Nitric Oxide and Its Putative Role in Hypertension

Dominiczak, Anna F.; Bohr, David F.

doi:10.1161/01.hyp.25.6.1202

Cited by 141 publications

(101 citation statements)

References 98 publications

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“…34 In the present study, the in vivo production of NO was not decreased in patients with renal failure, and was reduced without a significant alternation of systemic blood pressure following a single session of haemodialysis. Since there were no alternation of blood pressure on a non-dialysis day, the effect of diurnal blood pressure may limit interpretation.…”

Section: Discussionsupporting

confidence: 41%

Reduced production of nitric oxide during haemodialysis

Sumino

Sato

Sakamaki³

et al. 1999

J Hum Hypertens

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Objective: To examine the influence of systemic nitric oxide (NO) synthesis on blood pressure in patients with chronic renal failure undergoing haemodialysis, since nitric oxides are susceptible to renal excretion or are dialysed, a different indicator that is unaffected by renal function, such as the level of exhaled NO was evaluated. We examined the levels of the endogenous NO before and after a haemodialysis session. Design and methods: We evaluated the serum concentrations of nitrite/nitrate and the rate of nitric oxide release into exhaled air in 10 patients with hypertension who were receiving maintenance haemodialysis. Results: The serum concentrations of nitrite/nitrate before haemodialysis were significantly higher than those in 10 normal controls (183 ؎ 151 M vs 42 ؎ 17 M, P Ͻ 0.05). These levels decreased signifi-

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Section: Discussionsupporting

confidence: 41%

Reduced production of nitric oxide during haemodialysis

Sumino

Sato

Sakamaki³

et al. 1999

J Hum Hypertens

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“…Furthermore, NO may be involved in altering the release of ATP and NPY, which are cotransmitters with norepinephrine at the sympathetic vascular neuroeffector junction. NO is known to inhibit responses to NPY (33) and in hypertensive animals, a disease state characterized by a lack of available NO (13,18), NO potentiated responses to ATP and its nonhydrolyzable analog ␣,␤-methyl ATP (24, 38).Our laboratory (32) has observed that NO chemically reacts with catecholamines resulting in a decrease in catecholamine levels measured by high-performance liquid chromatography coupled to electrochemical detection (HPLC-EC). More importantly, we (32) have also seen a decrease in the biological activity of catecholamines after incubation with NO.…”

mentioning

confidence: 99%

Nitric oxide decreases the biological activity of norepinephrine resulting in altered vascular tone in the rat mesenteric arterial bed

Kolo

Westfall

Macarthur

2004

American Journal of Physiology-Heart and Circulatory Physiology

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Nitric oxide decreases the biological activity of norepinephrine resulting in altered vascular tone in the rat mesenteric arterial beds. Am J Physiol Heart Circ Physiol 286: H296-H303, 2004; 10.1152/ ajpheart.00668.2003 reacts with catecholamines resulting in their deactivation. In this study, we demonstrated that coincubation of NO donors with sympathetic neurotransmitters decreased the amount of norepinephrine detected but not ATP or neuropeptide Y (NPY). Furthermore, we found that the ability of norepinephrine to increase perfusion pressure in the isolated perfused mesenteric arterial bed of the rat was attenuated by the incubation of norepinephrine with the NO donor diethylamine NONOate. Conversely, the vasoconstrictive ability of NPY and ATP was unaffected by incubation with NONOate. Periarterial nerve stimulation in the presence of the NO synthase (NOS) inhibitor N -nitro-L-arginine methyl ester (L-NAME) resulted in an increase in both perfusion pressure response and norepinephrine levels. This was prevented by L-arginine, demonstrating that the effects of L-NAME were indeed specific to the inhibition of NOS. To confirm that NO was not altering the release of norepinephrine from the sympathetic nerve via presynaptic activation of guanylate cyclase, we repeated the experiments in the presence of the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]-quinoxaloine-one (ODQ). Unlike L-NAME, ODQ infusion did not increase norepinephrine overflow, demonstrating that modulation of norepinephrine by NO at the vascular neuroeffector junction of the rat mesenteric vascular bed is not the result of presynaptic guanylate cyclase activation. These results demonstrate that, in addition to being a direct vasodilatator, NO can also alter vascular reactivity at the sympathetic neuroeffector junction in the rat mesenteric bed by deactivating the vasoconstrictor norepinephrine. sympathetic neurotransmitters; nitric oxide synthase; adenosine 5Ј-triphosphate, neuropeptide Y; vascular tone IT HAS BEEN ESTABLISHED that the neurotransmitters norepinephrine, neuropeptide Y (NPY), and ATP are colocalized in and coreleased from many sympathetic neurons (10,16,47,50). It has also been demonstrated that the application of each transmitter mimics a phase of sympathetic nerve stimulation and that each phase can be blocked with appropriate antagonists (10,16,47,50). Moreover, norepinephrine, NPY, and ATP all have presynaptic inhibitory actions on sympathetic neurotransmission and can negatively regulate their own release as well as the release of each other (49,53).Nonneuronal mediators such as the well-characterized endothelium-derived vasodilator nitric oxide (NO) can also modulate sympathetic neurotransmission. Studies have shown that on sympathetic nerve stimulation, inhibition of NO synthesis results in an increase in vasoconstriction in the rat tail artery (51), in the large coronary artery of anesthetized dogs (55), and in the vessels of the isolated adrenal medulla of the dog (1).The enhancement of vasoconstriction may be du...

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“…Yapılan çalışmalar sayesinde bozulmuş NO aktivitesi ve hipertansiyondaki sistemik arteriyel tonus artışı arasındaki ilişki bilinmektedir (23) . Ancak bu ilişkinin etiyolojisi ve mekanizması çok iyi bilinmemekte olup, bozulmuş NO aktivitesinin hipertansiyondan önce mi geliştiği yoksa hipertansiyonun seyri sırasında mı geliştiği hala net değildir (24) . Bu nedenle NO seviyeleri çeşitli çalışmalarda hipertansif hastalarda yüksek (25) , etkilenmemiş (26) , düşük (27)(28)(29)(30) olarak bildirilmiştir.…”

Section: İstatistiksel Hesapunclassified

“…Bu nedenle NO seviyeleri çeşitli çalışmalarda hipertansif hastalarda yüksek (25) , etkilenmemiş (26) , düşük (27)(28)(29)(30) olarak bildirilmiştir. Bu çelişkili sonuçlar; nitrik oksid sentaz (NOS) polimorfizmi veya sentez üzerine etkili diyet, böbrek fonksiyonları ve hidrasyon durumu gibi birçok faktörden kaynaklanıyor olabilir (24) . Endotelin ise endotel hücrelerinden salgılanan ve düz kas hücrelerine endotelin reseptör A (ETA) üzerinden etki ederek vazokonstriksiyona neden olan bir peptiddir (31) .…”

Section: İstatistiksel Hesapunclassified