Sex differences and role of nitric oxide in blood flow of canine urinary bladder

1999 ◽  
Vol 276 (2) ◽  
pp. R407-R413 ◽  
Author(s):  
Michel A. Pontari ◽  
Michael R. Ruggieri
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Intravesical Pressure ◽  
Bladder Mucosa ◽  
Arterial Infusion ◽  
Nitric Oxide Synthase Inhibitor ◽  
Doppler Flowmetry ◽  
Muscle Perfusion ◽  
Anesthetized Dogs ◽  
Synthase Inhibitor

Continuous measurements were made of bladder blood flow by laser Doppler flowmetry in anesthetized dogs during bladder filling and emptying. In both mucosa and muscle, perfusion was inversely proportional to intravesical pressure. There was significantly greater perfusion in the bladder mucosa of males than females at baseline and up to 10 cm water filling pressure but not in the muscle. Intra-arterial infusion of the nitric oxide synthase inhibitor N G-nitro-l-arginine produced a significant decrease in resting bladder perfusion in the mucosa only, with no differences seen in the response to intravesical pressure. Intra-arterial infusion ofl-arginine produced a significant increase in the level of perfusion in the mucosa seen immediately after the bladder was drained. No changes were observed in muscle perfusion afterl-arginine. These results suggest that the perfusion of the bladder mucosa differs by gender and is regulated differently than the bladder muscle, possibly related to the different function of the two layers.

Nitric oxide as a regulator of adrenal blood flow

1993 ◽  
Vol 264 (2) ◽  
pp. H464-H469 ◽  
Author(s):  
M. J. Breslow ◽  
J. R. Tobin ◽  
D. S. Bredt ◽  
C. D. Ferris ◽  
S. H. Snyder ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Neural Control ◽  
Splanchnic Nerve ◽  
No Synthase ◽  
Catecholamine Secretion ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Synthase Inhibitor ◽  
Splanchnic Nerve Stimulation

To determine whether nitric oxide (NO) is involved in adrenal medullary vasodilation during splanchnic nerve stimulation (NS)-induced catecholamine secretion, blood flow (Q) and secretory responses were measured in pentobarbital-anesthetized dogs before and after administration of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). L-NAME (40 mg/kg iv over 5 min, followed by 40 mg.kg-1.h-1) reduced NO synthase activity of medullary and cortical homogenates from 5.2 +/- 0.3 to 0.7 +/- 0.1 pmol.min-1.mg protein-1 and from 1.2 +/- 0.2 pmol.min-1.mg protein-1 to undetectable levels, respectively. L-NAME reduced resting medullary and cortical Q by 42 and 60%, respectively. NS before L-NAME increased medullary Q from 181 +/- 16 to 937 +/- 159 ml.min-1.100 g-1 and epinephrine secretion from 1.9 +/- 0.8 to 781 +/- 331 ng/min. NS after L-NAME had no effect on medullary Q (103 +/- 14 vs. 188 +/- 34 ml.min-1.100 g-1), while epinephrine secretion increased to the same extent as in control animals (1.9 +/- 0.7 vs. 576 +/- 250 ng/min). L-NAME also unmasked NS-induced cortical vasoconstriction; cortical Q decreased from 96 +/- 8 to 50 +/- 5 ml.min-1.100 g-1. Administration of hexamethonium (30 mg/kg iv), a nicotinic receptor antagonist, reduced NS-induced epinephrine secretion by 90%. These data suggest independent neural control of medullary Q and catecholamine secretion, the former by NO and the latter by acetylcholine.

Inhibition of Acetylcholinesterase Selectively Potentiates NG-Monomethyl-l-Arginine-Resistant Actions of Acetylcholine in Human Forearm Vasculature

1995 ◽  
Vol 88 (1) ◽  
pp. 111-117 ◽  
Author(s):  
P. J. Chowienczyk ◽  
J. R. Cockcroft ◽  
J. M. Ritter
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Brachial Artery ◽  
Acetylcholinesterase Inhibitor ◽  
Sensory Nerve ◽  
High Dose ◽  
Nitric Oxide Synthase Inhibitor ◽  
Blood Flows ◽  
Human Forearm ◽  
Synthase Inhibitor

