Search PubMed⌕ Search

Biomedical subjects

A Carayon

Publications and source records attributed to A Carayon.

At least 91 records · Page 5Linked to original sources
PubMed1989

Atrial natriuretic factor messenger ribonucleic acid and peptide in the human heart during ontogenic development.

We have investigated the level of expression of the atrial natriuretic factor (ANF) gene in the human heart during ontogenic development by determining the concentrations of ANF messenger ribonucleic acid (ANF mRNA), of immunoreactive ANF (IR ANF) and of receptor reactive ANF (RR ANF), in myocardial samples of the various heart chambers. We found the level was high and almost identical in the left and right ventricles in utero. It gradually decreased during ontogenic development to reach the low adult levels, with a more rapid decrease in the right than in the left ventricle after birth. In the atria, ANF gene expression was high as early as the 13th week of gestation, was higher in the right than in the left atrium, and appeared little affected by ontogenic development.

Aging↗
PubMed1989

Opioid control of the in vitro release of calcitonin gene-related peptide from primary afferent fibres projecting in the rat cervical cord.

In vitro superfusion of slices from the dorsal half of the rat cervical enlargement allowed the measurement of spontaneous, K+ (30 mM)- and capsaicin (0.5 microM)-evoked release of calcitonin gene-related peptide-like immunoreactive material (CGRPLI). The greater part of this immunoreactive material originated in primary afferent fibres since dorsal rhizotomy from C4 to Th2 (8 days before sacrifice) resulted in a 85-90% decrease in CGRPLI release. CGRPLI outflow which persisted after dorsal rhizotomy could still be enhanced by K+-induced depolarization but was no longer sensitive to the stimulatory effect of 0.5 microM capsaicin. Both delta (DTLET, D-Pen2-D-Pen5-enkephalin) and mu (DAGO, PL 017) opioid receptor agonists reduced the K+ evoked release of CGRPLI from the dorsal half of the cervical enlargement. Morphine was also inhibitory but the selective K opioid agonist U 69593 was inactive. As expected from the involvement of delta and mu receptors, the selective opioid antagonist ICI 174864 and naloxone prevented the inhibitory effects of DTLET and DAGO, respectively. These data suggest that opioid-induced presynaptic inhibiton of CGRP-containing primary afferent fibres may be involved in the analgesic effect of intrathecally injected delta and mu opioid agonists in rats.

Afferent Pathways↗
PubMed1988

Plasma concentrations of atrial natriuretic peptide in patients with artificial and transplanted hearts.

Plasma atrial natriuretic peptide (ANP) concentrations were measured by radioimmunoassay 1 to 12 days after operation in six patients with artificial hearts. The mean levels were significantly higher in artificial heart recipients (58.2 pg.ml-1) than in controls (12.6 pg.ml-1). The mechanism underlying the raised values is not clear, although it is suggested that elevated atrial pressure may have been the stimulus for higher ANP release. In 3 patients plasma ANP concentrations were also measured 1 to 5 days after orthotopic transplantation. In all of them ANP concentrations had increased by 20 to 74% despite lower right atrial pressure. An increase in atrial tissue mass may have contributed to the raised plasma ANP after orthotopic transplantation. It also suggests that the functioning sympathetic nervous system is not a necessary condition for ANP release.

Adult↗
PubMed1988

Angiotensin II-like material extracted from the rat brain is distinct from authentic angiotensin II.

Specific radioimmunoassay and radioreceptor assay for angiotensin II (A II) were used for the possible identification of this peptide in the rat brain. An A II-like material (A II-LM) was detected with both assays applied to acidic extracts of various brain structures. The regional distribution of A II-LM was uneven, but absolute levels (in A II equivalents) could not be accurately determined, as they were highly dependent on the assay used. Partial purification of A II-LM by Sep-Pak C 18 chromatography and affinity chromatography using anti-A II antibodies bound to Ultrogel gave a compound coeluting with authentic A II in reverse-phase HPLC. However, gel filtration through Sephadex G-25 and TSK Spherogel 3000 SW as well as anion exchange HPLC demonstrated that A II-LM did not correspond to authentic A II. Partial characterization of A II-LM indicated that this compound was probably a peptide with an apparent molecular weight of 5,000-7,000 (instead of 1,046 for A II) and more polar but less positively charged than A II. Whether A II-LM is, in fact, the endogenous ligand of A II binding sites in brain remains an interesting hypothesis for further investigations.

Angiotensin II↗
PubMed1988

Effects of ciclosporin on plasma renin activity, catecholamines and prostaglandins in patients with idiopathic uveitis.

