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Biomedical subjects

G Petrescu

Publications and source records attributed to G Petrescu.

At least 19 recordsLinked to original sources
PubMed2004

New bioactive angiotensins formation pathways and functional involvements.

After a brief review of the actual knowledge concerning the circulating and tissue Renin-Angiotensin System (RAS) as a unitary hormonal system, the cognitive acquisitions regarding the formation and action mechanisms of the new biologically active angiotensins will be presented. The review of the enzymatic pathways for their synthesis and inactivation, as metabolism products of angiotensin II (1-8), will be followed by the presentation of the main physio-pharmacological actions of angiotensin III (2-8), angiotensin IV (3-8) and angiotensin (1-7). The functional involvements of the cerebral angiotensin IV in what concerns its possible participation in the normal neurochemical processes of memory and in the neurodegenerative processes of Alzheimer disease will be exposed, together with the vasodilating effects of angiotensin (1-7) as counteracting factor for the constricting effects of angiotensin II. The data concerning the bioactive fragments of angiotensin II will be accompanied by those regarding its implication in the cardiovascular modeling and the induction of oxidative stress, inflammation, atherogenesis, etc. In their turn, personal researches bring new experimental evidences in favor of interactions between angiotensin (1-7) and angiotensin II within the rat thoracic aorta. Biphasic, dose-dependent effects were observed for angiotensin (1-7), induced both through nitric oxide, kinins and prostaglandin release for counteracting the vasoconstricting effects of angiotensin II and the modulation of its own vasodilator action.

Angiotensins↗
PubMed2001

Contractile effects of angiotensin peptides in rat aorta are differentially dependent on tyrosine kinase activity.

It has been suggested that tyrosine kinase activity participates in the regulation of signal transduction associated with angiotensin II (Ang II)-induced pharmaco-mechanical coupling in rat aortic smooth muscle. We further tested the effects of genistein, a tyrosine-kinase inhibitor, and its inactive analogue, daidzein, on angiotensin I (Ang I), angiotensin III (Ang III) and angiotensin IV (Ang IV) contractions, as compared with those on Ang II. Genistein partially inhibited Ang II- and Ang I-induced contractions. The genistein-induced inhibition was more evident on Ang III and especially important on Ang IV contractile effects. Thus, Ang IV- and Ang III-induced contractions seem to be more dependent on tyrosine kinase activity than those evoked by Ang II or Ang I. Daidzein did not significantly affect the contractile effects of any of angiotensin peptides tested. These results clearly suggest that the inhibition of the action of angiotensin peptides actions by genistein is mediated by inhibition of endogenous tyrosine kinase activity. Furthermore, our data show that the type and/or intensity of tyrosine kinase activity is differentially associated with the contractile effects of different angiotensin peptides in rat aorta. Nifedipine, a blocker of membrane L-type Ca2+ channels, strongly inhibited Ang IV-induced contractions. At the same time, it significantly inhibited Ang III contractile effects as compared with Ang II and Ang I contractions. Meanwhile, we observed a close relationship between calcium influx and tyrosine kinase phosphorylation activity under the stimulatory effects of angiotensin peptides. Furthermore, genistein did not significantly influence the phasic contractions induced by angiotensin peptides in Ca2+-free Krebs-Henseleit solution. Thus, it appears that Ca2+ influx, rather than the release of Ca2+ from IP3-sensitive stores, may play a major role in the contractile effects of angiotensin peptides in rat aorta via tyrosine kinase activation. One argument against a direct action of genistein on the Ca2+ channel itself is that it did not markedly affect the K+-induced contraction (depolarisation) in rat aorta. At the same time, a potential role for tyrosine kinase activity in the process of calcium entry is suggested. An elevation of intracellular calcium via tyrosine kinase-mediated processes may mediate the actions of G-protein coupled receptor agonists in smooth muscle, including angiotensin peptides.

Angiotensin Receptor Antagonists↗
PubMed1998

Extracellular and intracellular arachidonic acid-induced contractions in rat aorta.

