Effect of DCA on development of renoprival hypertension

Langford, Herbert G.; Snavely, John Robert

doi:10.1152/ajplegacy.1959.196.2.449

Cited by 22 publications

(9 citation statements)

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“…However, the mechanism of corticosteroid-induced hypertension is not yet clear. Although renal sodium retention and intravascular volume overload contribute to the attendant hypertension, especially early in the course of the disease, non-renal mechanisms, such as the increase in peripheral vascular resistance, appear to play an important role in its development and maintenance [23]. It has been shown that corticosteroids potentiate the vasoconstrictor actions of vasoactive agonists such as 5-HT, NE and angiotensin II [8,9,11,[24][25][26][27][28][29][30][31][32].…”

Section: Discussionmentioning

confidence: 99%

Enhancement of receptor-operated cation current and TRPC6 expression in arterial smooth muscle cells of deoxycorticosterone acetate-salt hypertensive rats

Bae¹,

Kim

Lee

et al. 2007

Journal of Hypertension

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Section: Discussionmentioning

confidence: 99%

Enhancement of receptor-operated cation current and TRPC6 expression in arterial smooth muscle cells of deoxycorticosterone acetate-salt hypertensive rats

Bae¹,

Kim

Lee

et al. 2007

Journal of Hypertension

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“…Despite repeated demonstration of the effects of aldosterone in both in vitro and in vivo experimental settings [2,3], its physiologic significance as a regulator of vascular tone in health and disease remains to be established.…”

Section: Aldosterone and Vascular Tonementioning

confidence: 99%

Aldosterone and vascular damage

Duprez

Buyzere

Rietzschel

et al. 2000

Current Science Inc

105

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Although the aldosterone escape mechanism is well known, aldosterone has often been neglected in the pathophysiologic consequences of the activated renin-angiotensin-aldosterone system in arterial hypertension and chronic heart failure. There is now evidence for vascular synthesis of aldosterone aside from its secretion by the adrenal cortex. Moreover, aldosterone is involved in vascular smooth muscle cell hypertrophy and hyperplasia, as well as in vascular matrix impairment and endothelial dysfunction. The mechanisms of action of aldosterone may be either delayed (genomic) or rapid (nongenomic). Deleterious effects of aldosterone leading to vascular target-organ damage include (besides salt and water retention) decreased arterial and venous compliance, increased peripheral vascular resistance, and impaired autonomic vascular control due to baroreflex dysfunction.

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“…The downstream effects of GR activation within the arterial wall, and their influence on cardiovascular risk factors (such as hypertension), are imperfectly understood [5]. Glucocorticoids are essential for maintenance of blood pressure in healthy individuals [1], whilst their ability to increase peripheral vascular resistance in animals devoid of renal mass indicates that a non-renal mechanism contributes to glucocorticoid-induced hypertension [30]. A considerable body of evidence suggests that this non-renal mechanism may involve direct glucocorticoid-mediated alteration of EC and VSMC function [1].…”

Section: Introductionmentioning

confidence: 99%

Intra-vascular glucocorticoid metabolism as a modulator of vascular structure and function

Hadoke

Macdonald

Logie

et al. 2006

Cell. Mol. Life Sci.

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The ability of glucocorticoids to directly alter arterial function, structure and the inflammatory response to vascular injury may contribute to their well-established link with the development of cardiovascular disease. Recent studies have emphasised the importance of tissue-specific regulation of glucocorticoid availability by the 11 beta-hydroxysteroid dehydrogenase (11HSD) isozymes, which inter-convert active glucocorticoids and their inactive metabolites. The expression of both type 1 and type 2 11HSDs in the arterial wall suggests that prereceptor metabolism of glucocorticoids may have a direct impact on vascular physiology. Indeed there is evidence that 11HSDs influence glucocorticoid-mediated changes in vascular contractility, vascular structure, the inflammatory response to injury and the growth of new blood vessels. Hence, inhibition of 11HSD isozymes may provide a novel therapeutic target in vascular disease.

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Effect of DCA on development of renoprival hypertension

Abstract: The administration of DCA (desoxycorticosterone acetate) to nephrectomized dogs drinking 1% saline speeds the development of hypertension. Studies on nephrectomized rats given 0.9% saline intraperitoneally show that this is not due to increased sodium intake or overhydration.

Cited by 22 publications

References 0 publications

Enhancement of receptor-operated cation current and TRPC6 expression in arterial smooth muscle cells of deoxycorticosterone acetate-salt hypertensive rats

Enhancement of receptor-operated cation current and TRPC6 expression in arterial smooth muscle cells of deoxycorticosterone acetate-salt hypertensive rats

Aldosterone and vascular damage

Intra-vascular glucocorticoid metabolism as a modulator of vascular structure and function

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