Nitric Oxide Derived from Perivascular Nerves and Endothelium

2000 ◽  
pp. 85-98
Author(s):  
Tomio Okamura ◽  
Noboru Toda
Keyword(s):  
Nitric Oxide ◽  
Perivascular Nerves

Nitric oxide-synthesizing perivascular nerves in the rat middle cerebral artery

1997 ◽  
Vol 273 (2) ◽  
pp. R661-R668 ◽  
Author(s):  
C. S. Ignacio ◽  
P. E. Curling ◽  
W. F. Childres ◽  
R. M. Bryan
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Cerebral Arteries ◽  
Middle Cerebral Arteries ◽  
Nerve Bundles ◽  
Perivascular Nerves ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Ethmoidal Foramen ◽  
Active Precursor

Although perivascular nerves containing nitric oxide synthase (NOS) have been anatomically described for rat cerebral arteries, a dilator function for these nerves has eluded investigators when using isolated vessels. Rat middle cerebral arteries (MCAs) were isolated, pressurized, and electrically stimulated. The resting diameter of the MCAs after pressurization was 233 +/- 4 microns (n = 17) in one study. The MCAs showed a frequency-dependent dilation when stimulated. Maximum dilation (25-30% increase in diameter) occurred at a frequency of 8-16 Hz. Removal of endothelium or glibenclamide (10(-5) M), a blocker of ATP-sensitive potassium channels, had no effect on the dilations. The dilations were completely blocked with NG-nitro-L-arginine methyl ester (L-NAME) (10(-5) M), a general NOS inhibitor, and cold storage (24 h). The inhibition by L-NAME could be reversed by the addition of 10(-8) M L-arginine, the active precursor of NOS. Furthermore, 7-nitroindazole (10(-4) M), an inhibitor specific for the neuronal isoform of NOS, reduced the dilations by 43% (P < 0.05). Transections of nerve bundles originating from the sphenopalatine ganglia at the ethmoidal foramen blocked the dilations produced by electrical stimulations. We conclude that rat cerebral arteries have functionally intact perivascular nerves that dilate by releasing nitric oxide.

Pregnancy-induced alterations of neurogenic constriction and dilation of human uterine artery

1995 ◽  
Vol 268 (4) ◽  
pp. H1694-H1701 ◽  
Author(s):  
S. H. Nelson ◽  
O. S. Steinsland ◽  
R. L. Johnson ◽  
M. S. Suresh ◽  
A. Gifford ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Uterine Artery ◽  
Electrical Field Stimulation ◽  
Physiological Mechanisms ◽  
Electrical Field ◽  
Uterine Arteries ◽  
Perivascular Nerves ◽  
Arterial Constriction ◽  
Contraction And Relaxation ◽  
Oxide Synthase

The responses to electrical field stimulation (EFS) of perivascular nerves in human uterine arteries were characterized. The arteries were removed from pregnant and nonpregnant patients undergoing hysterectomy. Tetrodotoxin, guanethidine, and phentolamine blocked EFS (2 min, 80 V, 0.1-ms duration)-induced constriction. The constrictions and the endogenous norepinephrine levels were lower (P < 0.01) in uterine arteries from pregnant than from nonpregnant patients. When arterial rings were precontracted, the response to EFS was biphasic, consisting of an initial constriction followed by a postconstriction relaxation. The EFS-induced relaxation was endothelium independent and was greater (P < 0.01) in uterine arteries from pregnant than from nonpregnant patients. The relaxation was enhanced by guanethidine and superoxide dismutase, inhibited by nitric oxide synthase inhibitors, blocked by tetrodotoxin, and unaffected by atropine, propranolol, or indomethacin. The results demonstrate that human uterine arteries respond to EFS with contraction and relaxation and that these responses may be mediated, respectively, by norepinephrine and, in part, by nitric oxide released from periarterial nerves. The decrease in neuronally mediated uterine arterial constriction and the increase in dilation could be physiological mechanisms for ensuring appropriate uteroplacental perfusion.

Nitric oxide regulation of the central aortae of the toad Bufo marinus occurs independently of the endothelium

2002 ◽  
Vol 205 (19) ◽  
pp. 3093-3100 ◽  
Author(s):  
Brad R. S. Broughton ◽  
John A. Donald
Keyword(s):  
Nitric Oxide ◽  
Soluble Guanylyl Cyclase ◽  
Rat Aorta ◽  
Bufo Marinus ◽  
Organ Bath ◽  
Perivascular Nerves ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Toad Bufo

