Inhibition of Captopril-Induced Renin Release by Angiotensin II

Mersey, James H.; Ceballos, Laura; Swartz, Stephen L.

doi:10.1097/00005344-198711000-00013

Cited by 9 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Under conditions with pressures in the physiological range, ANG II is probably a very powerful regulator of renin secretion. During ACE inhibition, elimination of the short-loop feedback suppression by ANG II has great impact on renin secretion, a response that may be completely reversed by infusion of ANG II (22). Pressure-dependent renin release is, as shown by Reinhardt and Seeliger (26), another major regulator of PRA, but in the present study it seems that much larger changes in MAP are required to account for the large increase in PRA.…”

supporting

confidence: 43%

Effects of truncated angiotensins in humans after double blockade of the renin system

Plovsing

Wamberg²,

Sandgaard³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

We studied the effects of 3-h infusions of ANG III, ANG-(1-7), and ANG IV in doses equimolar to physiological amounts of ANG II (3 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 ), in six men on low-sodium diet (30 mmol/ day). The subjects were acutely pretreated with canrenoate and captopril to inhibit aldosterone actions and ANG II synthesis, respectively. ANG II infusion increased plasma angiotensin immunoreactivity to 53 Ϯ 6 pg/ml (ϩ490%), plasma aldosterone to 342 Ϯ 38 pg/ml (ϩ109%), and blood pressure by 27%. Glomerular filtration rate decreased by 16%. Concomitantly, clearance of endogenous lithium fell by 66%, and fractional proximal reabsorption of sodium increased from 77 to 92%; absolute proximal reabsorption rate of sodium remained constant. ANG II decreased sodium excretion by 70%, potassium excretion by 50%, and urine flow by 80%, whereas urine osmolality increased. ANG III also increased plasma aldosterone markedly (ϩ45%), however, without measurable changes in angiotensin immunoreactivity, glomerular filtration rate, or renal excretion rates. During vehicle infusion, plasma renin activity decreased markedly (ϳ700 to ϳ200 mIU/l); only ANG II enhanced this decrease. ANG-(1-7) and ANG IV did not change any of the measured variables persistently. It is concluded that 1) ANG III and ANG IV are cleared much faster from plasma than ANG II, 2) ANG II causes hypofiltration, urinary concentration, and sodium and potassium retention at constant plasma concentrations of vasopressin and atrial natriuretic peptide, and 3) a very small increase in the concentration of ANG III, undetectable by usual techniques, may increase aldosterone secretion substantially. healthy humans; angiotensin peptides; aldosterone secretion; sodium excretion THE RENIN-ANGIOTENSIN-ALDOSTERONE system (RAAS) is the single most important regulator of the sodium homeostasis. This specific role of the RAAS makes it a major determinant of extracellular fluid volume and arterial blood pressure. It has long been recognized that ANG II is the pivotal component of this system.

show abstract

supporting

confidence: 43%

Effects of truncated angiotensins in humans after double blockade of the renin system

Plovsing

Wamberg²,

Sandgaard³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…At 20 minutes of this Ang II infusion, just before captopril intake, PRA had already decreased to 2.9 ±0.8 ng/ ml/hr and the study design could not provide the PRA value obtained after the next 45 minutes of infusion of Ang II alone, which very likely would have been lower. A more exact conclusion from the experiment of Mersey et al 28 would be that captopril increased PRA from 2.9 to 4.6 ng/ml/hr. Therefore, in both experiments involving ACE inhibition and renin inhibition, the most obvious phenomenon is the reduction of renin release, confirmed by experimental data in rats.…”

Section: Discussionmentioning

confidence: 93%

“…However, after the combined administration of Ang II and Ro 42-5892 the plasma active renin level was 38 ±5 pg/ml, higher than its basal level (29±4 pg/ml) and more than threefold higher than the level observed at the end of the Ang II infusion (12±4 pg/ml). Mersey et al 28 used a similar methodology to investigate renin release during captopril administration in normal volunteers placed on a moderately low sodium diet. These authors concluded that the rise in PRA was mediated by the fall in plasma Ang II levels because an exogenous Ang II infusion (3-6 ng/kg/ min) maintained PRA at 4.6 ng/ml/hr (basal level 4.8±1.2 ng/ml/hr) compared with 15.2 ng/ml/hr when the Ang II infusion was ceased.…”

