Effects of ARB or ACE-Inhibitor Administration on Plasma Levels of Aldosterone and Adiponectin in Hypertension

Aldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie, aldosterone breakthrough). The angiotensin II receptor blocker (ARB) telmisartan can function as a ligand for peroxisome proliferator-activated re...

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Published inInternational Heart Journal Vol. 50; no. 4; pp. 501 - 512
Main Authors Kawachi, Kenji, Iwasaki, Tsutomu, Hoshino, Jin, Morishita, Koujurou, Ohyama, Yoshio, Nakamura, Tetsuya, Saito, Tomoko, Saito, Yuichiro, Kurabayashi, Masahiko, Hosoi, Tsutomu
Format Journal Article
LanguageEnglish
Published Japan International Heart Journal Association 2009
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Online AccessGet full text
ISSN1349-2365
1349-3299
1349-3299
DOI10.1536/ihj.50.501

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Abstract Aldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie, aldosterone breakthrough). The angiotensin II receptor blocker (ARB) telmisartan can function as a ligand for peroxisome proliferator-activated receptor (PPAR) γ. Stimulation of PPAR γ has been demonstrated to raise adiponectin production and suppress angiotensin II type 1 receptor expression. Thus, we investigated the effect of the ACE-I perindopril erbumin (perindopril) and the ARB telmisartan on plasma levels of aldosterone and adiponectin. Patients with essential hypertension were randomly assigned to receive 48 weeks of perindopril (2-8 mg/d) or telmisartan (20-80 mg/d). We measured adiponectin, aldosterone, angiotensin II, and renin at weeks 0, 8, 24, and 48. A total of 53 subjects were randomized. Data on 51 subjects (25 in the perindopril group and 26 in the telmisartan group; mean age, 65.1 years) were available for analyses. Plasma aldosterone decreased significantly in both the telmisartan (69.9 ± 5.6 to 58.1 ± 5.4 pg/mL) and perindopril (74.1 ± 4.7 to 64.7 ± 5.3 pg/mL) groups at 8 weeks, but returned toward the baseline in the perindopril group (67.9 ± 4.1 pg/mL) at 24 weeks. Plasma glycated hemoglobin levels or urine albumin did not change significantly after the treatment in either group. Telmisartan seemed to be more effective at suppressing aldosterone and raising adiponectin levels than perindopril; however, improvements in insulin sensitivity and albuminuria were not detected. These results are consistent with the idea that the use of an ARB with PPAR γ stimulating activity is equivalent to ACE-I for the treatment of hypertension.
AbstractList Aldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie, aldosterone breakthrough). The angiotensin II receptor blocker (ARB) telmisartan can function as a ligand for peroxisome proliferator-activated receptor (PPAR) gamma. Stimulation of PPAR gamma has been demonstrated to raise adiponectin production and suppress angiotensin II type 1 receptor expression. Thus, we investigated the effect of the ACE-I perindopril erbumin (perindopril) and the ARB telmisartan on plasma levels of aldosterone and adiponectin.Patients with essential hypertension were randomly assigned to receive 48 weeks of perindopril (2-8 mg/d) or telmisartan (20-80 mg/d). We measured adiponectin, aldosterone, angiotensin II, and renin at weeks 0, 8, 24, and 48.A total of 53 subjects were randomized. Data on 51 subjects (25 in the perindopril group and 26 in the telmisartan group; mean age, 65.1 years) were available for analyses. Plasma aldosterone decreased significantly in both the telmisartan (69.9+/-5.6 to 58.1+/-5.4 pg/mL) and perindopril (74.1+/-4.7 to 64.7+/-5.3 pg/mL) groups at 8 weeks, but returned toward the baseline in the perindopril group (67.9+/-4.1 pg/mL) at 24 weeks. Plasma glycated hemoglobin levels or urine albumin did not change significantly after the treatment in either group.Telmisartan seemed to be more effective at suppressing aldosterone and raising adiponectin levels than perindopril; however, improvements in insulin sensitivity and albuminuria were not detected. These results are consistent with the idea that the use of an ARB with PPAR gamma stimulating activity is equivalent to ACE-I for the treatment of hypertension.Aldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie, aldosterone breakthrough). The angiotensin II receptor blocker (ARB) telmisartan can function as a ligand for peroxisome proliferator-activated receptor (PPAR) gamma. Stimulation of PPAR gamma has been demonstrated to raise adiponectin production and suppress angiotensin II type 1 receptor expression. Thus, we investigated the effect of the ACE-I perindopril erbumin (perindopril) and the ARB telmisartan on plasma levels of aldosterone and adiponectin.Patients with essential hypertension were randomly assigned to receive 48 weeks of perindopril (2-8 mg/d) or telmisartan (20-80 mg/d). We measured adiponectin, aldosterone, angiotensin II, and renin at weeks 0, 8, 24, and 48.A total of 53 subjects were randomized. Data on 51 subjects (25 in the perindopril group and 26 in the telmisartan group; mean age, 65.1 years) were available for analyses. Plasma aldosterone decreased significantly in both the telmisartan (69.9+/-5.6 to 58.1+/-5.4 pg/mL) and perindopril (74.1+/-4.7 to 64.7+/-5.3 pg/mL) groups at 8 weeks, but returned toward the baseline in the perindopril group (67.9+/-4.1 pg/mL) at 24 weeks. Plasma glycated hemoglobin levels or urine albumin did not change significantly after the treatment in either group.Telmisartan seemed to be more effective at suppressing aldosterone and raising adiponectin levels than perindopril; however, improvements in insulin sensitivity and albuminuria were not detected. These results are consistent with the idea that the use of an ARB with PPAR gamma stimulating activity is equivalent to ACE-I for the treatment of hypertension.
Aldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie, aldosterone breakthrough). The angiotensin II receptor blocker (ARB) telmisartan can function as a ligand for peroxisome proliferator-activated receptor (PPAR) γ. Stimulation of PPAR γ has been demonstrated to raise adiponectin production and suppress angiotensin II type 1 receptor expression. Thus, we investigated the effect of the ACE-I perindopril erbumin (perindopril) and the ARB telmisartan on plasma levels of aldosterone and adiponectin. Patients with essential hypertension were randomly assigned to receive 48 weeks of perindopril (2-8 mg/d) or telmisartan (20-80 mg/d). We measured adiponectin, aldosterone, angiotensin II, and renin at weeks 0, 8, 24, and 48. A total of 53 subjects were randomized. Data on 51 subjects (25 in the perindopril group and 26 in the telmisartan group; mean age, 65.1 years) were available for analyses. Plasma aldosterone decreased significantly in both the telmisartan (69.9 ± 5.6 to 58.1 ± 5.4 pg/mL) and perindopril (74.1 ± 4.7 to 64.7 ± 5.3 pg/mL) groups at 8 weeks, but returned toward the baseline in the perindopril group (67.9 ± 4.1 pg/mL) at 24 weeks. Plasma glycated hemoglobin levels or urine albumin did not change significantly after the treatment in either group. Telmisartan seemed to be more effective at suppressing aldosterone and raising adiponectin levels than perindopril; however, improvements in insulin sensitivity and albuminuria were not detected. These results are consistent with the idea that the use of an ARB with PPAR γ stimulating activity is equivalent to ACE-I for the treatment of hypertension.
Aldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie, aldosterone breakthrough). The angiotensin II receptor blocker (ARB) telmisartan can function as a ligand for peroxisome proliferator-activated receptor (PPAR) gamma. Stimulation of PPAR gamma has been demonstrated to raise adiponectin production and suppress angiotensin II type 1 receptor expression. Thus, we investigated the effect of the ACE-I perindopril erbumin (perindopril) and the ARB telmisartan on plasma levels of aldosterone and adiponectin.Patients with essential hypertension were randomly assigned to receive 48 weeks of perindopril (2-8 mg/d) or telmisartan (20-80 mg/d). We measured adiponectin, aldosterone, angiotensin II, and renin at weeks 0, 8, 24, and 48.A total of 53 subjects were randomized. Data on 51 subjects (25 in the perindopril group and 26 in the telmisartan group; mean age, 65.1 years) were available for analyses. Plasma aldosterone decreased significantly in both the telmisartan (69.9+/-5.6 to 58.1+/-5.4 pg/mL) and perindopril (74.1+/-4.7 to 64.7+/-5.3 pg/mL) groups at 8 weeks, but returned toward the baseline in the perindopril group (67.9+/-4.1 pg/mL) at 24 weeks. Plasma glycated hemoglobin levels or urine albumin did not change significantly after the treatment in either group.Telmisartan seemed to be more effective at suppressing aldosterone and raising adiponectin levels than perindopril; however, improvements in insulin sensitivity and albuminuria were not detected. These results are consistent with the idea that the use of an ARB with PPAR gamma stimulating activity is equivalent to ACE-I for the treatment of hypertension.
Author Hosoi, Tsutomu
Ohyama, Yoshio
Kawachi, Kenji
Hoshino, Jin
Saito, Tomoko
Nakamura, Tetsuya
Kurabayashi, Masahiko
Saito, Yuichiro
Iwasaki, Tsutomu
Morishita, Koujurou
Author_xml – sequence: 1
  fullname: Kawachi, Kenji
  organization: Gunma Aldosterone Study Group
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  fullname: Iwasaki, Tsutomu
  organization: Gunma Aldosterone Study Group
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  fullname: Hoshino, Jin
  organization: Gunma Aldosterone Study Group
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  fullname: Morishita, Koujurou
  organization: Gunma Aldosterone Study Group
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  fullname: Ohyama, Yoshio
  organization: Gunma Aldosterone Study Group
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  fullname: Nakamura, Tetsuya
  organization: Clinical Investigation and Research Unit, Gunma University Hospital
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  fullname: Saito, Tomoko
  organization: Clinical Investigation and Research Unit, Gunma University Hospital
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  fullname: Saito, Yuichiro
  organization: Department of Medicine and Biological Science, Gunma University Graduate School of Medicine
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  fullname: Kurabayashi, Masahiko
  organization: Department of Medicine and Biological Science, Gunma University Graduate School of Medicine
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  organization: Gunma Aldosterone Study Group
BackLink https://www.ncbi.nlm.nih.gov/pubmed/19609054$$D View this record in MEDLINE/PubMed
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Snippet Aldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie,...
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SubjectTerms Adiponectin - blood
Adult
Aged
Aged, 80 and over
Aldosterone - blood
Angiotensin
Angiotensin II Type 1 Receptor Blockers - therapeutic use
Angiotensin-Converting Enzyme Inhibitors - therapeutic use
Benzimidazoles - therapeutic use
Benzoates - therapeutic use
Female
Follow-Up Studies
Humans
Hypertension - blood
Hypertension - complications
Hypertension - drug therapy
Leptin
Male
Middle Aged
Perindopril - therapeutic use
Peroxisome proliferator-activated receptor
Renin
Title Effects of ARB or ACE-Inhibitor Administration on Plasma Levels of Aldosterone and Adiponectin in Hypertension
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