scholarly journals Effects of Acidosis and CO2 on Vascular Tone in Newborn Piglet Pulmonary Resistance Vessels (PRV)

1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 308A-308A
Author(s):  
Nora Kovacs ◽  
Thuy K Smith ◽  
Mamta Fuloria ◽  
Judy L Aschner
Keyword(s):  
Vascular Tone ◽  
Newborn Piglet ◽  
Pulmonary Resistance ◽  
Resistance Vessels

N omega-nitro-L-arginine selectively inhibits vasodilator responses to acetylcholine and bradykinin in cats

1991 ◽  
Vol 260 (3) ◽  
pp. H1025-H1029 ◽  
Author(s):  
J. A. Bellan ◽  
R. K. Minkes ◽  
D. B. McNamara ◽  
P. J. Kadowitz
Keyword(s):  
Receptor Agonist ◽  
Vascular Tone ◽  
Nitroso Compound ◽  
Constant Flow ◽  
Flow Conditions ◽  
Relaxing Factor ◽  
Thromboxane Receptor ◽  
Vascular Bed ◽  
Resistance Vessels ◽  
Regulation Of Vascular Tone

The effects of N omega-nitro-L-arginine (nitroarginine), an inhibitor of endothelium-dependent relaxing factor (EDRF) production, on vascular tone and responses to vasodilator and vasoconstrictor agents were investigated in the hindquarters vascular bed of the cat. Under constant flow conditions, infusion of nitroarginine into the hindquarters vascular bed caused a significant increase in systemic arterial and hindquarters perfusion pressures. During infusion of nitroarginine, hindquarters vasodilator responses to acetylcholine and bradykinin were reduced significantly whereas vasodilator responses to isoproterenol, PGE1, nitroprusside, and 8-bromoguanosine 3',5'-cyclic monophosphate were not altered. Infusion of nitroarginine significantly enhanced vasoconstrictor responses to the thromboxane receptor agonist U 46619 and to phenylephrine. The results of these studies are consistent with the hypotheses that EDRF production may involve the formation of nitric oxide or a nitroso compound from L-arginine, and that EDRF production may play a role in the regulation of vascular tone and in the mediation of responses to the endothelium-dependent vasodilators, acetylcholine and bradykinin, in resistance vessels in the hindquarters. These data support the concept that EDRF is very likely an endogenous nitrovasodilator derived from L-arginine in the hindquarters vascular bed of the cat.

Influence of myeloperoxidase on vascular tone of conductance and resistance vessels in-vivo

2010 ◽  
Vol 58 (S 01) ◽  
Author(s):  
S Wipper ◽  
B Reiter ◽  
C Detter ◽  
K Knöll ◽  
M Kolk ◽  
...  
Keyword(s):  
Vascular Tone ◽  
Resistance Vessels

Perinatal pulmonary prostaglandin production

1981 ◽  
Vol 241 (5) ◽  
pp. H756-H759 ◽  
Author(s):  
C. W. Leffler ◽  
J. R. Hessler
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Electron Capture Detection ◽  
Pulmonary Resistance ◽  
Pulmonary Vasodilation ◽  
Resistance Vessels ◽  
Before And After ◽  
Fetal Lungs ◽  
Resistance Decrease

Products of reactions catalyzed by prostaglandin cyclo-oxygenase [prostaglandins (PG), thromboxanes] were analyzed by gas chromatography with electron-capture detection in the venous effluents of in situ Krebs-perfused lungs of exteriorized fetal goats and sheep before and after ventilation with air. The major products were 6-keto-PGF1 alpha and 6,15-diketo[13,14-dihydro] PGI2 without blood components. After ventilation, which decreased pulmonary vascular resistance to 63% of the before-ventilation value, lung production of 6-keto-PGF1 alpha and metabolite increased 50 and 230%, respectively. These data, in addition to earlier findings of inhibition of ventilation-induced pulmonary vasodilation by indomethacin and increased net production of PG-like material after ventilation of blood-perfused fetal lungs, support the hypothesis that ventilation of fetal lungs with air at birth increases synthesis of PGI2 by or near pulmonary resistance vessels, resulting in high local concentrations of PGI2 near its site of production. PGI2 appears to be important in the pulmonary vascular resistance decrease that is necessary for successful perinatal transition.

