Acute subcutaneous (s.c.) administration of aldosterone increases ex vivo 22Na efflux from rat tail artery smooth muscle, which appears to be due to a specific action on mineralocorticoid receptors. Indeed, this effect is blocked by the antimineralocorticoid compounds RU 28318 [17 beta-hydroxy-3-oxo,7 alpha-propyl(17 alpha)-pregn 4-ene, 21 potassium carboxylate] and spironolactone. The specific glucocorticoid receptor agonist RU 26988 [11 beta,17 beta-dihydroxy-17-(1-propynyl) androesta-1,4,6 trien-3-one] does not modify 22Na efflux. We show here that aldosterone has, at physiological concentrations, a mineralocorticoid specific stimulating effect on passive and sodium pump dependent transmembrane movements of sodium from the rat tail artery smooth muscle. Aldosterone exerts two types of action on sodium transport: 1) a delayed stimulation of ouabain-dependent 22Na efflux and ouabain-independent 22Na efflux, which are completely blocked by actinomycin D; and 2) a very rapid increase of passive 22Na efflux, which is insensitive to actinomycin D and therefore does not seem to depend on transcription of genomic information.

Aldosterone↗

PubMedDate not supplied

Effects of antiglucocorticoids on glucocorticoid hypertension in the rat.

The early phase of hypertension induced in rats by a glucocorticoid agonist RU 26988 was studied. Systolic blood pressure increased by 35 mm Hg. Water and sodium urinary excretion increased transiently, and plasma volume decreased. Total and ouabain-sensitive sodium efflux, as well as rubidium efflux, were enhanced by glucocorticoid administration. Low salt intake did not prevent hypertension. Pretreatment with RU 38486, a steroid with antiglucocorticoid properties, largely prevented the rise in blood pressure (+10 mm Hg) and suppressed transient natriuresis and the decrease in plasma volume. Changes in total and ouabain-sensitive sodium efflux were completely prevented, whereas changes in rubidium efflux were only partly reversed. Similarly, administration of progesterone, a steroid with antiglucocorticoid effects, prevented glucocorticoid hypertension (+11 mm Hg) and vascular ionic changes. In contrast administration of RU 28318, an antimineralocorticoid agent, was without effect on glucocorticoid hypertension (+38 mm Hg). Progesterone or RU 38486 administered after glucocorticoid also decreased blood pressure. Present data indicate that glucocorticoid hypertension may be prevented or reversed in its early phase by steroid drugs with antiglucocorticoid properties. These drugs also appeared to prevent the sodium and rubidium flux abnormalities induced by glucocorticoid. We suggest that activation of the vascular glucocorticoid receptors may be involved in the pathophysiology of glucocorticoid hypertension.

Androstanols↗

PubMedDate not supplied

[Thyroid activity of tadpoles of Alytes obstetricans Laur, deprived of diencephalon].

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Animals↗

PubMedDate not supplied

[Calcitonin, hypocalcemic factor of thyroid origin].

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Amino Acids↗

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Effects of angiotensin II on ionic fluxes in rat myometrium.

1. The action of angiotensin II (At II) on 24Na, 42K and 36 Cl fluxes was examined using longitudinal strips of rat myometrium as an experimental model. 2. In normally polarized muscles, At II 3.3 x 10(-6)M, a concentration 10 times higher than necessary to produce a maximal contraction of the muscle, increases 42K and 36 Cl efflux rates as well as 42K uptake. The action of At II on 42K and 36Cl effluxes is concentration-dependent. Under the same conditions 24Na efflux is not affected by At II, but a significant increase of 24Na uptake is obtained. In order to know whether the observed effects were membrane potential dependent, we reexamined the action of the peptide in preparations previously depolarized by a 101 mM K+ solution (K+ replacing Na+). In depolarized preparations, At II 3.3 x 10(-6)M still increases 24Na uptake, but the effects previously observed on 42K and 36Cl fluxes in normally polarized preparations are suppressed. It is concluded that At II produces a primary increase in the membrane permeability to Na+ and that the stimulation of 42K and 36Cl fluxes induced by At II in myometrial strips appears to be mainly potential dependent.

Angiotensin II↗