximal virus titers were reached by day 2 postinfection, whereas the multifocal pneumonia with mononuclear cell infiltration reached its maximum at the end of infection. We measured the cytokines IL-1 alpha, IL-1 beta, IL-2, IL-3, IL-4, IL-6, IFN-gamma, TNF-alpha, granulocyte (G)/macrophage (M)-CSF, G-CSF, M-CSF, and the lipid mediators leukotriene B4 and platelet-activating factor in the cellfree bronchoalveolar lavage fluid of mice during infection. We found an early increase of IL-1 alpha, IL-1 beta, IL-6, TNF-alpha, GM-CSF, IFN-gamma, and leukotriene B4. Levels of these factors peaked between 36 h and day 3 postinfection, with the exception of IL-6 that remained at elevated levels throughout infection. G-CSF and M-CSF increased slowly and reached a maximum by day 5 postinfection. We were unable to detect IL-2, IL-3, or IL-4. PAF remained at the same level throughout infection. Our results suggest that lung-resident cells, and possibly the alveolar macrophages, participate actively in the onset of the inflammatory response against the invading virus. The inability to detect the T cell products IL-2, IL-3, and IL-4 was unexpected considering the role of T cells in the elimination of the virus in infected mice. Our observation confirms thus earlier findings about the inability of specific T cell clones to elicit an unspecific antiviral effect.
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    The cofactor requirements of macrophage nitric oxide (NO.) synthase suggest involvement of an NADPH-dependent flavoprotein. This prompted us to test the effect of the flavoprotein inhibitors diphenyleneiodonium (DPI), di-2-thienyliodonium (DTI), and iodoniumdiphenyl (ID) on the NO. synthases of macrophages and endothelium. DPI, DTI, and ID completely inhibited NO. synthesis by mouse macrophages, their lysates, and partially purified macrophage NO. synthase. Inhibition of NO. synthase by these agents was potent (IC50's 50-150 nM), irreversible, dependent on time and temperature, and independent of enzyme catalysis. The inhibition by DPI was blocked by NADPH, NADP+, or 2'5'-ADP, but not by NADH. Likewise, FAD or FMN, but not riboflavin or adenosine 5-diphosphoribose, protected NO. synthase from inhibition by DPI. Neither NADPH nor FAD reacted with DPI. Once NO. synthase was inhibited by DPI, neither NADPH nor FAD could restore its activity. DPI also inhibited acetylcholine-induced relaxation of norepinephrine-preconstricted rabbit aortic rings (IC50 300 nM). Inhibition of acetylcholine-induced relaxation persisted for at least 2 h after DPI was washed out. In contrast, DPI had no effect on norepinephrine-induced vasoconstriction itself nor on vasorelaxation induced by the NO.-generating agent sodium nitroprusside. These results suggest that NO. synthesis in both macrophages and endothelial cells depends on an NADPH-utilizing flavoprotein. As a new class of NO. synthase inhibitors, DPI and its analogs are likely to prove useful in analyzing the physiologic and pathophysiologic roles of NO(.).