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      Aldosterone (ALDO) increases transmembrane influx of Na+ in vascular smooth muscle (VSM) cells through increased synthesis of Na+ channels.

      1 ,

      Steroids

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          Abstract

          We have previously reported our studies on glucocorticoid (GC) effects on Na+ influx in vascular smooth muscle (VSM) cells. We now report a parallel study on the effect of mineralocorticoid (MC) on Na+ influx in VSM cells. Unidirectional influx of Na+ was measured in cultured cells of rabbit aortic media with 22Na as tracer. Cells were treated with near physiologic (5 nM) or supraphysiologic (50 nM) aldosterone (ALDO) for 24 or 48 hours, or for 7 to 10 days, in the presence of competitive inhibitors of MC-receptor binding, K-prorenoate (PRN), or GC-receptor binding, RU 486. ALDO at 5 nM increased Na+ influx by 98% +/- 12%, but only after 7-10 days of treatment. This effect was inhibited by PRN, but not by RU 486, and blocked by amiloride but not by ethylisopropyl-amiloride or by dichlorobenzamil (DCB). In VSM cell membranes from aortae of rabbits treated in vivo with ALDO (2 mg/day) for 4 weeks. Na+ channels were quantified by determination of specific [3H]amiloride binding in the presence of excess of DCB and EIPA to exclude tracer binding from the Na+/Ca2+ exchanger and the Na+/H+ antiporter. ALDO doubled the number of of Na+ channels in such isolated cell membranes, as determined by Bmax per mg membrane protein. We propose that this vascular effect of ALDO may constitute an important pathogenetic mechanism of hypertension induced by chronic excess of MC, in addition to the well known renal mechanism.

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          Most cited references 25

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          Myosin phosphorylation and the cross-bridge cycle in arterial smooth muscle.

          Phosphorylation of the 20,000-dalton light chain of myosin is closely correlated with cross-bridge cycling in arterial smooth muscle. Evidence is presented that dephosphorylation can produce an attached, noncycling cross-bridge (latch-bridge) which is responsible for the high economy of force maintenance in this tissue.
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            Mineralocorticoid-induced hypertension in patients with orthostatic hypotension.

             L Liang,  L Volicer,  D Faxon (1979)
            The mechanism of recumbent hypertension induced by fludrocortisone was studied in seven patients with orthostatic hypotension. All showed increases in blood pressure in the recumbent and standing positions, and hypertensive levels were achieved on recumbency in four of them. Hypertensive retinopathy developed in two patients and cardiomegaly in one. Initial blood-pressure elevations were associated with sodium retention and plasma-volume expansion. However, with long-term treatment, plasma volume decreased to control levels despite further blood-pressure increases. Treatment did not affect plasma levels of catecholamines but did enhance pressor responsiveness to infused norepinephrine in some subjects. Hemodynamic studies indicated that hypertension in the recumbent position was related to increases in total peripheral-vascular resistance and not to changes in cardiac output. Clinically, hypertension in the recumbent position is an important risk of fludrocortisone treatment in patients with orthostatic hypotension. This unusual model of chronic mineralocorticoid-induced hypertension is not volume dependent but is related to increased peripheral-vascular resistance.
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              Mineralocorticoid binding in cultured smooth muscle cells and fibroblasts from rat aorta.

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                Author and article information

                Affiliations
                [1 ] Department of Medicine, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois, USA.
                Journal
                Steroids
                Steroids
                0039-128X
                0039-128X
                Jan 1995
                : 60
                : 1
                0039-128X(94)00016-6
                7792795

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