SUMMARY Nitric oxide (NO) signalling pathways were examined in the lateral aortae and dorsal aorta of the cane toad Bufo marinus. NADPH diaphorase histochemistry and nitric oxide synthase (NOS) immunohistochemistry found no evidence for endothelial NOS in the endothelium of toad aortae, but it could be readily demonstrated in rat aorta that was used as a control. Immunohistochemistry using a specific neural NOS antibody showed the presence of neural NOS immunoreactivity in the perivascular nerves of the aortae. The anatomical data was supported by in vitro organ bath physiology,which demonstrated that the vasodilation mediated by applied acetylcholine(10-5 mol l-1) was not dependent on the presence of the vascular endothelium; however, it was significantly reduced in the presence of a neural NOS inhibitor, vinyl-L-NIO (10-4 mol l-1). In addition, atropine (10-6 mol l-1) (a muscarinic receptor inhibitor), L-NNA (10-4 mol l-1) (a NOS inhibitor) and ODQ (10-5 mol l-1) (an inhibitor of soluble guanylyl cyclase) abolished the vasodilatory effect of applied acetylcholine. In conclusion, we propose that an endothelial NO system is absent in toad aortae and that NO generated by neural NOS in perivascular nerves mediates vasodilation.

Examination of the role of nitric oxide for the hypercapnic rise of cerebral blood flow in rats

1994 ◽  
Vol 266 (4) ◽  
pp. H1457-H1464 ◽  
Author(s):  
M. Fabricius ◽  
M. Lauritzen
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Topical Application ◽  
Baseline Level ◽  
Spreading Depression ◽  
Doppler Flowmetry ◽  
Perivascular Nerves ◽  
Oxide Synthase

We examined the effect of nitric oxide synthase (NOS) inhibition and tetrodotoxin (TTX) on the increase of cerebral blood flow (CBF) in parietal (CoBF) and cerebellar cortex (CeBF) in response to hypercapnia. Rats were anesthetized with halothane and artificially ventilated. Hypercapnia was induced by adding 5% CO2 to the inhalation mixture. CoBF and CeBF were measured by laser-Doppler flowmetry. NOS inhibition was achieved by intravenous (30 mg/kg) and/or topical application (1 mM) of NG-nitro-L-arginine (L-NNA). Activity in perivascular nerves around pial and cortical vessels was inhibited by topical application of TTX (20 microM). Under control conditions, hypercapnia (66 +/- 1 mmHg) increased CoBF by 70 +/- 4% and CeBF by 96 +/- 5%. Systemic L-NNA decreased the baseline level of CoBF and CeBF by 11 +/- 3%, but topical L-NNA did not affect baseline flow. Intravenous L-NNA attenuated the hypercapnic increase of CoBF by 77 +/- 5% and CeBF by 63 +/- 4% within 10-20 min. Topical L-NNA attenuated the hypercapnic increase of CoBF by 52 +/- 6% and CeBF by 29 +/- 5% after 45-min exposure. Both CoBF and CeBF decreased rapidly when L-NNA was infused during sustained hypercapnia, but not when L-NNA was applied topically. Effect of intravenous L-NNA was partially prevented by pretreatment with intravenous L-arginine. Intravenous or topical L-NNA enhanced the rise of CBF elicited by cortical spreading depression, adenosine (1 mM), or sodium nitroprusside (300 microM), except in the cerebellum where topical L-NNA attenuated the rise of CBF elicited by adenosine by 53%.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of nitric oxide synthase-containing vascular nerves in cerebrovasodilation elicited from cerebellum

1993 ◽  
Vol 264 (4) ◽  
pp. R738-R746 ◽  
Author(s):  
C. Iadecola ◽  
F. Zhang ◽  
X. Xu
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cervical Spinal Cord ◽  
Systemic Administration ◽  
Doppler Probe ◽  
Perivascular Nerves ◽  
Dose Dependent Fashion ◽  
Cortical Cerebral Blood Flow ◽  
Nos Inhibitor ◽  
Oxide Synthase

We studied whether the increases in cortical cerebral blood flow (CBF) elicited by stimulation of the cerebellar fastigial nucleus (FN) are attenuated by systemic administration of inhibitors of nitric oxide synthase (NOS) and, if so, whether NOS-containing perivascular nerves arising from the sphenopalatine ganglia (SPG) are the source of NO during FN stimulation. Rats were anesthetized (1-3% halothane) and artificially ventilated. The FN or the pontine reticular formation (PRF) was stimulated electrically through a stereotaxically implanted microelectrode. To eliminate the elevation in arterial pressure (AP) elicited by FN or PRF stimulation the cervical spinal cord was transected and AP was maintained by intravenous phenylephrine. CBF was measured by a laser-Doppler probe placed over the parietal cortex. Systemic administration of the NOS inhibitor N omega-nitro-L-arginine methyl ester (L-NAME; 5-40 mg/kg) reduced resting CBF, an effect that was maximal at 10 mg/kg (-30 +/- 4%; n = 6; P < 0.003, analysis of variance). L-NAME, but not its inactive isomer D-NAME, attenuated the increases in CBF elicited by FN stimulation or hypercapnia in a dose-dependent fashion (10-40 mg/kg). At 40 mg/kg, the response to FN stimulation was reduced by 80 +/- 6% (n = 6; P < 0.05) and that to hypercapnia was reduced by 70 +/- 9% (P < 0.05). In contrast, the increases in CBF elicited by PRF stimulation were not affected (10-40 mg/kg; P > 0.05; n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

l-Citrulline conversion tol-arginine in sphenopalatine ganglia and cerebral perivascular nerves in the pig