1. NG-monomethyl-l-arginine (l-NMMA, a nitric oxide synthase inhibitor) inhibits vasodilator responses to acetylcholine but not methacholine in human forearm vasculature. To investigate whether this difference results from the relative susceptibility of these agonists to hydrolysis by acetylcholinesterase, we studied vasodilator responses to brachial artery administration of acetylcholine alone and in the presence of the acetylcholinesterase inhibitor edrophonium. 2. Vasodilator responses to constant-rate brachial artery infusions of acetylcholine were biphasic, with an initial peak response fading over 2 min to a plateau. Fade [(peak—plateau)/peak × 100%] was dose dependent (P < 0.02), ranging from 43 ± 7% (mean ± SEM) at low dose (16 nmol/min) to 9 ± 8% at high dose (83 nmol/min). 3. Edrophonium (0.5 μmol/min intra-arterially) alone produced no change in forearm blood flow but increased blood flow responses to acetylcholine (P < 0.01), causing an approximately 10-fold reduction in the dose required to increase plateau blood flow by 10 ml min−1 100 ml−1. 4. Responses to low doses of acetylcholine alone (16 and 41 nmol/min) faded more (P < 0.01) than those to doses of acetylcholine with edrophonium chosen to produce similar plateau blood flows. Responses to acetylcholine (41 nmol/min) also faded more (P < 0.01) than those to methacholine (5 nmol/min), producing matched plateau flows. 5. Peak and plateau responses to acetylcholine (41 nmol/min) were reduced (P < 0.01) by similar amounts (47 ± 15% and 37 ± 13% respectively, P = 0.39) by coinfusion of l-NMMA (4 μmol/min). l-NMMA inhibited responses to acetylcholine more than matched responses to acetylcholine with edrophonium (P < 0.01). 6. These results suggest that the actions of acetylcholine in human forearm resistance vessels are mediated both through an l-NMMA-sensitive pathway (l-arginine/nitric oxide pathway) that exhibits biphasic characteristics and through an l-NMMA-resistant pathway. The l-NMMA-resistant pathway is selectively potentiated by edrophonium. Inhibition of acetylcholinesterase by edrophonium may increase concentrations of acetylcholine deep to the endothelium and favour NO-independent actions on smooth muscle or sensory nerve endings mediating vasodilatation.

Nitric Oxide Modulation of Pulmonary Blood Flow Distribution in Lobar Hypoxia 

1995 ◽  
Vol 82 (5) ◽  
pp. 1216-1225 ◽  
Author(s):  
Filip Freden ◽  
Shao Z. Wei ◽  
Jan E. Berglund ◽  
Claes Frostell ◽  
Goran Hedenstierna
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Lower Lobe ◽  
Nitric Oxide Production ◽  
Nitric Oxide Synthase Inhibitor ◽  
Endogenous Nitric Oxide ◽  
Nitric Oxide Inhalation ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Background Nitric oxide, endogenously produced or inhaled, has been shown to play an important role in the regulation of pulmonary blood flow. The inhalation of nitric oxide reduces pulmonary arterial pressure in humans, and the blockade of endogenous nitric oxide production increases the pulmonary vascular response to hypoxia. This study was performed to investigate the hypothesis that intravenous administration of an nitric oxide synthase inhibitor and regional inhalation of nitric oxide can markedly alter the distribution of pulmonary blood flow during regional hypoxia. Methods Hypoxia (5% O2) was induced in the left lower lobe of the pig, and the blood flow to this lobe was measured with transit-time ultrasound. Nitric oxide was administered in the gas ventilating the hypoxic lobe and the hyperoxic lung regions with and without blockade of endogenous nitric oxide production by means of N omega-nitro-L-arginine methyl ester (L-NAME). Results Hypoxia in the left lower lobe reduced blood flow to that lobe to 27 +/- 3.9% (mean +/- SEM) of baseline values (P &lt; 0.01). L-NAME caused a further reduction in lobar blood flow in all six animals to 12 +/- 3.5% and increased arterial oxygen tension (PaO2) (P &lt; 0.01). Without L-NAME, the inhalation of nitric oxide (40 ppm) to the hypoxic lobe increased lobar blood flow to 66 +/- 5.6% of baseline (P &lt; 0.01) and, with L-NAME, nitric oxide delivered to the hypoxic lobe resulted in a lobar blood flow that was 88 +/- 9.3% of baseline (difference not significant). When nitric oxide was administered to the hyperoxic lung regions, after L-NAME infusion, the blood flow to the hypoxic lobe decreased to 2.5 +/- 1.6% of baseline and PaO2 was further increased (P &lt; 0.01). Conclusions By various combinations of nitric oxide inhalation and intravenous administration of an nitric oxide synthase inhibitor, lobar blood flow and arterial oxygenation could be markedly altered during lobar hypoxia. In particular, the combination of intravenous L-NAME and nitric oxide inhalation to the hyperoxic regions almost abolished perfusion of the hypoxic lobe and resulted in a PaO2 that equalled the prehypoxic values. This possibility of adjusting regional blood flow and thereby of improving PaO2 may be of value in the treatment of patients undergoing one-lung ventilation and of patients with acute respiratory failure.