Animals and humans undergoing treatment with ciclosporin (CS) show a reversible increase in renal vascular resistance and a decrease in glomerular filtration rate. The causes of these abnormalities have not yet been established. We evaluated the effects of a 1-week treatment with CS on creatinine clearance, renal arachidonic acid metabolites, plasma renin activity (PRA), plasma aldosterone levels, urinary excretion and plasma levels of catecholamines in 7 patients with idiopathic uveitis. We show that CS treatment induces a significant (p less than 0.05) decrease in creatinine clearance (from 132 +/- 0.5 to 108 +/- 8 ml/min); urinary 6-keto-PGF1 excretion (from 17.8 +/- 4.9 to 10.9 +/- 3.3 ng/mmol creatinine), urinary thromboxane B2 excretion (from 7.0 +/- 1.0 to 3.6 +/- 0.9 ng/mmol creatinine), upright PRA (from 4.2 +/- 0.9 to 2.3 +/- 0.8) and supine PRA (from 2.0 +/- 0.5 to 1.1 +/- 0.3). We found no change in plasma aldosterone levels and plasma levels and urinary excretion of catecholamines. We suggest that the reversible renal vasoconstriction observed in patients treated with CS may be induced by inhibition of renal prostacyclin synthesis. In this setting inhibition of PRA and angiotensin II formation may impair autoregulation of effective filtration pressure and therefore glomerular filtration rate.

Adult↗
PubMed1988

Aldosterone secretion and adrenal angiotensin II receptors in the Brattleboro rat.

The basal secretion of aldosterone, measured in adrenal venous blood, was three- to fourfold lower in Brattleboro than in Long-Evans rats used as controls. Infusion of a low dose of angiotensin II (1 ng/min per 100 g body/wt) to Long-Evans rats caused a fourfold increase in aldosterone release but neither the low dose nor a tenfold higher dose changed the rate of release in Brattleboro rats. Only a very high dose (300 ng/min per 100 g body wt) succeeded in increasing the secretion of aldosterone in Brattleboro rats but throughout the time-course of the infusion, secretion remained about fivefold lower than in Long-Evans rats and the incremental response was reduced by 74.9%. Adrenal zona glomerulosa angiotensin II receptor sites had similar affinity and maximum binding capacity in the two groups of rats. It is suggested that the reduced corticosteroidogenic capacity of the adrenal cortex of Brattleboro rats results from an impairment of the post-receptor mechanisms involved in the biosynthesis of aldosterone.

Adrenal Cortex↗
PubMed1988

[Atrial natriuretic factor, catecholamines and the renin-angiotensin system in cardiac insufficiency. Relation to hemodynamic parameters].

Plasma concentrations of atrial natriuretic factor (ANF), catecholamines (adrenaline, noradrenaline, dopamine) and aldosterone, and plasma renin activity (PRA) were measured in a group of 20 patients with moderate to medium heart failure (NYHA class II 7 patients, class III 13 patients), 24 hours after treatment was discontinued. Compared with a control group, plasma concentrations of ANF (p less than 0.01), noradrenaline (p less than 0.05), aldosterone (p less than 0.01) and PRA (p less than 0.01) were significantly increased. There was a significant difference between class II patients and class III patients in plasma ANF (p less than 0.01) and noradrenaline (p less than 0.02) concentrations, but not in PRA and aldosterone levels. A significant correlation was observed between plasma ANF concentration and left ventricular end-diastolic pressure (r = 0.68, p less than 0.001), pulmonary arterial pressure (r = 0.59, p less than 0.01), pulmonary capillary pressure (r = 0.51, p less than 0.02), cardiac index (r = 0.46, p less than 0.05) and left ventricular end-diastolic volume (r = 0.50, p less than 0.05). However, ANF concentration was not correlated with mean right atrial pressure. Plasma adrenaline concentration correlated with systemic arterial resistance (r = 0.80, p less than 0.001), pulmonary arterial pressure (r = 0.57, p less than 0.02), mean pulmonary capillary pressure (r = 0.62, p less than 0.001), cardiac index (r = 0.53, p less than 0.05) and left ventricular end-diastolic pressure (r = 0.58, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Atrial natriuretic factor in cardiovascular pathology].

Atrial natriuretic factor (ANF) is a cardiac peptide hormone whose detection led to the discovery of a new natriuretic vasomotor relaxant hormonal system where the heart plays the role of an endocrine gland. Atrial distension represents the main stimulus for the release of ANF. Its cardiovascular effects consist primarily of hypotension related to its relaxant properties, a decrease in cardiac output and a negative inotropic effect. The close relations between ANF and the heart implicate this hormone as a major factor in all cardiovascular disorders, and in particular in congestive heart failure where its plasma concentration represents an index of hemodynamic and functional disease severity. Hemodynamic changes related to valvular heart disease, whether of the mitral or aortic valve, as well as dysrhythmias have a significant effect on release of ANF. Thus, it is now well recognized that ANF, released by the heart, is implicated in the pathophysiology of cardiovascular disorders.

