Acute and chronic effects of angiotensin converting enzyme inhibitors on the essential hypertensive kidney

Reams, Garry P.; Bauer, John H.

doi:10.1007/bf01857635

Cited by 7 publications

(9 citation statements)

References 169 publications

(119 reference statements)

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“…In this hypertensive strain, there is a congenital reduction in afferent arteriolar diameter that results in renal ischemia. An increase in BP ensues, but the autoregulatory response of the preglomerular vasculature is functional and vasoconstricts appropriately to prevent the development of glomerular and peritubular capillary hypertension (66,67). In addition, renal ischemia is minimal because the increase in systemic and renal perfusion pressure will act to relieve it (55).…”

Section: Relevance Of Stages Of Hypertension With the Progression Of mentioning

confidence: 99%

Essential Hypertension, Progressive Renal Disease, and Uric Acid

Johnson

Segal

Srinivas

et al. 2005

Journal of the American Society of Nephrology

263

171

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Hypertension and hypertension-associated ESRD are epidemic in society. The mechanisms responsible for renal progression in mild to moderate hypertension and those groups most at risk need to be identified. Historic, epidemiologic, clinical, and experimental studies on the pathogenesis of hypertension and hypertension-associated renal disease are reviewed and an overview/hypothesis for the mechanisms involved in renal progression is presented. There is increasing evidence that hypertension may exist in one of two forms/stages. The first stage, most commonly observed in early or borderline hypertension, is characterized by salt-resistance, normal or only slightly decreased GFR, relatively normal or mild renal arteriolosclerosis, and normal renal autoregulation. This group is at minimal risk for renal progression. The second stage, characterized by salt-sensitivity, renal arteriolar disease, and blunted renal autoregulation, defines a group at highest risk for the development of microalbuminuria, albuminuria, and progressive renal disease. This second stage is more likely to be observed in blacks, in subjects with gout or hyperuricemia, with low level lead intoxication, or with severe obesity/metabolic syndrome. The two major mechanistic pathways for causing impaired autoregulation at mild to moderate elevations in BP appear to be hyperuricemia and/or low nephron number. Understanding the pathogenetic pathways mediating renal progression in hypertensive subjects should help identify those subjects at highest risk and may provide insights into new therapeutic maneuvers to slow or prevent progression.

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Section: Relevance Of Stages Of Hypertension With the Progression Of mentioning

confidence: 99%

Essential Hypertension, Progressive Renal Disease, and Uric Acid

Johnson

Segal

Srinivas

et al. 2005

Journal of the American Society of Nephrology

263

171

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“…[6] ACE inhibitors have recently developed as a popular therapy for hypertension because they not only reduce blood pressure, but also have renoprotective effects, leading to reductions in proteinuria, glomerulosclerosis, and progressive renal disease. [7][8][9][10][11][12] Indeed, there have been many studies both in humans and experimental animals detailing the benefits of ACE inhibition on kidney function. [7][8][9][10][11][12][13] ACE inhibition has been reported to reduce glomerular capillary pressure, lower renal vascular resistance, and improve or preserve both renal blood flow and glomerular filtration rate.…”

Section: Introductionmentioning

confidence: 99%

“…[7][8][9][10][11][12] Indeed, there have been many studies both in humans and experimental animals detailing the benefits of ACE inhibition on kidney function. [7][8][9][10][11][12][13] ACE inhibition has been reported to reduce glomerular capillary pressure, lower renal vascular resistance, and improve or preserve both renal blood flow and glomerular filtration rate. [7,14] The aim of our study was to compare the effects of the AT 1 receptor blocker, Irb, and the ACE inhibitor, Q, in STZ-induced diabetes in rats by assessing nephron function, renal morphology, and renal TGF-β 1 expression.…”

Section: Introductionmentioning

confidence: 99%

“…[7][8][9][10][11][12][13] ACE inhibition has been reported to reduce glomerular capillary pressure, lower renal vascular resistance, and improve or preserve both renal blood flow and glomerular filtration rate. [7,14] The aim of our study was to compare the effects of the AT 1 receptor blocker, Irb, and the ACE inhibitor, Q, in STZ-induced diabetes in rats by assessing nephron function, renal morphology, and renal TGF-β 1 expression. We also determined whether combined use of Q and Irb is superior over the use of these agents alone.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Angiotensin-Converting Enzyme Inhibition and Angiotensin II Type 1 Receptor Blockade on Streptozotocin-Induced Diabetic Nephropathy

