Role of nitric oxide in vasopressinergic pulmonary vasodilatation

Russ, R. D.; Walker, Benjimen R.

doi:10.1152/ajpheart.1992.262.3.h743

Cited by 46 publications

(37 citation statements)

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“…In this model, NO synthase inhibitors did not increase pulmonary vascular resistance unless pulmonary vessels were first preconstricted by hypoxia 14 or a thromboxane analogue. 15 Additionally, shearstress-induced NO release was lower in lungs perfused with a low-viscosity salt/albumin solution (low shear stress) than in lungs perfused with a high-viscosity blood solution (high shear stress), suggesting that increased shear stress increases NO synthesis in rat lungs. 16 Similarly, Endlich et al 17 demonstrated in perfused kidneys isolated from normal rats that NO, released by shear stress, modulated the renal angiotensin II vasoconstriction.…”

Section: Ne Infusion In the Absence And In The Presence Of Increased mentioning

confidence: 91%

Shear stress modulates the vascular tone in perfused livers isolated from normal rats

Pastor

2000

Hepatology

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Fluid shear stress can be increased either by increasing the flow rate or perfusing increasing doses of norepinephrine (NE) at a constant flow rate. Concomitantly, increased fluid shear stress at the surface of endothelial cells releases nitric oxide (NO). To better understand the role of NO released by shear stress in regulating intrahepatic vascular resistances, we increased fluid shear stress either by changing the flow rate or by perfusing increasing doses of NE at a constant flow rate in perfused livers isolated from normal rats. When concentration-response curves to NE were studied at low, mild, and high flow rates, portal pressure increased during NE perfusion. The higher the flow rate, the lower the response to NE. NO synthase inhibition similarly increased the response to NE at each flow rate. Thus, NO was released by NE-induced increased shear stress, but other vasodilators are likely to be responsible for the flowinduced increased shear stress. In additional experiments, when flow rate was decreased while infusing increasing doses of NE to maintain the portal pressure constant, shear stress remained steady and NO was not released. Hepatic NO production in the different conditions of shear stress could not be detected. Our data are consistent with the fact that in the liver, NO released by shear stress decreases the vasoconstriction to NE and regulates the intrahepatic vascular resistances. (HEPATOLOGY 2000;32:786-791.)Forces generated by blood flow act on vessels either perpendicular to the wall to induce blood pressure or parallel to the wall to create a frictional force or shear stress. 1,2 Although the entire vessel wall is subject to stretch, the fluid shear stress predominates on endothelial cells. Increased fluid shear stress at the surface of endothelial cells is then responsible for the release of nitric oxide (NO), but the precise mechanism coupling the increased shear stress and the enhanced production and release of NO remains unknown. Moreover, evidence exists that fluid shear stress (and consequently, endothelial NO release) is greatly modulated by the vasomotor tone, blood flow rate, and pulsatility. Shear-stress-dependent NO release constitutes a local feed-back mechanism to counteract vasoconstriction.Few data are available on the role of NO released by shear stress in modulating the hepatic vascular tone. Using a perfusion circuit to regulate hepatic blood pressure and flow in anesthetized cats, Macedo and Lautt 3 demonstrated that increased shear stress releases NO in the hepatic artery and the portal vein. Additionally, Shah et al. 4 showed that the exposure of isolated sinusoidal endothelial cells to increasing levels of flow increased the release of NO. Moreover, Mittal et al. 5 demonstrated that NO modulates the hepatic circulation in livers isolated from normal rats and perfused with increasing doses of NE at a constant flow rate. However, whether hepatic NO originated from a baseline production or from the effect of shear stress on endothelial cells is unknown. Recently, Shah e...

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Section: Ne Infusion In the Absence And In The Presence Of Increased mentioning

confidence: 91%

Shear stress modulates the vascular tone in perfused livers isolated from normal rats

Pastor

2000

Hepatology

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“…Vasopressin has been shown to lower pulmonary arterial pressure in rats with hypoxic pulmonary hypertension, through activation of the V 1 receptor (34). It has been speculated that these pulmonary vasodilator properties may be mediated, in part, by modulation of nitric oxide release (35,36). Canine pulmonary arteries, mounted in an organ bath and preconstricted with phenylephrine, have been shown to vasodilate in response to vasopressin (37).…”

Section: Impact Of Vasopressin On Myocardial Performancementioning

confidence: 99%

Vasopressin improves survival compared with epinephrine in a neonatal piglet model of asphyxial cardiac arrest