Arrhythmias, Cardiac↗
PubMed1986

Identification of urinary metabolites of penticainide in the rat, dog, baboon and man.

[14C]-Penticainide, 2-[2-(diisopropylamino) ethyl]-4-methyl-2-(2-pyridyl)pentanamide, a new antiarrhythmic agent, was administered as a single oral dose to rats, dogs, baboons (30 mg kg-1) and to healthy, informed volunteers (300 mg). Excretion of radioactivity was followed for 3 days in urine and faeces. In man, about 95% of the administered radioactivity was eliminated in the urine and levels ranging from 56 to 86% were observed in animals. The radioactivity that did not appear in the urine was almost quantitatively recovered in the faeces. Metabolites in urine were isolated by thin-layer chromatography and identified by mass spectrometry and nuclear magnetic resonance. In addition to the unchanged drug, nine metabolites and an artifact compound resulting from the partial degradation of one metabolite, were identified among the thirteen radioactive compounds detected. The major metabolites resulted from N-dealkylation of the diisopropyl moiety, oxidation of the isobutyl side-chain and hydrolytic cleavage of the amide. Comparison of the excretion and metabolic patterns of animals with those of man revealed that the dog should be a most suitable model for predicting the pharmacological and toxicological effects of penticainide in man.

Animals↗
PubMed1986

Renin-angiotension-aldosterone system, urinary prostaglandins and kallikrein in pregnancy-induced hypertension: evidence for a dysregulation of the renin-angiotensin-prostacyclin loop.

Plasma renin activity (PRA) and aldosterone concentrations were measured simultaneously with urinary excretion of kallikrein and of four prostaglandins (PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TXB2) in 23 patients with pregnancy-induced hypertension (PIH; 17 with permanent PIH (PH) and six with labile PIH (LH), i.e. patients whose hypertension was controlled only by home bed-rest) and in 16 normotensive pregnant women. Plasma renin activity was lower in PH than in controls or in LH. No difference between the three groups was observed for plasma aldosterone and urinary excretion of kallikrein and prostaglandins except that TXB2 was higher in LH than in PH. Thus patients with LH have a different biological profile from that of PH, since they have higher PRA and higher TXB2 excretion, an association that suggests a more pronounced ureteral compression by the gravid uterus in this group. Although no decreased synthesis of vasodilating prostaglandins was found in PH, a dysregulation of the renin-angiotensin-prostacyclin loop is suggested by a negative correlation between PRA and 6-keto-PGF1 alpha. An independent vasopressive substance which would stimulate PGI2 and suppress renin secretion is therefore postulated.

Female↗
PubMed1986

Partial characterization of angiotensin II-like material extracted from the rat brain.

Angiotensin II (ANG II)-like material was detected in acid extracts of rat brain using radio-immunoassay (RIA) and a radioreceptor assay (RRA). This material, expressed as ANG II equivalents, corresponded to 131 +/- 20 fmol/g and 33 +/- 4 pmol/g as assessed by RIA and RRA respectively. Such quantitative differences indicated that the brain material did not behave as authentic ANG II in both assays, and further chromatographic investigations confirmed this inference. In particular, gel filtration through Sephadex G-25 and TSK Spherogel 3000 SW revealed that the apparent molecular weight of ANG II-like material was much higher (approximately 5000-7000) than that of authentic ANG II. Furthermore, in contrast to the marked hypertension due to ANG II, a decrease in blood pressure (BP) was observed in rats following the systemic administration of chromatographic eluates enriched with brain ANG II-like material.

Angiotensin II↗
PubMed1985

Plasma ferritin in old age. Influence of biological and pathological factors in a large elderly population.

The effects of biological (age, sex, weight) and pathological factors on plasma ferritin concentrations were documented in 776 unselected elderly patients aged 80.9 +/- 9.7 yr. A marked shift towards high values (159 +/- 142 micrograms/l) was observed in this elderly population together with the persistence of the well-known sex-related difference in ferritin levels (higher levels in men). Twenty-five percent of the population had high levels of ferritin (greater than or equal to 220 micrograms/l) but 75% of these high values (i.e. 18.5% of the population) could be readily explained by their known association with a particular pathology (inflammatory syndrome, renal failure, cardiovascular diseases, alcoholism). Only 6% of the population had unexplained high ferritin concentrations. Therefore, our data strongly suggest that the repeatedly reported increase of ferritin in the aged population is merely related to an age-associated pathology and may not be a normal physiological event occurring during the process of aging.

Aged↗