Arachidonic acid induced contractions of de-endothelized rat aortic rings. A more potent effect was obtained after intracellular administration of arachidonic acid using liposomes. Contractions induced by extracellular arachidonic acid were inhibited similarly to phenylephrine-induced contractions by the L-type Ca2+ channel blocker, methoxyverapamil (D600), and the calmodulin inhibitor, calmidazolium. In contrast, contractions induced by arachidonic acid-filled liposomes were not affected by these compounds. Indomethacin did not affect the contractions induced by either extra- or intracellular arachidonic acid, whereas nordihydroguaiaretic acid relaxed contractions induced by extracellular arachidonic acid but not those induced by arachidonic acid-filled liposomes. Apart from a relaxing effect on contractions induced by extracellular arachidonic acid or by phenylephrine, protein kinase C inhibition with 1-(5-isoquinolinesulphonyl-2-methylpiperazine (H7)) had an even more prominent relaxing effect on contractions induced by arachidonic acid-filled liposomes. Therefore, arachidonic acid exerts a contractile effect on rat aorta, and this effect is regulated differently depending on the site of application.

Animals↗
PubMed1981

Possible hormonal role of the angiotensin-like peptides in mammals' pineal gland.

An isorenin is synthetized in the pineal gland cells. The amount of isorenin as well as the synthesis of angiotensin I and II in the pineal gland depends on the circadian rhythm, osmotic stimuli and stimulation of the cervical sympathetic postganglionar fibres. Pineal angiotensin is released both into the blood and in the cerebrospinal fluid (CFS). The major site of the pineal angiotensin action are the circumventricular organs, the preiventricular receptors of the anterior hypothalamus and the epiphysis cerebri itself. Except its participation in regulating arterial pressure and the hydroelectrolytic metabolism, through its central effects on the brain, pineal angiotensin-like peptides also participate in the pool of circulating angiotensin and it may represent Farrell's pineal glomerulotropic factor.

Angiotensin I↗
PubMed1980

Influence of angiotensin II on dog pineal serotonin content.

Intravenous infusion of angiotensin II in different concentrations for 2 h induced an increase in the serotonin contents of pineal gland, hypothalamus and brain stem in dogs. The maximal stimulatory effect was obtained with a concentration of 50 ng angiotensin II/kg body wt./min. Results are interpreted with regard to the concept of an intrinsic isorenin-angiotensin system and its implications at the level of brain nervous tissue and accessory glands. Experimental data indicating the possible existence of positive and negative feedback relationships between the brain isorenin-angiotensin system and serotonin metabolism in the pineal gland, are presented.

Angiotensin II↗
PubMed1978

Iso-renin secretion from rat brain cortex slices in vitro under the influence of ions and electrical stimulation.

The aim of this study was to obtain additional data concerning the influence of changes in osmolarity and ionic composition on iso-renin secretion from rat brain cortex slices. The slices were isolated and superfused in vitro according to the technique of Pull and McIlwain (1972). The secretion of iso-renin was strongly stimulated by an increase of Na+ concentration. Iso-renin output almost doubled upon raising NaCl from 120 to 240 mM. Decrease of the NaCl concentration to 60 mM resulted in a reduced iso renin secretion while addition of tetrodotoxin (TTX) (60 micron) did not significantly alter the iso-renin content of brain slices. Changes in osmotic pressure were without significant influence. Electrical stimulation or elevation of extracellular K+ concentrations enhanced iso-renin secretion. Furthermore, Ca2+ ions seem to increase both the content and the release of cerebral iso-renin.

Animals↗
PubMedDate not supplied

TLC characterization of liposomes containing angiotensinogen, angiotensine I, angiotensine II and saralazin.

Recent studies have described intracellular binding sites for angiotensine II. In vascular smooth muscle it was found that intracellular injection of angiotensin II increases the Ca2+ level. An alternative method for intracellular delivery of drugs is represented by using liposomes. Thus, the aim of this study was to characterize liposomes filled with angiotensinogen, angiotensine I (Ang I), angiotensine II (Ang II), and saralasin by a TLC method and examine the physiological effects of these on rat vascular smooth muscle. Ang II (for all concentrations tested in the aqueous phase) and Ang I (for concentrations less than 10(-4)M) did not affect the thin-layer chromatography migration of this type of vesicle, suggesting that dose-dependent effects on physio-pharmacological experiments could be studied. On the other hand, this type of experiment could not be performed for salarasin- or angiotensinogen-filled liposomes. Administration of liposomes containing Ang II (10(-6)M), Ang I (10(-6)M), angiotensinogen (10(-6)M) and saralasine (10(-6)M) caused the contraction to isolated rat aorta smooth muscle, suggesting the presence of active intracellular binding sites.

Angiotensin I↗