�ber die Wirkung der Heparinbehandlung auf das histologische Bild der Nebennierenrinde und auf den Index der juxtaglomerul�ren granulierten Zellen im Nierengewebe

Vallent, K; Fachet, J; Palkovits, M; Devenyi, I

doi:10.1007/bf00339919

Cited by 12 publications

(4 citation statements)

References 15 publications

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“…The heparin dose used in the in vivo experiment was about 10-fold that employed in the clinical situation. In addition, prolonged heparin or heparinoid treatment in vivo is known to cause a reduction in the width of the zona glomerulosa in man (Wilson & Goetz 1964) and rats (Valient et al 1964;Abbott et al 1966;Levine et al 1972). Such a morphological change could influence the heparin effect on the All receptors and the All-induced aldosterone production be¬ cause of decreased mass of tissue.…”

Section: Discussionmentioning

confidence: 92%

See 1 more Smart Citation

Effects of heparin treatments in vivo and in vitro on adrenal angiotensin II receptors and angiotensin II-induced aldosterone production in rats

Azukizawa

Iwasaki²,

Kigoshi³

et al. 1988

Acta Endocrinologica

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To evaluate the heparin effects in vivo and in vitro on adrenal angiotensin II receptors and angiotensin II-induced aldosterone production, we examined the angiotensin II binding and the maximum angiotensin II-induced aldosterone production using adrenal glomerulosa cells from rats treated with a heparin preparation containing benzyl alcohol (1500 IU/kg, twice daily for 6 weeks) or cells to which heparin (300 IU/l) was directly added. Comparison was made using the cells from rats treated with vehicle or the cells to which vehicle was directly added. Specific binding of [125I]iodo-angiotensin II was decreased in the cells from heparin-treated rats or in the heparin-treated cells. Scatchard analysis showed that the decrease in binding was due to a decrease in both the number and the affinity of angiotensin II receptors in the cells from heparin-treated rats and a decrease in the number, but not the affinity, of the receptors in the heparin-treated cells. Heparin also caused a decrease in the maximum angiotensin Il-induced production, but not the basal production, of aldosterone in the cells from hepari n\x=req-\ treated rats and in the heparin-treated cells. These data suggest that heparin interacts with adrenal angiotensin II receptors to inhibit the angiotensin Il-induced aldosterone production.

show abstract

Section: Discussionmentioning

confidence: 92%

“…It may be related to the duration of expo¬ sure to heparin. Prolonged exposure to heparin in vivo could alter not only the number but also the affinity of All receptors directly or by forming some active substance, in addition to a heparininduced decrease in the mass of the glomerulosa tissue (Valient et al 1964;Wilson & Goetz 1964).…”

Section: Discussionmentioning

confidence: 99%

Effects of heparin treatments in vivo and in vitro on adrenal angiotensin II receptors and angiotensin II-induced aldosterone production in rats

Azukizawa

Iwasaki²,

Kigoshi³

et al. 1988

Acta Endocrinologica

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show abstract

“…In man (Wilson & Goetz 1964) and rats (Valient et al 1964;Abbott et al 1966b;Levine et al 1972), prolonged treatment with heparin or heparinoid is shown to decrease the width of the adrenal zona glomerulosa. Such a morphological change could also contribute to lowering basal levels and subse¬ quent responses of aldosterone and its precursor steroids to a given stimulus because of a reduction in the mass of zona glomerulosa cells.…”

Section: Discussionmentioning

confidence: 96%

Effect of angiotensin II on aldosterone and its precursor steroid production in adrenal zona glomerulosa cells from heparin-treated rats

Uchida

Azukizawa

Imaizumi

et al. 1986

Acta Endocrinologica

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To assess the nature of the heparin-induced aldosterone deficiency, we investigated the stimulatory effect of angiotensin II (All) on aldosterone and its precursor steroids in adrenal zona glomerulosa cells from heparin-treated rats compared with those in the cells from vehicle-treated rats. Heparin-treated rats had low plasma aldosterone levels, high plasma renin activity and plasma All levels, and normal plasma corticosterone level 6 weeks after the treatment (1500 IU/kg, twice daily). Basal aldosterone production, when corrected to a uniform number of cells per group, was similar in the cells from heparin-and vehicle-treated rats. The cells from heparin-treated rats had a less sensitive and lower response of aldosterone production to All; an increase by 4 orders of magnitude in the threshold dose for All and a decrease in the maximum All-stimulated level.The maximum All-stimulated levels, but not the basal levels, of pregnenolone, corticosterone and 18-OHB production were low in the cells from heparin-treated rats.ACTH caused a similar stimulatory effect on aldosterone production in the cells from heparin-and vehicle-treated rats. The cells from heparin-treated rats had a less sensitive and lower response of aldosterone production to potassium; an increase by one order of magnitude in the threshold dose for potassium and a decrease in the maximum potassium-stimulated level, presumably because of the glomerulosa hyporesponsivness to AII. These results suggest that our heparin-treated rats have selective impairment of adrenal zona glomerulosa cells, involving the specific receptors and the aldosterone bio¬ synthesis, to AIL

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“…This explanation is in accordance with the histological findings in rats treated with these drugs. Vallent et al (35) reported a decreased width of the zona glomerulosa of salt-depleted rats after administration of heparin. Abbott et al (2,3) found atrophy of the zona glomerulosa of rats on normal sodium intake without clearcut alterations in the zona fasciculata after treatment with Ro 1-8307, and Chremos et al (14) obtained identical results in regenerating rat adrenal glands and in intact adrenals of sodium-deprived rats.…”

Section: Subjmentioning

confidence: 98%

INHIBITION OF ADRENAL FUNCTION IN MAN BY HEPARIN OR HEPARINOID Ro 1‐8307

Kloppenborg

Casparie

Benraad

et al. 1975

Journal of Internal Medicine

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Heparin and the heparinoid Ro 1‐8307 inhibited the secretory rate of aldosterone in physiological or pathological aldosteronism to the level found in normal subjects on liberal sodium intake. In addition, these compounds inhibited corticosterone biosynthesis, although less markedly than that of aldosterone. Indications of interference with Cortisol production have not been found. During drug treatment angiotensin, in doses of 5–10 ng/kg b.wt./min, did not stimulate aldosterone secretion. ACTH responsiveness of the adrenals—indicated by the fractional increases of both aldosterone and corticosterone secretory rates—remained unchanged. In two studies heparin had no consistent effect on plasma renin activity.

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�ber die Wirkung der Heparinbehandlung auf das histologische Bild der Nebennierenrinde und auf den Index der juxtaglomerul�ren granulierten Zellen im Nierengewebe

Cited by 12 publications

References 15 publications

Effects of heparin treatments in vivo and in vitro on adrenal angiotensin II receptors and angiotensin II-induced aldosterone production in rats

Effects of heparin treatments in vivo and in vitro on adrenal angiotensin II receptors and angiotensin II-induced aldosterone production in rats

Effect of angiotensin II on aldosterone and its precursor steroid production in adrenal zona glomerulosa cells from heparin-treated rats

INHIBITION OF ADRENAL FUNCTION IN MAN BY HEPARIN OR HEPARINOID Ro 1‐8307

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