et al. 2014

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Background: Epinephrine is a component of all resuscitation algorithms. Vasopressin is a pulmonary vasodilator and systemic vasopressor. We investigated the effect of epinephrine vs. vasopressin on survival and hemodynamics after neonatal porcine cardiac arrest (CA). Methods: A 4-min asphyxial CA was induced, after which cardiopulmonary resuscitation (CPR) was commenced. Animals were randomized to low-(LDE: 0.01 mg/kg) or high-dose epinephrine (HDE: 0.03 mg/kg), low-(LDV: 0.2 U/kg) or high-dose vasopressin (HDV: 0.4 U/kg), or control (saline). Clinical and echocardiography indexes were monitored. results: Sixty-nine animals were randomized. Survival was greater in HDV (n = 8 (89%); P < 0.05 ANOVA) vs. control (n = 7 (43%)) and LDE (n = 5 (36%)) but not vs. HDE (n = 7 (64%)) or LDV (n = 6 (75%)). Animals resuscitated with LDE required more shocks (2.5 (interquartile range: 2-6); P < 0.05) and higher doses of energy (15 J (interquartile range: 10-20); P < 0.05). Left ventricular output was comparable between groups, but a greater increase in superior vena caval flow was seen after HDV (P < 0.001 vs. control, LDE, and HDE). Plasma troponin was greatest in the HDE group (P < 0.05 vs. control and HDV). conclusion: Vasopressin results in improved survival, lower postresuscitation troponin, and less hemodynamic compromise after CA in newborn piglets. Vasopressin may be a candidate for testing in human neonates. t he need for active neonatal resuscitation is common with an incidence of 5-10%, although there is likely to be regional variability (1). Guidelines for drug use in neonatal resuscitation guidelines are based on extrapolations from adult literature. Pressors, almost invariably epinephrine, are recommended as core therapy during cardiopulmonary resuscitation (CPR) in order to enhance systemic perfusion (especially cerebral and coronary perfusion) by maintaining vascular tone while forward flow is generated by chest compressions. Epinephrine, although an integral part of every published protocol for neonatal resuscitation, may be associated with adverse effects (2-6); similar concerns exist in pediatric and adult cardiac arrest (CA). However, because of concerns associated with epinephrine (2,7), vasopressin was studied in the setting of asystolic CA. Vasopressin is an intense systemic vasoconstrictor, which may explain why it increases cerebral (and systemic) perfusion during experimental cardiac massage, as well as increasing cerebral oxygenation, neurological outcome, and resuscitation success following experimental .Vasopressin was first proposed as a resuscitation agent after endogenous vasopressin levels were found to be higher in successfully resuscitated patients compared with those who died (13). Evidence from a large, adult, multicenter, randomized controlled trial suggests it to be superior to epinephrine, when the nature of the CA was primary asystole (14). For the following reasons, vasopressin may be a good candidate for pressor support during CPR. First, CA in neonates is almost always due to asphy...

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“…Preconstricted and cyclo-oxygenase-inhibited isolated rat pulmonary vessels [5] respond to AVP with vasodilation. Vasopressin also causes vasodilation in the basilar artery of the brain.…”

Section: Introductionmentioning

confidence: 99%

“…The p values re flect the significance of changes from con trol. [5]. A report of isolated basilar artery dilation [6] also showed that the femoral artery could only con strict in response to AVP.…”

mentioning

confidence: 99%

Arginine Vasopressin-lnduced Renal Vasodilation Mediated by Nitric Oxide

Rudichenko

Beierwaltes²

1995

J Vasc Res

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The vasconstrictor vasopressin has been reported to induce paradoxical local vasodilation in the basilar vasculature through stimulation of the endothelium-derived relaxing factor nitric oxide (NO). We investigated the possibility that at subpressor doses, exogenous arginine vasopressin (AVP) might have a similar effect in the kidney. Ten Inactin-anesthetized rats were infused with sequential doses of AVP from 25 to 6,400 µU/min in 30-min increments. Subpressor infusion resulted in progressive renal vasodilation; renal blood flow (RBF) increased significantly going from 14 ± 6% above basal at 200 µU/min (p < 0.02) to 27 ± 5% (p < 0.01) at 1,600 µU/min accompanied by a 24 ± 5% decrease in renal vascular resistance (RVR). At 6,400 µU/min, blood pressure (BP) increased 29 ± 6 mm Hg and RVR increased. A second group of 8 rats were first given 10 mg/kg b.w. of the NO synthesis inhibitor N^G-nitro-L-arginine methyl ester (L-NAME) before infusion of AVP. L-NAME increased BP 22 ± 3 mm Hg (p < 0.001), and decreased RBF 16 ± 3% (p < 0.005). After L-NAME, no dose of AVP had any further effect on either BP, RBF, or RVR. Continuous infusion of a single subpressor dose of 100 µU AVP resulted in a 26% increase in RBF (from 7.52 ± 0.68 to 9.49 ± 0.54 ml/min/g kidney weight, p < 0.001). AVP doubled urinary cyclic guanosine monophosphate excretion, a marker for renal NO synthesis, from 8.51 ± 1.01 to 17.48 ± 4.26 pM/min (p < 0.025). We conclude that AVP at subpressor doses induces renal vasodilation, which is eliminated by prior inhibition of NO synthesis.

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Role of nitric oxide in vasopressinergic pulmonary vasodilatation

Cited by 46 publications

References 0 publications

Shear stress modulates the vascular tone in perfused livers isolated from normal rats

Shear stress modulates the vascular tone in perfused livers isolated from normal rats

Vasopressin improves survival compared with epinephrine in a neonatal piglet model of asphyxial cardiac arrest

Arginine Vasopressin-lnduced Renal Vasodilation Mediated by Nitric Oxide

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