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M A Devynck

Publications and source records attributed to M A Devynck.

At least 181 records · Page 10Linked to original sources
PubMed1979

Plasma renin activity and adrenal angiotensin II receptors in fetal, newborn, adult and pregnant rabbits.

Plasma renin activity (PRA) and adrenal angiotensin II receptors have been studied simultaneously in the rabbit at various stages of development. In the fetus both parameters show very low values but increase rapidly during the last 4 days of gestation. PRA reaches a maximal level in the early post-natal period but the concentration of adrenal angiotensin II receptors continues to increase further up to the adult state. In adult females, pregnancy results in an initial rise in PRA and adrenocortical angiotensin II receptors. However, PRA remains at a high level throughout the gestation period whereas the number of adrenocortical angiotensin II receptors decreases progressively as pregnancy progresses. The role of circulating angiotensin in the regulation of the concentration and affinity of its receptor sites is discussed.

Adrenal Cortex↗
PubMed1978

Alterations of adrenal and uterine angiotensin II receptors during variation of sodium intake and/or experimental hypertension.

1. Angiotensin II receptors from rat adrenal gland and myometrium were studied during variation of sodium intake. 2. In both target-tissues low Na+ diet increased the number of receptors whereas a high Na+ diet did not modify the adrenocortical receptors but increased the number of uterine receptors. 3. Deoxycorticosterone and one kidney Goldblatt hypertension were associated with a decrease in the number of adrenal receptors. 4. Alterations of angiotensin II receptors alone cannot explain satisfactorily the variations of sensitivity of target-cells to angiotensin II during sodium balance changes.

Adrenal Glands↗
PubMed1977

Post-nephrectomy changes in adrenal angiotensin II receptors in the rat; influence of exogenous angiotensin and a competitive inhibitor.

3H-angiotensin binding sites have been studied in a particulate fraction prepared from rat adrenal glands. This binding is rapid and reversible, of high affinity (KD29 degrees C = 3-5 X 10(-9) M) and with demonstrable specificity for the angiotensin II octapeptide. The number of binding sites varies with endogenous angiotensin levels: nephrectomy is followed by an increase in number of binding sites. This increase can be prevented by chronic angiotensin II administration and, to a lesser extent, by administration of Sar1,Ala8-angiotensin II, a competitive antagonist of the hormone. No variation in the equilibrium dissociation constant accompanied these changes in binding capacity. The post-nephrectomy increase in capacity is time-dependent, with a lag period of 24-40 h. The observed changes in receptor concentration do not appear explicable on the basis of receptor occupancy. Accordingly, angiotensin II receptors in the rat adrenal appear to be dependent on circulating angiotensin levels as previously reported for rat uterus.

Adrenal Glands↗
PubMed1977

[Demonstration of specific receptors for angiotensin III in rat adrenal glands].

Distinct and specific binding sites for 3H-angiotensin II (A II) AND 3H-angiotensin III (A III) have been demonstrated in Rat adrenal gland preparations. A III binding sites have the highest affinity (KD29C1-2.10(-10)M) for the 2-8 heptapeptide. This suggests the possibility of a separate and distinct physiological role for the 2-8 heptapeptide, mediated via such A III binding sites.

Angiotensin II↗
PubMed1977

Specific receptors for des-Asp1-angiotensin II (("angiotensin III") in rat adrenals.

The specific binding of angiotensin II and des-Asp1-angiotensin II ("angiotensin III") III") to rat adrenals was studied with the use of the tritiated peptides. The binding sites having maximal affinity for angiotensin II were characterized by an equilibrium dissociation constant of 3.3 to 5.2 X 10(-9) M. Angiotensin III was able to interact with these sites, and also with a class of sites with very high affinity, characterized by an equilibrium dissociation constant of 1 to 2 X 10(-10) M. These sites exhibited a greater affinity for the heptapeptide angiotensin III than for the octapeptide angiotensin II. These findings, together with the known potent aldosterone stimulating effect of angiotensin III and its presence in rat plasma, suggest that this heptapeptide could be the physiologically important steroidogenic angiotensin in this species.

Adrenal Glands↗
PubMed1977

Arterial glucocorticoid receptors: the binding of tritiated dexamethasone in rabbit aorta.

Current concepts of the mechanism of the physiological action of both mineralocorticoids and glucocorticoids include an initial step in interaction between the steroid and specific receptors in the cytoplasm of target tissue cells. Using cells from rabbit aorta as a model system, we have studied the cytoplasmic binding of 3H-dexamethasone and 3H-aldosterone. Aorta cells appear to contain binding sites with a high affinity (Kd 4 degrees C approximately 1.3 X 10(-8) mol) for dexamethasone, and with specificity appropriate for glucocorticoid receptors. Under similar experimental conditions, mineralocorticoid receptors could not be demonstrated.

