Effect of ACE inhibition and angiotensin AT1 receptor blockade on renal and blood pressure response to L-arginine in humans

Radko Komers, Karla Komersova, Ludmila Kazdova, Jana Ruzickova, Terezie Pelikanova

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Objective. Nitric oxide (NO) may contribute to the actions of angiotensin converting enzyme (ACE) inhibitors. In contrast, angiotensin type 1 (AT1) receptor blockers (AT1 B) have been considered to act exclusively by inhibiting angiotensin II actions. However, recent experimental findings suggest that AT1B actions may be also partly mediated by NO. In this study, we explored whether ACE inhibitors and AT1B modulate hemodynamic responses to L-arginine (L-arg), a NO precursor. Methods. Systemic (Finapres) and renal hemodynamic responses to L-arg (200 mg/kg body weight), associated with markers of systemic and renal NO production, were assessed before (control) and after 3 weeks of randomized pretreatment with the ACE inhibitor ramipril (5 mg/day for 3 weeks) or the AT1B losartan (50 mg/day for 3 weeks) in nine healthy male subjects (33 ± 2 years; body mass index 25.5 ± 0.5 kg/m2). Results. Control L-arg did not influence mean arterial pressure (MAP) (92 ± 5 versus 90 ± 5 mmHg; not significant). In contrast, L-arg decreased MAP when administered after pretreatment with ramipril (89 ± 5 versus 83 ± 4 mmHg; P <0.01) or losartan (90 ± 44 versus 86 ± 4; P <0.05). Control L-arg infusion had no effect on renal plasma flow (RPF) (paraminohippuric acid clearance) and renal vascular resistance (RVR), whereas the glomerular filtration rate (GFR) (inulin clearance) decreased (98 ± 4 versus 89 ± 5 ml/min; P <0.05), resulting in a decrease in filtration fraction (P <0.05). After ramipril, L-arg induced renal vasodilation as indicated by significant changes in RPF (576 ± 41 versus 669 ± 21 ml/min; P <0.01) and RVR (P <0.05). The GFR did not change statistically after ramipril pretreatment (91 ± 3 versus 97 ± 4 ml/min; not significant); however, the trend was different as compared with control (F = 5.7, P <0.05). L-Arg-induced renal vasodilation was also observed after losartan (RPF, 637 ± 34 versus 706 ± 40 ml/min; P <0.05). Enhanced renal and systemic responses to L-arg after ACE inhibitor and AT1B were associated with a rise in plasma L-citrulline levels, which was greater than after control L-arg (P <0.05). However, other indicators of NO activity such as plasma and urinary cyclic guanosine 3',5'-monophosphate, and nitrates, remained unchanged throughout all experiments. Conclusion. The results indicate that ACE inhibitors and AT1B have a potential to enhance L-arg-induced vasodilation both in systemic and renal vascular beds. However, these hemodynamic responses were not associated with convincing changes in indicators of systemic or renal NO activity, suggesting a contribution of NO-independent vasodilator mechanisms. (C) Lippincott Williams and Wilkins.

Original languageEnglish (US)
Pages (from-to)51-59
Number of pages9
JournalJournal of Hypertension
Volume18
Issue number1
StatePublished - 2000

Fingerprint

Angiotensin Type 1 Receptor
Angiotensins
Peptidyl-Dipeptidase A
Arginine
Blood Pressure
Kidney
Nitric Oxide
Ramipril
Angiotensin-Converting Enzyme Inhibitors
Renal Plasma Flow
Losartan
Vasodilation
Hemodynamics
Glomerular Filtration Rate
Vascular Resistance
Arterial Pressure
Angiotensin II Type 1 Receptor Blockers
Citrulline
Inulin
Cyclic GMP

Keywords

  • Blood pressure
  • Endothelium-dependent vasodilation
  • L-arginine
  • Losartan
  • Ramipril
  • Renal

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology

Cite this

Komers, R., Komersova, K., Kazdova, L., Ruzickova, J., & Pelikanova, T. (2000). Effect of ACE inhibition and angiotensin AT1 receptor blockade on renal and blood pressure response to L-arginine in humans. Journal of Hypertension, 18(1), 51-59.

Effect of ACE inhibition and angiotensin AT1 receptor blockade on renal and blood pressure response to L-arginine in humans. / Komers, Radko; Komersova, Karla; Kazdova, Ludmila; Ruzickova, Jana; Pelikanova, Terezie.

In: Journal of Hypertension, Vol. 18, No. 1, 2000, p. 51-59.

Research output: Contribution to journalArticle

Komers, R, Komersova, K, Kazdova, L, Ruzickova, J & Pelikanova, T 2000, 'Effect of ACE inhibition and angiotensin AT1 receptor blockade on renal and blood pressure response to L-arginine in humans', Journal of Hypertension, vol. 18, no. 1, pp. 51-59.
Komers, Radko ; Komersova, Karla ; Kazdova, Ludmila ; Ruzickova, Jana ; Pelikanova, Terezie. / Effect of ACE inhibition and angiotensin AT1 receptor blockade on renal and blood pressure response to L-arginine in humans. In: Journal of Hypertension. 2000 ; Vol. 18, No. 1. pp. 51-59.
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TY - JOUR

T1 - Effect of ACE inhibition and angiotensin AT1 receptor blockade on renal and blood pressure response to L-arginine in humans

