Renal vascular responses to captopril and to candesartan in patients with type 1 diabetes mellitus
BACKGROUND: Enhanced renal vasodilator responses to angiotensin-converting enzyme (ACE) inhibition in diabetes mellitus despite a normal or low plasma renin activity level have suggested intrarenal activation of the renin-angiotensin system in this disease. There is, however, a continuing debate as to the mediators of the renal hemodynamic response to ACE inhibition-reduced angiotensin II formation or pathways involving kinins, prostaglandins, and nitric oxide.
METHODS: Twelve patients with type 1 diabetes mellitus of 18 +/- 3.2 (SEM) years of duration (7 females and 5 males, ages 17 to 50, 32 +/- 4.0 years) who were free of sustained microalbuminuria and on a high-salt diet were given the ACE inhibitor captopril (25 mg orally) on one day and the AT1 receptor blocker candesartan (16 mg orally) on another day. Renal plasma flow (RPF) and glomerular filtration rate were measured before and for four hours after administration.
RESULTS: Both drugs caused a significant increase in RPF (captopril 574 +/- 26 to 625 +/- 37 mL/min/1.73 m2, P = 0.008; candesartan 577 +/- 26 to 643 +/- 37, P = 0.004). There was a highly significant correlation between the responses to captopril and to candesartan (r = 0.86, P < 0.001). Seven subjects had an RPF response to captopril that was accentuated (90 +/- 13 mL/min/1.73 m2), while five had a response that was normal (-4 +/- 9). There was no significant change in glomerular filtration rate on either drug.
CONCLUSION: The remarkable rise in RPF in response to captopril and candesartan despite high-salt balance suggests the intrarenal activation of the renin-angiotensin system in diabetes that is not reflected in plasma renin levels. The high correlation between the renal hemodynamic response to captopril and to candesartan indicates that reduced angiotensin II formation is the main mechanism of action of the ACE inhibitor.
| Medienart: |
Artikel |
|---|
| Erscheinungsjahr: |
2001 |
|---|---|
| Erschienen: |
2001 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:59 |
|---|---|
| Enthalten in: |
Kidney international - 59(2001), 4 vom: 01. Apr., Seite 1432-8 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Lansang, M C [VerfasserIn] |
|---|
| Anmerkungen: |
Date Completed 14.06.2001 Date Revised 03.12.2021 published: Print Citation Status MEDLINE |
|---|
| Förderinstitution / Projekttitel: |
|
|---|
| PPN (Katalog-ID): |
NLM111708230 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM111708230 | ||
| 003 | DE-627 | ||
| 005 | 20231222160202.0 | ||
| 007 | tu | ||
| 008 | 231222s2001 xx ||||| 00| ||eng c | ||
| 028 | 5 | 2 | |a pubmed24n0373.xml |
| 035 | |a (DE-627)NLM111708230 | ||
| 035 | |a (NLM)11260405 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Lansang, M C |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Renal vascular responses to captopril and to candesartan in patients with type 1 diabetes mellitus |
| 264 | 1 | |c 2001 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ohne Hilfsmittel zu benutzen |b n |2 rdamedia | ||
| 338 | |a Band |b nc |2 rdacarrier | ||
| 500 | |a Date Completed 14.06.2001 | ||
| 500 | |a Date Revised 03.12.2021 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a BACKGROUND: Enhanced renal vasodilator responses to angiotensin-converting enzyme (ACE) inhibition in diabetes mellitus despite a normal or low plasma renin activity level have suggested intrarenal activation of the renin-angiotensin system in this disease. There is, however, a continuing debate as to the mediators of the renal hemodynamic response to ACE inhibition-reduced angiotensin II formation or pathways involving kinins, prostaglandins, and nitric oxide | ||
| 520 | |a METHODS: Twelve patients with type 1 diabetes mellitus of 18 +/- 3.2 (SEM) years of duration (7 females and 5 males, ages 17 to 50, 32 +/- 4.0 years) who were free of sustained microalbuminuria and on a high-salt diet were given the ACE inhibitor captopril (25 mg orally) on one day and the AT1 receptor blocker candesartan (16 mg orally) on another day. Renal plasma flow (RPF) and glomerular filtration rate were measured before and for four hours after administration | ||
| 520 | |a RESULTS: Both drugs caused a significant increase in RPF (captopril 574 +/- 26 to 625 +/- 37 mL/min/1.73 m2, P = 0.008; candesartan 577 +/- 26 to 643 +/- 37, P = 0.004). There was a highly significant correlation between the responses to captopril and to candesartan (r = 0.86, P < 0.001). Seven subjects had an RPF response to captopril that was accentuated (90 +/- 13 mL/min/1.73 m2), while five had a response that was normal (-4 +/- 9). There was no significant change in glomerular filtration rate on either drug | ||
| 520 | |a CONCLUSION: The remarkable rise in RPF in response to captopril and candesartan despite high-salt balance suggests the intrarenal activation of the renin-angiotensin system in diabetes that is not reflected in plasma renin levels. The high correlation between the renal hemodynamic response to captopril and to candesartan indicates that reduced angiotensin II formation is the main mechanism of action of the ACE inhibitor | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Research Support, U.S. Gov't, P.H.S. | |
| 650 | 7 | |a Angiotensin-Converting Enzyme Inhibitors |2 NLM | |
| 650 | 7 | |a Antihypertensive Agents |2 NLM | |
| 650 | 7 | |a Benzimidazoles |2 NLM | |
| 650 | 7 | |a Biphenyl Compounds |2 NLM | |
| 650 | 7 | |a Tetrazoles |2 NLM | |
| 650 | 7 | |a Captopril |2 NLM | |
| 650 | 7 | |a 9G64RSX1XD |2 NLM | |
| 650 | 7 | |a candesartan |2 NLM | |
| 650 | 7 | |a S8Q36MD2XX |2 NLM | |
| 700 | 1 | |a Price, D A |e verfasserin |4 aut | |
| 700 | 1 | |a Laffel, L M |e verfasserin |4 aut | |
| 700 | 1 | |a Osei, S Y |e verfasserin |4 aut | |
| 700 | 1 | |a Fisher, N D |e verfasserin |4 aut | |
| 700 | 1 | |a Erani, D |e verfasserin |4 aut | |
| 700 | 1 | |a Hollenberg, N K |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Kidney international |d 1972 |g 59(2001), 4 vom: 01. Apr., Seite 1432-8 |w (DE-627)NLM000007188 |x 1523-1755 |7 nnns |
| 773 | 1 | 8 | |g volume:59 |g year:2001 |g number:4 |g day:01 |g month:04 |g pages:1432-8 |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 59 |j 2001 |e 4 |b 01 |c 04 |h 1432-8 | ||