Mechanism of the response to captopril in glucocorticoid hypertension

F. Elijovich; L. R. Krakoff

doi:10.3109/10641968209061642

Mechanism of the response to captopril in glucocorticoid hypertension

F. Elijovich, L. R. Krakoff

Icahn School of Medicine at Mount Sinai

Research output: Contribution to journal › Article › peer-review

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Abstract

The effect of captopril was explored in salt-depleted methylprednisolone (MP)-hypertensive rats. MP treatment raised BP by 41±2 mmHg over 2 weeks. Controls (C) had no change in BP. Sodium balance and weight data indicated a greater salt depletion in MP than in C. On day 15, captopril reduced BP in both MP (20±4 mmHg) and C (31±4 mmHg). The effect was significantly smaller in MP than in C (p<0.05). Plasma renin activity (PRA) was similarly elevated in both groups, consistent with salt depletion. Serum (SCE) and lung-converting enzyme (LCE) activity were similar in MP and C. The diminished antihypertensive effect of captopril in MP is therefore not attributable to differences in PRA, SCE, or LCE. Our data suggest that depressor actions of captopril unrelated to the renin-angiotensin system are impaired in MP. Glucocorticoid-induced changes in vasodilator systems may explain these findings.

Original language	English
Pages (from-to)	1795-1814
Number of pages	20
Journal	Clinical and Experimental Hypertension
Volume	A4
Issue number	9-10
DOIs	https://doi.org/10.3109/10641968209061642
State	Published - 1982

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title = "Mechanism of the response to captopril in glucocorticoid hypertension",

abstract = "The effect of captopril was explored in salt-depleted methylprednisolone (MP)-hypertensive rats. MP treatment raised BP by 41±2 mmHg over 2 weeks. Controls (C) had no change in BP. Sodium balance and weight data indicated a greater salt depletion in MP than in C. On day 15, captopril reduced BP in both MP (20±4 mmHg) and C (31±4 mmHg). The effect was significantly smaller in MP than in C (p<0.05). Plasma renin activity (PRA) was similarly elevated in both groups, consistent with salt depletion. Serum (SCE) and lung-converting enzyme (LCE) activity were similar in MP and C. The diminished antihypertensive effect of captopril in MP is therefore not attributable to differences in PRA, SCE, or LCE. Our data suggest that depressor actions of captopril unrelated to the renin-angiotensin system are impaired in MP. Glucocorticoid-induced changes in vasodilator systems may explain these findings.",

author = "F. Elijovich and Krakoff, \{L. R.\}",

note = "Funding Information: Supported by USPHS Grant HLB 13595, and a New York",

year = "1982",

doi = "10.3109/10641968209061642",

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journal = "Clinical and Experimental Hypertension",

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T1 - Mechanism of the response to captopril in glucocorticoid hypertension

AU - Elijovich, F.

AU - Krakoff, L. R.

N1 - Funding Information: Supported by USPHS Grant HLB 13595, and a New York

PY - 1982

Y1 - 1982

N2 - The effect of captopril was explored in salt-depleted methylprednisolone (MP)-hypertensive rats. MP treatment raised BP by 41±2 mmHg over 2 weeks. Controls (C) had no change in BP. Sodium balance and weight data indicated a greater salt depletion in MP than in C. On day 15, captopril reduced BP in both MP (20±4 mmHg) and C (31±4 mmHg). The effect was significantly smaller in MP than in C (p<0.05). Plasma renin activity (PRA) was similarly elevated in both groups, consistent with salt depletion. Serum (SCE) and lung-converting enzyme (LCE) activity were similar in MP and C. The diminished antihypertensive effect of captopril in MP is therefore not attributable to differences in PRA, SCE, or LCE. Our data suggest that depressor actions of captopril unrelated to the renin-angiotensin system are impaired in MP. Glucocorticoid-induced changes in vasodilator systems may explain these findings.

AB - The effect of captopril was explored in salt-depleted methylprednisolone (MP)-hypertensive rats. MP treatment raised BP by 41±2 mmHg over 2 weeks. Controls (C) had no change in BP. Sodium balance and weight data indicated a greater salt depletion in MP than in C. On day 15, captopril reduced BP in both MP (20±4 mmHg) and C (31±4 mmHg). The effect was significantly smaller in MP than in C (p<0.05). Plasma renin activity (PRA) was similarly elevated in both groups, consistent with salt depletion. Serum (SCE) and lung-converting enzyme (LCE) activity were similar in MP and C. The diminished antihypertensive effect of captopril in MP is therefore not attributable to differences in PRA, SCE, or LCE. Our data suggest that depressor actions of captopril unrelated to the renin-angiotensin system are impaired in MP. Glucocorticoid-induced changes in vasodilator systems may explain these findings.

UR - https://www.scopus.com/pages/publications/0020382774

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DO - 10.3109/10641968209061642

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AN - SCOPUS:0020382774

SN - 1064-1963

VL - A4

SP - 1795

EP - 1814

JO - Clinical and Experimental Hypertension

JF - Clinical and Experimental Hypertension

IS - 9-10

ER -

Mechanism of the response to captopril in glucocorticoid hypertension

Abstract

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