Does an adequate control of blood pressure protect the kidney in essential hypertension?

Ruilope, Luis; Alcázar, J M; Hernández, Eduardo; Moreno, F; Martinez, Miguel A.; Rodicio, J. L.

doi:10.1097/00004872-199006000-00005

Cited by 54 publications

(18 citation statements)

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“…Adequate blood pressure control does not necessarily resolve all target-organ injury. 29 - 30 The metabolism of vasoactive substances generated regionally in the vascular wall and the kidney is important in producing a regression of organ damage.…”

Section: Discussionmentioning

confidence: 99%

Long-term infusion of kallikrein attenuates renal injury in Dahl salt-sensitive rats.

et al. 1994

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We investigated whether long-term infusion of kallikrein would attenuate renal injury in salt-induced hypertension in Dahl salt-sensitive rats. A subdepressor dose of purified rat urinary kallikrein (700 ng/d IV) was infused by osmotic minipump for 4 weeks in male Dahl salt-sensitive rats fed a high salt (2% NaCl) diet. This dose did not affect the time-dependent elevation of blood pressure; however, urinary protein excretion was significantly decreased, and glomerular filtration rate was increased. These beneficial effects were reflected morphologically by an attenuation of the glomerulosclerotic lesions and tubular injury seen in the hypertensive Dahl salt-sensitive rats. Kallikrein infusion increased urinary A ngiotensin-converting enzyme (ACE) inhibitors affect both the renin-angiotensin and kallikrein-kinin-prostaglandin systems, inhibiting different catalytic sites on the same ACE. The cardiovascular protection induced by ACE inhibitors is primarily due to inhibition of the renin-angiotensin system. Recent advances in vascular biology suggest that the vasodepressor system participates in the progression or regression of cardiovascular injury.12 Vasodepressor eicosanoid directly delays the transition from the resting G0/G1 to DNA-synthetic (S) period progression in the proliferative cycle of vascular smooth muscle cells. 3 Moreover, enhancement of the endogenous production of prostacyclin attenuates vascular and renal injury in salt-induced hypertension in Dahl salt-sensitive (Dahl S) rats, a genetic model for salt-induced hypertension in humans. 4 Kinins stimulate the formation of nitric oxide, which also retards vascular smooth muscle cell proliferation. 56 The activity of the kallikrein-kinin-prostaglandin system is reduced in the kidneys of Dahl S rats. "9 Recently, kallikrein-like activity and its corresponding mRNAs have been found in the vascular wall.1012 More intriguingly, it has been reported that blood pressure cosegregates with a kallikrein gene restrictive fragment length polymorphism.13 These data Correspondence to Yoshio Uehara, MD, The Second Department of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan.© 1994 American Heart Association, Inc.excretion of bradykinin and stimulated excretion of cyclic GMP, suggesting that the kallikrein-kinin-prostaglandin and nitric oxide axes were enhanced by rat urinary kallikrein infusion. The alterations induced by kallikrein infusion were potentiated by the concomitant administration of the angiotensin-converting enzyme inhibitor alacepril. These studies indicated that long-term replacement with rat tissue kallikrein attenuates renal injury in hypertensive Dahl salt-sensitive rats. (Hypertension. 1994;24:770-778.) Key Words • kallikrein • renin-angiotensin system • rats, inbred Dahl • angiotensin-converting enzyme inhibitor • prostaglandins • kallikrein-kinin system clearly suggest that dysfunction of the kallikrein-kininprostaglandin system is involved in the genesis of saltinduced hypertension of Dahl S rats.We have ...

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Section: Discussionmentioning

confidence: 99%

Long-term infusion of kallikrein attenuates renal injury in Dahl salt-sensitive rats.

et al. 1994

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“…Hypertensive patients with persistent proteinuria under intensive antihypertensive therapy have shown a significantly higher prevalence of end-organ damage. 3 In view of the correlation between proteinuria progression and subsequent renal impairment, it is not unrealistic to anticipate a beneficial effect on clinical events in our population. This finding may provide a new strategy to treat persistent proteinuria in patients with well-controlled hypertension and may be of particular importance for the future design of combination drugs.…”

