Mechanism of Mineralocorticoid-induced Hypertension

Mitchell, John W.; Bohr, David F.

doi:10.1007/978-3-642-69081-5_8

Cited by 6 publications

(1 citation statement)

References 39 publications

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“…Taken together these data suggest that there is no simple relation between the ability of a steroid to retain Na a 'mineralocorticoid' effect and its ability to raise blood pressure. A large number of studies in a wide range of species has failed to characterise the physiological mechanisms by which 'mineralocorticoid' hor¬ mones such as DOC raise blood pressure (Scoggins et al 1982: Mitchell & Bohr 1983Schalekamp et al 1981). Although manv different mechanisms have been proposed these cannot individually ex¬ plain DOC" hypertension under all circumstances.…”

Section: Discussionmentioning

confidence: 99%

The effect of potassium loading and sodium depletion on DOC induced hypertension in sheep

Mills

Coghlan

Denton

et al. 1984

Acta Endocrinologica

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Abstract. This study examines the physiological effects of 1 1-deoxycorticosterone (DOC) at 2 rates of continuous iv infusion for 5 days in conscious sheep. DOC treatment, in sheep on Na and K intake 80 and 120 mmol/day respectively, increased mean arterial pressure (MAP) by 12 mmHg at 50 mg/day and by 10 mmHg at 5 mg/day. Both rates of infusion raised plasma [Na] and lowered plasma [K]. Urinary Na excretion fell on the first day of infusion. On cessation of infusion there was a natriuresis. A high K intake of approximately 800 mmol/day for 7 to 10 days prior to and during DOC (5 mg/day) treatment abolished the rise in blood pressure, the rise in plasma [Na], the intitial Na retention and the post-DOC natriuresis. Plasma [K] rose with high K intake and fell with DOC. Na depletion prior to DOC infusion (5 mg/day) prevented the rise in MAP. Urinary Na excretion remained low and plasma [K] fell. This study shows that K loading abolishes DOC hypertension in sheep by a mechanism which may involve modification of the Na retaining effects of the steroid.

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Section: Discussionmentioning

confidence: 99%

The effect of potassium loading and sodium depletion on DOC induced hypertension in sheep

Mills

Coghlan

Denton

et al. 1984

Acta Endocrinologica

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The Effects of Enalapril on Urinary Protein Excretion in Patients with Idiopathic Membranous Nephropathy

Sauter

Bakris

1990

The Journal of Clinical Pharma

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High doses of the angiotensin converting enzyme inhibitor, captopril, is known to cause significant increases in urinary protein excretion in patients with idiopathic membranous nephropathy. To find whether other angiotensin converting enzyme inhibitors yield similar results, we prospectively examined the effect of enalapril in five consecutive patients with idiopathic membranous nephropathy, elevated arterial pressure, and proteinuria and compared them to age-matched controls receiving clonidine. Glomerular filtration rate, 24-hour urinary protein excretion, and arterial pressure were measured. All patients served as their own controls. Those who received enalapril demonstrated an initial increase in proteinuria (-0.3 +/- 0.7 delta gm/day, clonidine vs 3.9 +/- 0.9 delta gm/day, enalapril: P less than .05) despite similar decreases in arterial pressure (-18 +/- 6 delta mm Hg, clonidine vs -22 +/- 6 delta mm Hg, enalapril: NS) and glomerular filtration rate (-1.1 +/- 0.8 delta mL/min, clonidine vs -1.9 +/- 1.2 delta mL/min, enalapril: NS) when compared to the clonidine group. This increase in proteinuria, however, did not occur when these patients were rechallenged with enalapril. To our knowledge, this is the first report to document a significant increase in preexisting nephrotic range proteinuria following administration of nonsulfhydryl ACE inhibitor. This increase, however, appears to be unique to the initial treatment phase of the disease and does not affect long-term management.

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