Effects of nitric oxide synthase inhibitor on cochlear blood flow

2002 ◽  
Vol 171 (1-2) ◽  
pp. 32-42 ◽  
Author(s):  
Hideaki Hoshijima ◽  
Kazuo Makimoto ◽  
Osamu Noi ◽  
Yoshimitsu Ohinata ◽  
Hiroshi Takenaka
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Cochlear Blood Flow ◽  
Nitric Oxide Synthase Inhibitor ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Superoxide scavenging attenuates renal responses to ANG II during nitric oxide synthase inhibition in anesthetized dogs

2005 ◽  
Vol 288 (2) ◽  
pp. F412-F419 ◽  
Author(s):  
Dewan S. A. Majid ◽  
Akira Nishiyama ◽  
Keith E. Jackson ◽  
Alexander Castillo
Keyword(s):  
Nitric Oxide ◽  
Urinary Sodium Excretion ◽  
Ang Ii ◽  
Arterial Infusion ◽  
Anesthetized Dogs ◽  
Significant Attenuation ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
Renal Responses

To assess the role of superoxide (O2−) and nitric oxide (NO) interaction in mediating the renal actions of ANG II, we examined the renal responses to intra-arterial infusion of ANG II (0.5 ng·kg−1·min−1) before and during administration of a superoxide dismutase mimetic, tempol (0.5 mg·kg−1·min−1), in the presence or absence of NO synthase inhibitor, nitro-l-arginine (NLA; 50 μg·kg−1·min−1), in anesthetized dogs pretreated with enalaprilat (33 μg·kg−1·min−1). In one group of dogs ( n = 7), ANG II infusion before tempol infusion caused decreases of 24 ± 4% in renal blood flow (RBF), 55 ± 7% in urine flow (V), and 53 ± 8% in urinary sodium excretion (UNaV) with a slight decrease in glomerular filtration rate (GFR; −7.8 ± 3.4%). Tempol infusion alone did not cause significant alterations in RBF, GFR, V, or UNaV; however, ANG II in the presence of tempol caused a smaller degree of decreases in RBF (−12 ± 2%), in V (−16 ± 5%), and in UNaV (−27 ± 10%) with a slight increase in GFR (6.6 ± 2.8%) than the responses observed before tempol. In another group of NLA-treated dogs ( n = 6), tempol infusion also caused significant attenuation in the ANG II-induced responses on RBF (−13 ± 3% vs. −22 ± 7%), GFR (−19 ± 5% vs. −33 ± 3), V (−15 ± 12% vs. −28 ± 4%), and UNaV (−11 ± 14% vs. −32 ± 7%). These data demonstrate that renal responses to ANG II are partly mediated by O2− generation and its interaction with NO. The sodium-retaining effect of ANG II is greatly influenced by O2− generation, particularly in the condition of NO deficiency.

