Effect of norepinephrine and acetylcholine on outer medullary descending vasa recta

1995 ◽  
Vol 269 (2) ◽  
pp. H710-H716 ◽  
Author(s):  
S. Yang ◽  
E. P. Silldorff ◽  
T. L. Pallone
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Regional Blood Flow ◽  
Renal Medulla ◽  
Cholinergic Innervation ◽  
Vascular Bundles ◽  
Nitric Oxide Synthase Inhibitor ◽  
Vasa Recta ◽  
Oxide Synthase

To examine their responsiveness to norepinephrine (NE) and acetylcholine (ACh), outer medullary descending vasa recta (OMDVR) have been dissected from vascular bundles of the rat and perfused in vitro. Abluminal application of NE produced graded vasoconstriction in a concentration range of 10(-9)-10(-6) M. When applied with NE, ACh at concentrations of 10(-8)-10(-5) M dilated NE-preconstricted OMDVR. In contrast, ACh applied in the absence of NE caused vasoconstriction. ACh-induced vasodilation was blocked by addition of the nitric oxide synthase inhibitor N omega-nitro-L-arginine (L-NNA, 2 x 10(-4) M). L-NNA in the absence of ACh enhanced NE-induced vasoconstriction. Supraphysiological (10(-3) M) L-arginine (L-Arg) reversed the effects of L-NNA, and abluminal application of L-NNA alone resulted in OMDVR vasoconstriction. At concentrations of 10(-6)-10(-3) M, abluminal application of L-Arg produced graded vasodilation of NE-constricted OMDVR. These results suggest that adrenergic and cholinergic innervation could influence OMDVR vasomotor tone to modulate total and regional blood flow to the renal medulla. The data also favor a role for the activity of constitutively expressed nitric oxide synthase to modulate OMDVR vasoactivity.

Vasoconstriction of outer medullary vasa recta by angiotensin II is modulated by prostaglandin E2

1994 ◽  
Vol 266 (6) ◽  
pp. F850-F857 ◽  
Author(s):  
T. L. Pallone
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Regional Blood Flow ◽  
Renal Medulla ◽  
Hydraulic Pressure ◽  
Vascular Bundles ◽  
Ang Ii ◽  
Vasa Recta ◽  
Anatomical Arrangement

Vasa recta were dissected from outer medullary vascular bundles in the rat and perfused in vitro. Examination by transmission electron microscopy reveals them to be only outer medullary descending vasa recta (OM-DVR). To establish a method for systematic examination of vasoconstriction, OMDVR were perfused at 5 nl/min with collection pressure increased to 5 mmHg. Under these conditions, transmembrane volume flux was found to be near zero, and the transmural hydraulic pressure gradient was found to be < 15 mmHg. Over a concentration range of 10(-12) to 10(-8) M, abluminal application of angiotensin II (ANG II) caused graded focal vasoconstriction of OMDVR that is blocked by saralasin. Luminal application of ANG II over the same concentration range was much less effective. Abluminal application of prostaglandin E2 (PGE2) shifted the vasoconstrictor response of OMDVR to higher ANG II concentrations. PGE2 reversibly dilated OMDVR that had been preconstricted by ANG II. These results demonstrate that OMDVR are vasoactive segments. Their anatomical arrangement suggests that they play a key role in the regulation of total and regional blood flow to the renal medulla.

Influence of chronic ethanol consumption on arterial tone in young and aged rats

1999 ◽  
Vol 276 (2) ◽  
pp. H464-H471 ◽  
Author(s):  
Mika Kähönen ◽  
Kirsi Karjala ◽  
Nina Hutri-Kähönen ◽  
Xiumin Wu ◽  
Pia Jaatinen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ethanol Consumption ◽  
Ethanol Exposure ◽  
Aged Rats ◽  
Nitric Oxide Synthase Inhibitor ◽  
Chronic Ethanol Consumption ◽  
Oxide Synthase

The aim of this work was to evaluate the effects of long-term ethanol consumption on arterial responses in vitro in young and aged rats. Therefore, Wistar rats (ages 3 and 29 mo, respectively) were allocated to six groups: control-young, sucrose-young, ethanol-young, control-aged, sucrose-aged, and ethanol-aged. The ethanol-fed groups were given 25% ethanol by intragastric gavage three times a day 4 days a week. Responses of mesenteric arterial rings were examined in standard organ chambers after 5 treatment weeks. In norepinephrine-precontracted arterial rings, endothelium-dependent relaxations to acetylcholine, as well as endothelium-independent relaxations to isoproterenol, were attenuated in aged rats when compared with young controls. Relaxation responses to isoproterenol, but not to acetylcholine and nitroprusside, were clearly improved by ethanol treatment in both young and aged rats. The cyclooxygenase inhibitor diclofenac, which reduces the synthesis of dilating and constricting prostanoids, enhanced the relaxation to acetylcholine in all three aged rat groups but was without significant effect in the young rats. In the presence of the nitric oxide synthase inhibitor N G-nitro-l-arginine methyl ester the relaxation to acetylcholine in control and sucrose-fed aged rats was markedly reduced compared with control rats, whereas in the young controls and in both young and aged ethanol-exposed groups, distinct relaxations to higher concentrations of acetylcholine were still present. The endothelium-independent relaxations to cromakalim, a hyperpolarizing vasodilator acting via ATP-sensitive potassium channels, were also markedly augmented by ethanol feeding in both young and aged rats. In conclusion, ethanol consumption in both young and aged rats was associated with markedly improved arterial relaxations to isoproterenol and cromakalim, as well as clearly augmented relaxation to acetylcholine during inhibition of cyclooxygenase and nitric oxide synthase. These findings suggest that especially the potassium channel-related component of arterial relaxation was augmented by long-term ethanol exposure.

Ultrasound Improves Tissue Perfusion in Ischemic Tissue through a Nitric Oxide Dependent Mechanism

2002 ◽  
Vol 88 (11) ◽  
pp. 865-870 ◽  
Author(s):  
Valentina Suchkova ◽  
Raymond Baggs ◽  
Sanjeev Sahni ◽  
Charles Francis
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Rabbit Model ◽  
Tissue Perfusion ◽  
Nitric Oxide Synthase Inhibitor ◽  
Doppler Probe ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
Dependent Mechanism

SummaryUltrasound accelerates enzymatic fibrinolysis in vitro and in animal models and may be used as an adjunct to thrombolytic therapy. Ultrasound can also affect vascular tone directly, and we have now investigated the effect of ultrasound on tissue perfusion in a rabbit model of acute muscle ischemia to characterize the magnitude and temporal course of vasodilation and determine its mechanism. After ligation of the femoral artery of rabbits, tissue perfusion in the gracilis muscle as determined using a laser Doppler probe declined by 53% from 13.7 ± 0.3 U to 6.4 ± 0.2 U. The tissue became acidotic as pH declined from normal to 7.05 ± 0.2. Application of 40 kHz ultrasound at intensities from 0.25 to 0.75 W/cm2 progressively improved perfusion over 60 min and reversed acidosis, but these effects were both completely blocked by pre-treatment with the nitric oxide synthase inhibitor LNAME. Nitric oxide synthase activity in muscle was measured using an assay based on the conversion of radiolabeled L-arginine to L-citrulline and demonstrated an increase of 3.6-fold following ultrasound exposure. This effect was greatest at locations close to the transducer and declined progressively away from it. Histologic examination showed greater capillary circumference in ultrasound exposed muscle compared to unexposed tissue with no other histologic changes. We conclude that the application of 40 kHz at low intensity improves perfusion and reverses acidosis in acutely ischemic muscle through a nitric oxide dependent mechanism.

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