1997 ◽  
Vol 273 (5) ◽  
pp. H2192-H2199 ◽  
Author(s):  
J. G. Yu ◽  
T. Ishine ◽  
T. Kimura ◽  
W. E. O’Brien ◽  
T. J. F. Lee
Keyword(s):  
Nitric Oxide ◽  
Cerebral Arteries ◽  
Neuronal Cell ◽  
Histochemical Staining ◽  
Nerve Fibers ◽  
Neuronal Cell Bodies ◽  
Nos Inhibitors ◽  
Perivascular Nerves ◽  
Almost All

The presence of nitric oxide synthase (NOS), argininosuccinate synthetase (ASS), and argininosuccinate lyase (ASL) and their coexistence with NADPH-diaphorase (NADPHd), a marker for NOS, in the porcine sphenopalatine ganglia (SPG), pial veins, and the anterior cerebral arteries was examined using immunohistochemical and histochemical staining techniques. NOS-immunoreactive (I), ASS-I, and ASL-I fibers were found in pial veins and the anterior cerebral arteries. NOS, ASS, and ASL immunoreactivities were also found in neuronal cell bodies in the SPG. Almost all neuronal cell bodies in the SPG and nerve fibers in pial veins and the anterior cerebral arteries that were reactive to ASS, ASL, and NOS were also stained positively with NADPHd, suggesting that ASS, ASL, and NOS were colocalized in the same neurons in the SPG and perivascular nerves. With the use of in vitro tissue bath techniques,l-citrulline but notd-citrulline reversed inhibition of neurogenic vasodilation in isolated porcine pial veins produced by NOS inhibitors such as N G-nitro-l-arginine methyl ester. In the presence of l-aspartate,l-arginine was synthesized froml-citrulline in homogenates of SPG and endothelium-denuded cerebral arteries and pial veins. These results provide evidence indicating that perivascular nerves in pial veins like cerebral arteries can convertl-citrulline tol-arginine for synthesizing nitric oxide. The conversion is most likely via an argininosuccinate pathway.

Nitric oxide from perivascular nerves modulates cerebral arterial pH reactivity

2001 ◽  
Vol 281 (3) ◽  
pp. H1353-H1363 ◽  
Author(s):  
Ute Lindauer ◽  
Alexander Kunz ◽  
Sigrid Schuh-Hofer ◽  
Johannes Vogt ◽  
Jens P. Dreier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vessel Diameter ◽  
Arterial Ph ◽  
Perivascular Nerves ◽  
Vessel Response ◽  
Chronic Denervation ◽  
Ph Dependent ◽  
Baseline Diameter

In the isolated rat middle cerebral artery (MCA) we investigated the role of nitric oxide (NO)/cGMP in the vasodilatory response to extraluminal acidosis. Acidosis increased vessel diameter from 140 ± 27 μm (pH 7.4) to 187 ± 30 μm (pH 7.0, P < 0.01). NO synthase (NOS) inhibition by N ω-nitro-l-arginine (l-NNA, 10 μM) reduced baseline diameter (103 ± 20 μm, P < 0.01) and attenuated response to acidosis (9 ± 8 μm). Application of the NO-donors 3-morpholinosydnonimine (1 μM) or S-nitroso- N-acetylpenicillamine (1 μM), or of 8-bromoguanosine 3′,5′-cyclic monophosphate (8-BrcGMP, 100 μM) reestablished pre-l-NNA diameter at pH 7.4 and reversedl-NNA-induced attenuation of the vessel response to acidosis. Restoration of pre-l-NNA diameter (pH 7.4) by papaverine (20 μM) or nimodipine (30 nM) had no effect on the attenuated response to acidosis. Guanylyl cyclase inhibition with 1H-[1,2,4]oxadiazolo[4,3-a]-quinoxalin-1-one (5 μM) or NOS-inhibition with 7-nitroindazole (7-NI, 100 μM) reduced baseline vessel diameter (109 ± 8 or 127 ± 11 μm, respectively) and vasodilation to acidosis, and restoration of baseline diameter with 8-BrcGMP (30 μM) completely restored dilation to pH 7.0. Chronic denervation of NOS-containing perivascular nerves in vivo 14 days before artery isolation significantly reduced pH-dependent reactivity in vitro (diameter increase sham: 48 ± 14 μm, denervated: 14 ± 8 μm), and 8-BrcGMP (30 μM) restored dilation to pH 7.0 (denervated: 49 ± 31 μm). Removal of the endothelium did not change vasodilation to acidosis. We conclude that NO, produced by neuronal NOS of perivascular nerves, is a modulator in the pH-dependent vasoreactivity.

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