Section: Discussionmentioning

confidence: 99%

“…These authors concluded that the rise in PRA was mediated by the fall in plasma Ang II levels because an exogenous Ang II infusion (3-6 ng/kg/ min) maintained PRA at 4.6 ng/ml/hr (basal level 4.8±1.2 ng/ml/hr) compared with 15.2 ng/ml/hr when the Ang II infusion was ceased. The protocol of Mersey et al 28 did not permit a comparison between PRA values measured during the combined administration of Ang II and captopril and PRA values measured during the infusion of Ang II alone. Captopril was given after the Ang II infusion was started, and the reported PRA of 4.6 ±1.2 ng/ml/hr 45 minutes after captopril intake was already influenced by a previous 65 minutes of Ang II infusion.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Renin release regulation during acute renin inhibition in normal volunteers.

et al. 1991

View full text Add to dashboard Cite

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.

show abstract

“…This is consistent with a negative-feedback effect of Ang II on renin synthesis and release. 30,31 In group 3 animals in which Ang II infusion was provided without pacing, Ang II levels declined toward baseline by the 7-day time point (37Ϯ3.9 -baseline; 135Ϯ40.4 -4-day Ang II; 61.8Ϯ11-7-day Ang II, pg/mL, PϽ.05 for baseline vs 4-day Ang II only). This suggests some interaction between the …”

Section: Plasma Ang I and Ii Levelsmentioning

confidence: 99%

Synergistic Exacerbation of Diastolic Stiffness From Short-term Tachycardia–Induced Cardiodepression and Angiotensin II

Senzaki

Gluzband

Pak

et al. 1998

Circulation Research

View full text Add to dashboard Cite

Synergistic interaction between angiotensin II (Ang II) and evolving cardiodepression may play an important role in worsening chamber function, particularly in diastole. To test this hypothesis, Ang II was infused at 10 or 17 ng.kg(-1).min(-1) in 18 conscious dogs 4 days before and during induction of subacute cardiodepression by 48-hour tachypacing. The lower dose yielded negligible systemic pressure changes. Twelve additional animals served as paced-only controls. Pressure-dimension relations were recorded, and serial endocardial biopsies were obtained to assess histological and metalloproteinase (MMP) changes. Forty-eight-hour pacing alone depressed systolic function but had little effect on diastolic stiffness. Ang II alone only modestly raised diastolic stiffness at both doses and enhanced contractility at the higher dose. These changes recovered toward baseline after a 7-day infusion. However, Ang II (at either dose) combined with 48-hour pacing markedly increased ventricular stiffness (110+/-26% over baseline) and end-diastolic pressure (22+/-1.7 mm Hg). In contrast, pacing-induced inotropic and relaxation abnormalities were not exacerbated by Ang II. Zymography revealed MMP activation (72- and 92-kD gelatinases and 52-kDa caseinase) after a 4-day Ang II infusion (at both doses), which persisted during pacing. Tachypacing initiated 24 hours after cessation of a 7-day Ang II infusion also resulted in diastolic stiffening and corresponded with MMP reactivation. Ang II also induced myocyte necrosis, inflammation, and subsequent interstitial fibrosis, but these changes correlated less with chamber mechanics. Thus, Ang II amplifies and accelerates diastolic dysfunction when combined with evolving cardiodepression. This phenomenon may also underlie Ang II influences in late-stage cardiomyopathy, when chamber distensibility declines.

show abstract

Inhibition of Captopril-Induced Renin Release by Angiotensin II

Cited by 9 publications

References 0 publications

Effects of truncated angiotensins in humans after double blockade of the renin system

Effects of truncated angiotensins in humans after double blockade of the renin system

Renin release regulation during acute renin inhibition in normal volunteers.

Synergistic Exacerbation of Diastolic Stiffness From Short-term Tachycardia–Induced Cardiodepression and Angiotensin II

Contact Info

Product

Resources

About