Section: Perspectivesmentioning

confidence: 96%

“…1 Hypertension has been shown to be an important cause of end-stage renal disease. 2 Ruilope et al 3 illustrated the existance of overt proteinuria in 17.5% of patients with chronic and well-controlled hypertension. Therefore, although tight blood pressure control is known to be a crucial factor in preventing progression of renal disease, other factors are undoubtedly involved.…”

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confidence: 99%

Effect of Pravastatin on Proteinuria in Patients With Well-Controlled Hypertension

2002

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Abstract-Proteinuria is an important risk factor for cardiovascular and renal morbidity and mortality. The effects of 3-hydroxy-3-methyglutaryl coenzyme A reductase inhibitor (statin) therapy on proteinuria in normolipidemic patients with well-controlled hypertension have not been studied. A total of 63 normolipidemic (total cholesterol Ͻ240 mg/dL) and proteinuric (300 to 3000 mg/d) patients with well-controlled blood pressure (Ͻ140/90 mm Hg) were randomized to receive either placebo (nϭ32) or pravastatin (10 mg/d; nϭ31) after a 3-month placebo period. Pravastatin lowered proteinuria after 6 months by 54% (PϽ0.0001). Creatinine clearance was stable throughout the study in the 2 groups. Despite unchanged plasma endothelin-1 levels throughout the study, urinary excretion of the peptide was decreased and significantly correlated with improvement in urinary protein excretion in pravastatin-treated patients (rϭ0.64, Pϭ0.001). The urinary excretion of retinol-binding protein decreased after pravastatin administration, probably reflecting an improvement in tubular function. In contrast, the urinary excretion of IgG did not change significantly throughout the study in either group. Multivariate analysis revealed that proteinuria was only significantly correlated with statin use (PϽ0.0001, R 2 ϭ0.66). Linear regression analysis in the statin-treated group did not show any correlation between changes in lipid profiles and proteinuria regression. Thus, in addition to their primary function of antilipidemia, the addition of pravastatin to treatment for well-controlled hypertension may have an additive effect on reducing proteinuria independent of hemodynamics and lipid-lowering effects, possibly through inhibiting renal endothelin-1 synthesis and improving tubular function.

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“…Thus, the discrepancy in the renal protection between indapamide and trichloromethiazide could not be explained by blood pressure reduction alone. A number of studies have reported dissociation of blood pressure reduction from target organ protection (25,26). To explain such discrepancy, much attention has been paid thus far to metabolic changes induced by antihypertensive drugs, e.g.…”

Section: Discussionmentioning

confidence: 99%

Radical Scavenging Properties of Indapamide and Renal Protection in Dahl Salt-Sensitive Rats.

et al. 1992

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We have found that indapamide has free radical scavenging properties and stimulates prostacyclin generation in vascular smooth muscle cells. In this study, we investigated whether indapamide exhibits radical scavenging effects in vivo and whether these properties are related to renal protection in Dahl salt-sensitive (Dahl S) rats. Indapamide (4 mg/kg body weight per day for 5 weeks) ameliorated the development of hypertension in Dahl S rats fed a high salt (6% NaCI) diet. The blood pressure reduction was associated with a decrease in proteinuria, a decrease in urinary n-acetyl-/9-D-glucosaminidase excretion, and an increase in glomerular filtration rate. Moreover, morphological investigation revealed improvement in glomerulosclerosis, renal tubular damage and intrarenal arterial injuries, seen in the saltinduced hypertension. These beneficial properties were accompanied by a significant decrease in the capacity for lipid peroxide formation in the renal homogenates. In contrast, trichloromethiazide, which reduced the blood pressure to the same extent as indapamide, did not lower lipid peroxide formation in the kidney or exert protective effects on the renal glomeruli or arteries. Thus, the evidence suggests that the diuretic indapamide exhibits radical scavenging effects on the kidney which may contribute to attenuating the renal injuries seen in salt-induced hypertension in Dahl S rats. (Hypertens Res 1992; 15: 17-26)

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Does an adequate control of blood pressure protect the kidney in essential hypertension?

Cited by 54 publications

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Long-term infusion of kallikrein attenuates renal injury in Dahl salt-sensitive rats.

Long-term infusion of kallikrein attenuates renal injury in Dahl salt-sensitive rats.

Effect of Pravastatin on Proteinuria in Patients With Well-Controlled Hypertension

Radical Scavenging Properties of Indapamide and Renal Protection in Dahl Salt-Sensitive Rats.

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