scholarly journals Interactions Between Nitric Oxide and Endothelin in the Regulation of Vascular Tone of Human Resistance Vessels In Vivo

Hypertension ◽  
2000 ◽  
Vol 35 (6) ◽  
pp. 1237-1241 ◽  
Author(s):  
Carmine Cardillo ◽  
Crescence M. Kilcoyne ◽  
Richard O. Cannon ◽  
Julio A. Panza
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Resistance Vessels ◽  
Regulation Of Vascular Tone

Distribution of NOS in normoxic vs. hypoxic rat lung: upregulation of NOS by chronic hypoxia

1994 ◽  
Vol 267 (6) ◽  
pp. L667-L678 ◽  
Author(s):  
C. Xue ◽  
A. Rengasamy ◽  
T. D. Le Cras ◽  
P. A. Koberna ◽  
G. C. Dailey ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Chronic Hypoxia ◽  
De Novo ◽  
Rat Lung ◽  
Pulmonary Resistance ◽  
Pulmonary Vessels ◽  
Resistance Vessels ◽  
Staining Techniques ◽  
Oxide Synthase

Expression and localization of nitric oxide synthase (NOS) in the lungs of chronically hypoxic and normoxic rats were studied using both immunohistochemistry and NADPH diaphorase (NADPH-d) staining techniques. In the normoxic and in the hypoxic rat, NOS was detected by both methods in the endothelium of large pulmonary vessels and in the epithelium of bronchi and bronchioli. NOS expression was not detected in the endothelium of normoxic pulmonary resistance vessels but was prominently expressed in the endothelium of these vessels after 2-4 wk of chronic hypoxia. In contrast to small pulmonary vessels, the endothelium of small bronchial vessels exhibited NOS immunostaining in both normoxic and hypoxic lungs. Hypoxia was also found to induce de novo NOS expression in the smooth muscle of large and small pulmonary vessels and in bronchial smooth muscle. NOS enzyme activity in lung homogenates was assessed by [3H]arginine to [3H]citrulline conversion. The activity of soluble NOS, but not particulate NOS, was increased in the hypoxic lungs. These results demonstrate chronic hypoxia-induced upregulation of NOS protein expression and activity in the rat lung, suggesting a potentially important role of nitric oxide in adaptation of the pulmonary circulation to chronic hypoxia. The lack of immunostaining in small pulmonary resistance vessels is also consistent with physiological studies suggesting that NO may not be involved in the mechanism for maintaining the normally low pulmonary vascular resistance.

scholarly journals Inflammation and autoimmunity in pulmonary hypertension: is there a role for endothelial adhesion molecules? (2017 Grover Conference Series)

2018 ◽  
Vol 8 (2) ◽  
pp. 204589321875759 ◽  
Author(s):  
Wolfgang M. Kuebler ◽  
Sébastien Bonnet ◽  
Arata Tabuchi
Keyword(s):  
Pulmonary Hypertension ◽  
Potential Role ◽  
Disease Process ◽  
Experimental Models ◽  
Therapeutic Interventions ◽  
Pulmonary Resistance ◽  
Resistance Vessels ◽  
Endothelial Adhesion Molecules ◽  
Inflammatory Component

While pulmonary hypertension (PH) has traditionally not been considered as a disease that is directly linked to or, potentially, even caused by inflammation, a rapidly growing body of evidence has demonstrated the accumulation of a variety of inflammatory and immune cells in PH lungs, in and around the wall of remodeled pulmonary resistance vessels and in the vicinity of plexiform lesions, respectively. Concomitantly, abundant production and release of various inflammatory mediators has been documented in both PH patients and experimental models of PH. While these findings unequivocally demonstrate an inflammatory component in PH, they have fueled an intense and presently ongoing debate as to the nature of this inflammatory aspect: is it a mere bystander of or response to the actual disease process, or is it a pathomechanistic contributor or potentially even a trigger of endothelial injury, smooth muscle hypertrophy and hyperplasia, and the resulting lung vascular remodeling? In this review, we will discuss the present evidence for an inflammatory component in PH disease with a specific focus on the potential role of the endothelium in this scenario and highlight future avenues of experimental investigation which may lead to novel therapeutic interventions.

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