Captopril-Stimulated Renin Secretion in the Diagnosis of Renovascular Hypertension

Gaul, Mary K.; Linn, William D.; Mulrow, Cynthia D.

doi:10.1093/ajh/2.5.335

Cited by 9 publications

(2 citation statements)

References 22 publications

(35 reference statements)

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“…These animal results have been largely confirmed in hypertensive patients, and the increase in renin release after the administration of saralasin 4 or captopril 5 has been used as a dynamic test to investigate the reactivity of renin release in various forms of hyper-tension. 6 The development of direct immunoradiometric plasma renin assays, using different pairs of monoclonal anti-human renin antibodies, 7 -8 has allowed the demonstration of a rise in renin release after the administration of renin inhibitor to monkeys or human beings; the plasma concentrations of active and total renin are increased 910 and PRA is suppressed. The interruption of Ang IFs tonic renin release inhibition can be mediated by either a fall in the plasma Ang II level or the suppression of local Ang II production in the juxtaglomerular apparatus (JGA), where Ang II and renin have been codetected by immunohistochemistry.…”

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confidence: 99%

Renin release regulation during acute renin inhibition in normal volunteers.

et al. 1991

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Blockade of the renin-angiotensin system by an angiotensin converting enzyme (ACE) inhibitor or an angiotensin II (Ang II) antagonist is accompanied by a reactive rise in renin release. This rise is generally attributed to interruption of the short feedback loop between Ang II and renin release. Similarly, after the administration of a renin inhibitor, the plasma concentrations of active and total renin are increased and plasma renin activity is suppressed. The aim of the present study was to investigate if a fall in the plasma Ang II level is the unique determinant of the rise in the active renin (AR) level that follows renin Inhibition. Six normal male volunteers participated in three successive 240-minute experiments at weekly intervals according to a single-blind randomized Latin square design. For experiment 1, Ang II was infused at 2 ng/kg/min from 0 to 60 minutes and at 4 ng/kg/min from 60 to 120 minutes. For experiment 2, 0.3 mg/kg of the new potent renin inhibitor Ro 42-5892 was injected at 30 minutes followed by infusion at 0.1 mg/kg/hr from 30 to 240 minutes. For experiment 3, Ang II and Ro 42-5892 were administered simultaneously at the same doses as described above. The mean±SEM Ang II concentration increased from 10.2±1.6 to 33.7±11.2 pg/ml after infusion of exogenous peptide. It decreased from 9.5±0.9 to 1.4±03 pg/ml after the injection of Ro 42-5892 and increased from 15.6±2.9 to 37.1 ±11.8 pg/ml after the simultaneous infusion of both compounds. At 120 minutes, Ang II infusion decreased the AR level from 30±5 to 12±4 pg/ml and Ro 42-5892 increased it from 28±4 to 209 ±40 pg/ml. After the combined infusion of Ang II and Ro 48-5892, the AR level rose by only 42% (from 22±4 to 38±5 pg/ml) and was still threefold higher than during the infusion of Ang II only. It is concluded that the exogenous infusion of an excess of Ang II minimizes but does not completely suppress the renin stimulation secondary to the administration of renin inhibitor. Although the fall in the plasma Ang II level appears to be a major stimulus of renin release, our results suggest that Ro 42-5892 may also have a direct intrarenal effect, possibly at the level of the juxtaglomerular cells, where renin and Ang II have been codetected and are locally produced.

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confidence: 99%

Renin release regulation during acute renin inhibition in normal volunteers.

et al. 1991

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“…However, these available antihypertensive agents are short-lasting, nonspecific, and have side effects. In addition, blockade of AT 1 receptors or inhibition of ACE results in a reactive rise in renin release and an excessive accumulation of angiotensin I (Ang I), which are generally attributed to interruption of the short feedback loop between angiotensin II (Ang II) and renin release [4][5][6][7][8][9]. Ang I, though less potent than Ang II, has pressor effect and can stimulate aldosterone release, which may make hypertension difficult to control [10].…”

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Prolonged attenuation of cold-induced hypertension by adenoviral delivery of renin antisense

Wang¹,

Sun²,

Cade³

2005

Kidney International

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Newer Tests for the Diagnosis of Renovascular Disease

Davidson¹

1992

JAMA

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Among the newer diagnostic tests, both magnetic resonance imaging and Doppler ultrasonography hold promise for the anatomic detection of renal artery stenosis, but clear diagnostic criteria have not been universally accepted. There is more information concerning the captopril test, which has a sufficiently high sensitivity to be useful in the screening of high-risk patients for renovascular hypertension. Scans after captopril administration, which appear to be more specific, may enable the prediction of a blood pressure response to angioplasty or surgery.

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Captopril-Stimulated Renin Secretion in the Diagnosis of Renovascular Hypertension

Cited by 9 publications

References 22 publications

Renin release regulation during acute renin inhibition in normal volunteers.

Renin release regulation during acute renin inhibition in normal volunteers.

Prolonged attenuation of cold-induced hypertension by adenoviral delivery of renin antisense

Newer Tests for the Diagnosis of Renovascular Disease

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