Aldosterone↗
PubMed1976

Angiotensin receptors in vascular tissue.

The biologic effect of angiotensin II is triggered by its interaction with components of target organs, which specifically recognize the hormone. These receptors have been studied with the use of radioactive angiotensin and, as for other peptidic hormones, have been localized in the plasma membrane of target cells. Such angiotensin receptors have been characterized in three target organs: vascular tissue, uterus and adrenal cortex. The binding characteristics differ in contractile tissue and in adrenal glands, the N and C terminal ends of angiotensin being involved in the former, whereas the N terminus does not appear to have the same importance in the latter. Numerous factors, including ionic composition, seem to be able to modify angiotensin-receptor interaction in vascular smooth muscle. However, the molecular mechanisms responsible for angiotensin binding and for the transmission of the signal determined by receptor-angiotensin interaction are not yet understood. As observed with other peptidic hormones, the number of angiotensin receptors seems to be susceptible to variation under certain conditions. In uterine smooth muscle, it was shown that the number of receptors increased after nephrectomy, a phenomenon which was prevented by the prolonged infusion of angiotensin. The significance of such a variation remains unknown, but it may be partially responsible for the inverse relationship that exists between the endogenous angiotensin level and the pressor effect of exogenous angiotensin. In the near future, investigation of the angiotensin-receptor mechanism will probably answer whether the variation in angiotensin receptors is similar in all target tissues and whether an angiotensin-receptor mechanism is involved in the pathogenesis of certain varieties of hypertension. In addition, a precise understanding of the angiotensin-receptor interaction with help the development of new angiotensin antagonists.

Adrenal Cortex↗
PubMed1976

Variations in the number of uterine angiotensin receptors following changes in plasma angiotensin levels.

3H-labelled angiotensin II binding to receptor sites was studied in plasma membranes isolated from myometrial homogenates of uterine horns. Removal of the kidneys, which results in the disappearance of plasma angiotensin II, was followed 19 h after nephrectomy by an increase in the number of uterine receptor sites without significant variation in the apparent dissociation constant. Acute pressor i.v. injection of angiotensin II into nephrectomized rats immediately before removing uteri, did not affect the number of uterine angiotensin receptors, whereas long-lasting angiotensin infusion did reduce the number of receptors. These changes cannot be accounted for by variations in the occupancy of receptor sites. These results demonstrate that the number of angiotensin receptors, at least in uterine contractile cells, is affected by chronic variations of endogenous angiotensin levels. The relation between the specific supersensitivity to angiotensin II observed in uteri from nephrectomized rats and the variations at the receptor level is discussed.

Angiotensin II↗
PubMed1976

Lack of hypotensive effect on central injection of angiotensin inhibitors in spontaneously hypertensive (SH) and normotensive rats.

1. Injections of antagonists of angiotensin II into the cerebral ventricles of normotensive and spontaneously hypertensive rats were performed in order to assess the role of the isorenin-angiotensin system in the brain. 2. No hypotensive effect was obtained in either normotensive or hypertensive rats, suggesting that intracranial isoangiotensin has little role in the pathogenesis of spontaneous hypertension in the rat.

Angiotensin II↗
PubMed1976

Variations in the number of uterine angiotensin receptors following changes in plasma angiotensin levels.

3H-labelled angiotensin II binding to receptor sites was studied in plasma membranes isolated from myometrial homogenates of uterine horns. Removal of the kidneys, which results in the disappearance of plasma angiotensin II, was followed by an increase in the number of uterine receptor sites without significant variation in the apparent dissociation constant, which became significant 15 h after nephrectomy. Acute pressor intravenous injection of angiotensin II into nephrectomized rats immediately before removing uteri, did not affect the number of uterine angiotensin receptors, whereas long-lasting angiotensin infusion did reduce the number of receptors. These results provided an explanation for the specific supersensitivity to angiotensin II, observed in uteri excised from nephrectomized rats, which cannot be accounted for by variations in the occupancy of receptor sites. These results also demonstrate that the number of angiotensin receptors, at least in uterine contractile cells, is affected by chronic variations of endogenous angiotensin levels.

Angiotensin II↗
PubMed1976

[Variations of membrane hormonal receptors induced by their ligands].

A great deal of research has been carried out on hormonal receptors and their quantitative variations, in particular, those which may be induced by their ligands. Insulin receptors, growth hormone, TRH and catecholamine receptors are already good examples of these variations. The authors have particularly studied angiotensin receptors which also vary with the plasma concentration of the hormone. Numerous questions of molecular biology are raised by these observations and are then discussed. The possible consequences of these discoveries on the physiopathology of endocrine diseases are finally discussed.

Cell Membrane↗