AU - Komers, Radko

AU - Komersova, Karla

AU - Kazdova, Ludmila

AU - Ruzickova, Jana

AU - Pelikanova, Terezie

PY - 2000

Y1 - 2000

N2 - Objective. Nitric oxide (NO) may contribute to the actions of angiotensin converting enzyme (ACE) inhibitors. In contrast, angiotensin type 1 (AT1) receptor blockers (AT1 B) have been considered to act exclusively by inhibiting angiotensin II actions. However, recent experimental findings suggest that AT1B actions may be also partly mediated by NO. In this study, we explored whether ACE inhibitors and AT1B modulate hemodynamic responses to L-arginine (L-arg), a NO precursor. Methods. Systemic (Finapres) and renal hemodynamic responses to L-arg (200 mg/kg body weight), associated with markers of systemic and renal NO production, were assessed before (control) and after 3 weeks of randomized pretreatment with the ACE inhibitor ramipril (5 mg/day for 3 weeks) or the AT1B losartan (50 mg/day for 3 weeks) in nine healthy male subjects (33 ± 2 years; body mass index 25.5 ± 0.5 kg/m2). Results. Control L-arg did not influence mean arterial pressure (MAP) (92 ± 5 versus 90 ± 5 mmHg; not significant). In contrast, L-arg decreased MAP when administered after pretreatment with ramipril (89 ± 5 versus 83 ± 4 mmHg; P <0.01) or losartan (90 ± 44 versus 86 ± 4; P <0.05). Control L-arg infusion had no effect on renal plasma flow (RPF) (paraminohippuric acid clearance) and renal vascular resistance (RVR), whereas the glomerular filtration rate (GFR) (inulin clearance) decreased (98 ± 4 versus 89 ± 5 ml/min; P <0.05), resulting in a decrease in filtration fraction (P <0.05). After ramipril, L-arg induced renal vasodilation as indicated by significant changes in RPF (576 ± 41 versus 669 ± 21 ml/min; P <0.01) and RVR (P <0.05). The GFR did not change statistically after ramipril pretreatment (91 ± 3 versus 97 ± 4 ml/min; not significant); however, the trend was different as compared with control (F = 5.7, P <0.05). L-Arg-induced renal vasodilation was also observed after losartan (RPF, 637 ± 34 versus 706 ± 40 ml/min; P <0.05). Enhanced renal and systemic responses to L-arg after ACE inhibitor and AT1B were associated with a rise in plasma L-citrulline levels, which was greater than after control L-arg (P <0.05). However, other indicators of NO activity such as plasma and urinary cyclic guanosine 3',5'-monophosphate, and nitrates, remained unchanged throughout all experiments. Conclusion. The results indicate that ACE inhibitors and AT1B have a potential to enhance L-arg-induced vasodilation both in systemic and renal vascular beds. However, these hemodynamic responses were not associated with convincing changes in indicators of systemic or renal NO activity, suggesting a contribution of NO-independent vasodilator mechanisms. (C) Lippincott Williams and Wilkins.

AB - Objective. Nitric oxide (NO) may contribute to the actions of angiotensin converting enzyme (ACE) inhibitors. In contrast, angiotensin type 1 (AT1) receptor blockers (AT1 B) have been considered to act exclusively by inhibiting angiotensin II actions. However, recent experimental findings suggest that AT1B actions may be also partly mediated by NO. In this study, we explored whether ACE inhibitors and AT1B modulate hemodynamic responses to L-arginine (L-arg), a NO precursor. Methods. Systemic (Finapres) and renal hemodynamic responses to L-arg (200 mg/kg body weight), associated with markers of systemic and renal NO production, were assessed before (control) and after 3 weeks of randomized pretreatment with the ACE inhibitor ramipril (5 mg/day for 3 weeks) or the AT1B losartan (50 mg/day for 3 weeks) in nine healthy male subjects (33 ± 2 years; body mass index 25.5 ± 0.5 kg/m2). Results. Control L-arg did not influence mean arterial pressure (MAP) (92 ± 5 versus 90 ± 5 mmHg; not significant). In contrast, L-arg decreased MAP when administered after pretreatment with ramipril (89 ± 5 versus 83 ± 4 mmHg; P <0.01) or losartan (90 ± 44 versus 86 ± 4; P <0.05). Control L-arg infusion had no effect on renal plasma flow (RPF) (paraminohippuric acid clearance) and renal vascular resistance (RVR), whereas the glomerular filtration rate (GFR) (inulin clearance) decreased (98 ± 4 versus 89 ± 5 ml/min; P <0.05), resulting in a decrease in filtration fraction (P <0.05). After ramipril, L-arg induced renal vasodilation as indicated by significant changes in RPF (576 ± 41 versus 669 ± 21 ml/min; P <0.01) and RVR (P <0.05). The GFR did not change statistically after ramipril pretreatment (91 ± 3 versus 97 ± 4 ml/min; not significant); however, the trend was different as compared with control (F = 5.7, P <0.05). L-Arg-induced renal vasodilation was also observed after losartan (RPF, 637 ± 34 versus 706 ± 40 ml/min; P <0.05). Enhanced renal and systemic responses to L-arg after ACE inhibitor and AT1B were associated with a rise in plasma L-citrulline levels, which was greater than after control L-arg (P <0.05). However, other indicators of NO activity such as plasma and urinary cyclic guanosine 3',5'-monophosphate, and nitrates, remained unchanged throughout all experiments. Conclusion. The results indicate that ACE inhibitors and AT1B have a potential to enhance L-arg-induced vasodilation both in systemic and renal vascular beds. However, these hemodynamic responses were not associated with convincing changes in indicators of systemic or renal NO activity, suggesting a contribution of NO-independent vasodilator mechanisms. (C) Lippincott Williams and Wilkins.

KW - Blood pressure

KW - Endothelium-dependent vasodilation

KW - L-arginine

KW - Losartan

KW - Ramipril

KW - Renal

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