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Biomedical subjects

O Bălţatu

Publications and source records attributed to O Bălţatu.

4 recordsLinked to original sources
PubMedDate not supplied

[Experimental data on epithelial factors modulating bronchial reactivity].

A tracheobronchial smooth muscle reactivity study on isolated guinea pig tracheal rings was done. The presence of two different factors active on smooth muscle, an inhibiting one, as well as an activating one was identified. Generated on different pathways, the epithelial derived relaxing factor is a cyclooxygenase dependent prostaglandin, while the activating epithelial factor seems to be a thromboxane derivate.

Animals↗
PubMedDate not supplied

Cardiovascular effects of L-arginine as physiological precursor of nitric oxide.

In this study the cardiovascular effects of L-arginine were investigated. Perfusion with sorbitol L-arginine 5% solution induced a significant decrease of the systolic blood pressure in the human arterial hypertension. The hypotensive effects of L-arginine are accompanied by an increase of the ventricular ejection fraction. In vitro, L-arginine as physiologic precursor of nitric oxide induced a smooth muscle relaxation more evident in the coronary vessels than in the thoracic aorta rings. Selective inhibition of NO-synthetise with L-NAME reduced the L-arginine vasodilation and intensified the vasoconstrictor effect of phenylephrine.

Amino Acid Oxidoreductases↗
PubMedDate not supplied

Modulatory role of nitric oxide on angiotensins vasoconstriction.

Using aortic rings from male Wistar rats, we studied the influence of nitric oxide (NO) on the vascular reactivity to angiotensins. The inhibition of NO-synthesis by L-NAME produced on both intact and desendothelised rings an augmentation of vascular reactivity to angiotensins. NO inhibition did not affect the blocking effects of Saralasin to angiotensins vasoconstriction, suggesting that NO cannot act directly on angiotensin II receptor. Nifedipin inhibited the stimulatory effect of L-NAME on angiotensins vasoconstriction. The results of our study provide functional evidence that NO production can interfere with vascular RAS at two levels: 1. by modulating the activity of Ang II-forming enzymes; 2. at intracellular level, by modulating the concentration of calcium. Also, our results suggest the existence of an alternative pathway on Ang II formation, that become more evident with removal of endothelium.

Angiotensin I↗