et al. 2008

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The aim of this study was designed to investigate the possible beneficial effects of the angiotensin-converting enzyme (ACE) inhibitor, Quinapril (Q) and, the angiotensin (ang) II T 1 (AT1) receptor blocker, irbesartan (Irb), in streptozotocin (STZ)-induced diabetes in rats. The rats were randomly allotted into one of five experimental groups: A (control), B (diabetic untreated), C (diabetic treated with Q), D (diabetic treated with Irb), and E (diabetic treated with Q&Irb), each group containing 10 animals. Groups B-E received STZ. Diabetes was induced in four groups by a single intraperitoneal (i.p) injection of STZ (50 mg/kg, freshly dissolved in 5 mmol/L citrate buffer, pH 4.5). Two days after STZ treatment, development of diabetes in four experimental groups was confirmed by measuring blood glucose levels in a tail vein blood samples. Rats with blood glucose levels of 250 mg/dL or higher were considered to be diabetic. The rats in Q-, Irb-, and Q&Irb-treated groups were given Q (in a dose of 3 mg/kg body weight), Irb (5 mg/kg body weight), and Q&Irb (in a dose of 1.5 mg/kg + 2.5 mg/kg body weight) once a day orally by using intra-gastric intubation for 12 weeks starting two days after STZ injection. Treatment of Q and especially Irb reduced the glomerular size and thickening of capsular, glomerular, and tubular basement membranes; and increased amounts of mesangial matrix and tubular dilatation and renal function as compared with diabetics untreated. Notably, the better effects were obtained when Q and Irb given together. We conclude that Q, Irb, and especially Q+Irb therapy causes renal morphologic and functional improvement after STZ-induced diabetes in rats. We believe that further preclinical research into the utility of Q and Irb treatment, alone or its combination, may indicate its usefulness as a potential treatment in diabetic nephropathy (DNp).

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“…Indeed, there have been many studies both in humans and experimental animals detailing the benefits of ACE inhibition on kidney function 1–7 . Angiotensin‐converting enzyme inhibition has been reported to reduce glomerular capillary pressure, lower renal vascular resistance and improve or preserve both renal blood flow and glomerular filtration rate 1,8 …”

Section: Introductionmentioning

confidence: 99%

Angiotensin‐converting enzyme inhibition in adult hypertensive rats: A stereological study of renal filtration surface area

Dunstan

Briscoe

Bertram

et al. 2003

Clin Exp Pharma Physio

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1. Angiotensin-converting enzyme (ACE) inhibitor treatment leads to beneficial effects on kidney function. The aim of the present study was to determine whether ACE inhibition at high or low doses affects glomerular capillary surface area and length, glomerular number or total renal filtration surface area in rats with established hypertension and, if so, to determine whether these effects are mediated through bradykinin potentiation. 2. Spontaneously hypertensive rats (SHR) were treated with the ACE inhibitor perindopril at either 3 or 0.1 mg/kg per day (high and low doses, respectively) from 16 to 24 weeks of age. Some rats were concomitantly treated with the bradykinin B2 receptor antagonist S16118 (10 nmol/kg per day). Blood pressure was measured twice weekly during the treatment period. At 24 weeks of age, rats were perfusion fixed at 140 mmHg, the kidneys removed, embedded in resin and examined stereologically to estimate glomerular number and volume, length and surface area of glomerular capillaries and total renal filtration surface area. 3. High- and low-perindopril treatment significantly reduced systolic blood pressure compared with control SHR. However, the rats treated with low-dose perindopril were still considered hypertensive. Neither low-dose nor high-dose perindopril treatment had any observable effect on glomerular number (23 876 +/- 1201 vs 26 240 +/- 1465 glomeruli/kidney, respectively) or volume (2.25 +/- 0.21 and 1.96 +/- 0.06 x 10-3 mm3, respectively) compared with controls (glomerular number 25866 +/- 1210 glomeruli/kidney; glomerular volume 2.24 +/- 0.21 x 10-3 mm3). As a result, there was no significant difference in total renal filtration surface area between any of the experimental groups (8161.6 +/- 550.9, 8699.7 +/- 427.6, 9081.9 +/- 453.6, 8830.2 +/- 521.2 and 8559.4 +/- 341.4 mm2 for SHR, SHR low-dose perindopril, SHR low-dose perindopril + B2 antagonist, SHR high-dose perindopril and SHR high-dose perindopril + B2 antagonist, respectively). Coadministration of the bradykinin antagonist had no observable effect on any of the parameters studied. 4. In conclusion, because neither high-dose nor low-dose perindopril had any effect on total renal filtration surface area, the observed beneficial effects of ACE inhibition on kidney function are not the result of enhancement in glomerular capillary surface area.

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Acute and chronic effects of angiotensin converting enzyme inhibitors on the essential hypertensive kidney

Cited by 7 publications

References 169 publications

Essential Hypertension, Progressive Renal Disease, and Uric Acid

Essential Hypertension, Progressive Renal Disease, and Uric Acid

Effect of Angiotensin-Converting Enzyme Inhibition and Angiotensin II Type 1 Receptor Blockade on Streptozotocin-Induced Diabetic Nephropathy

Angiotensin‐converting enzyme inhibition in adult hypertensive rats: A stereological study of renal filtration surface area

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