Comparison of Forearm Vasodilatation to Substance P and Acetylcholine: Contribution of Nitric Oxide

1997 ◽  
Vol 92 (2) ◽  
pp. 133-138 ◽  
Author(s):  
David E. Newby ◽  
Nicholas A. Boon ◽  
David J. Webb
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Substance P ◽  
Cell Function ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Nitric Oxide Synthase Inhibitor ◽  
Endothelial Cell Function ◽  
Synthase Inhibitor ◽  
Oxide Synthase

1. Forearm blood flow responses to incremental challenges of acetylcholine and substance P, administered via the brachial artery, were measured by venous occlusion plethysmography in eight subjects in the presence of saline, the nitric oxide synthase inhibitor, NG-monomethyl-l-arginine, and a control vasoconstrictor, noradrenaline. 2. Substance P and acetylcholine caused dose-dependent increases in forearm blood flow (P < 0.001). When separated by 30 min saline infusions, repeated responses did not undergo tachyphylaxis. 3. Noradrenaline caused a mean reduction in basal blood flow of 34–51% (P < 0.001), and augmented the percentage increases in blood flow with both substance P (P = 0.05) and acetylcholine (P = 0.03) infusions. 4. NG-Monomethyl-l-arginine caused a mean reduction in basal blood flow of 42–45% (P < 0.001) and significantly inhibited the responses to both substance P (P < 0.001) and acetylcholine (P = 0.05). 5. In comparison with saline responses, NG-monomethyl-l-arginine caused a mean inhibition of 69 ± 8% for substance P-induced vasodilatation and 40 ± 5% for acetylcholine-induced vasodilatation. However, comparing responses with those to the control vasoconstrictor noradrenaline, NG-monomethyl-l-arginine caused a mean inhibition of 81 ± 5% for substance P responses and 58 ± 3% for acetylcholine responses. Inhibition by NG-monomethyl-l-arginine of the response to substance P was significantly greater than inhibition of the response to acetylcholine (P = 0.02). 6. Hence, in healthy men, a greater proportion of the forearm vasodilatation to substance P than to acetylcholine appears to be nitric oxide-mediated. Given its greater stability, substance P may be more suitable as a pharmacological tool in the investigation of stimulated nitric oxide production and endothelial cell function.

scholarly journals Nitric oxide is the predominant mediator of cerebellar hyperemia during somatosensory activation in rats

1999 ◽  
Vol 277 (6) ◽  
pp. R1760-R1770 ◽  
Author(s):  
Guang Yang ◽  
Gang Chen ◽  
Timothy J. Ebner ◽  
Costantino Iadecola
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Synaptic Function ◽  
Kainate Receptors ◽  
No Production ◽  
Field Potentials ◽  
Doppler Flowmetry ◽  
Somatosensory Stimuli ◽  
Synthase Inhibitor ◽  
Stimulation Of

Crus II is an area of the cerebellar cortex that receives trigeminal afferents from the perioral region. We investigated the mechanisms of functional hyperemia in cerebellum using activation of crus II by somatosensory stimuli as a model. In particular, we sought to determine whether stimulation of the perioral region increases cerebellar blood flow (BFcrb) in crus II and, if so, whether the response depends on activation of 2-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-kainate receptors and nitric oxide (NO) production. Crus II was exposed in anesthetized rats, and the site was superfused with Ringer. Field potentials were recorded, and BFcrb was measured by laser-Doppler flowmetry. Crus II was activated by electrical stimulation of the perioral region (upper lip). Perioral stimulation evoked the characteristic field potentials in crus II and increased BFcrb (34 ± 6%; 10 Hz-25 V; n = 6) without changing arterial pressure. The BFcrb increases were associated with a local increase in glucose utilization (74 ± 8%; P < 0.05; n = 5) and were attenuated by the AMPA-kainate receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo-[f]quinoxaline (−71 ± 3%; 100 μM; P < 0.01; n = 5). The neuronal NO synthase inhibitor 7-nitroindazole (7-NI, 50 mg/kg; n = 5) virtually abolished the increases in BFcrb(−90 ± 2%; P < 0.01) but did not affect the amplitude of the field potentials. In contrast, 7-NI attenuated the increase in neocortical cerebral blood flow produced by perioral stimulation by 52 ± 6% ( P < 0.05; n = 5). We conclude that crus II activation by somatosensory stimuli produces localized increases in local neural activity and BFcrbthat are mediated by activation of glutamate receptors and NO. Unlike in neocortex, in cerebellum the vasodilation depends almost exclusively on NO. The findings underscore the unique role of NO in the mechanisms of synaptic function and blood flow regulation in cerebellum.

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