Nephroprotective effect of antihypertensive drugs in essential hypertension

Sušić, Dinko; Fröhlich, Edward D.

doi:10.1097/00004872-199816050-00001

Cited by 22 publications

(13 citation statements)

References 141 publications

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“…In many patients, terminal renal failure can occur despite the presence of an efficient antihypertensive drug treatment. 28,29 We suggest that such a development should be explained not only on the basis of studies of small arteries but also of large arteries, as the latter may be damaged independent of atherosclerosis and even of increased BP levels.…”

Section: Discussionmentioning

confidence: 93%

Arterial Stiffness and Plasma Creatinine in Untreated Hypertensive Patients

Gosse

Safar

2005

American Journal of Hypertension

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Background: Increased arterial stiffness is a common feature of hypertensive subjects with renal failure, independently of age, office blood pressure (BP), and traditional cardiovascular risk factors including atherosclerosis but not diabetes mellitus. Recently a reduction in creatinine clearance was shown to be associated with increased arterial stiffness in patients with normal or elevated BP and mild renal failure, and the association was noted to be stronger in subjects Ͻ55 years of age. We wanted to study this relationship in a population of newly recognized hypertensive subjects with preserved renal function using another method to assess arterial stiffness and to see whether it was independent of 24-h BP.

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Section: Discussionmentioning

confidence: 93%

Arterial Stiffness and Plasma Creatinine in Untreated Hypertensive Patients

Gosse

Safar

2005

American Journal of Hypertension

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“…It should be noted that our study involved drugs that were deemed to offer better nephroprotection than, perhaps, other antihypertensive agents. 15 Question may be raised as to whether our finding that the renal vascular response to dipyridamole may be compromised in hypertension has any biological significance or whether it is just another marker of hypertension. We believe that the altered responses of renal vasculature to dipyridamole may be one of the first signs of renal involvement in hypertension.…”

Section: Susic Et Al Renal Vasculature and Dipyridamole In Shrmentioning

confidence: 99%

Abnormal Renal Vascular Responses to Dipyridamole-Induced Vasodilation in Spontaneously Hypertensive Rats

2001

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Abstract-The objective of this study was to determine whether there were differences in hemodynamic responses of different vascular beds to systemic administration of dipyridamole between spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. To this end, systemic hemodynamics and organ blood flows (using labeled microspheres) were determined in conscious rats before and 10 minutes after dipyridamole (4 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 ) infusion. In both the normotensive and hypertensive rats, the dipyridamole infusion reduced arterial pressure by Ϸ20 mm Hg, associated with a decreased total peripheral resistance and an increased cardiac output. Renal blood flow decreased significantly in SHR after dipyridamole but remained unchanged or increased slightly in the WKY rats. There were no other differences in regional hemodynamics, including those of brain, liver, skin, and muscle, between the WKY and SHR. Antihypertensive treatment completely restored normal renal vascular response to dipyridamole. Previous reports had demonstrated an abnormal coronary hemodynamic response of the SHR. Our data demonstrate that, as with coronary hemodynamics, hypertension selectively induced alterations in renal vasculature. These findings may be of importance in identifying the earliest hemodynamic evidence of developing hypertensive nephrosclerosis. Key Words: hypertension Ⅲ renal vasculature Ⅲ dipyridamole Ⅲ regional hemodynamics S ustained increase in arterial pressure alters function as well as structure of systemic vasculature. 1-3 These hypertension-induced vascular alterations eventually lead to target organ damage of brain, heart, and kidneys. Fortunately, antihypertensive therapy seems to ameliorate these hypertensive vascular changes, reducing morbidity and mortality from strokes and coronary heart disease. 4,5 In contrast, the incidence and prevalence of end-stage hypertensive renal disease continue to increase. 6 Moreover, renal vascular involvement in hypertension is seldom detected during its early stages. At the moment when clear clinical signs of renal insufficiency become apparent, renal damage is usually so extensive that therapy can only delay, but not prevent, the development of end-stage renal failure. For this reason, early signs of renal involvement in hypertensive disease are highly desirable.In our studies dealing with the coronary circulation in spontaneously hypertensive rats (SHR), early hemodynamic alterations were demonstrated by dipyridamole infusion. [7][8][9][10] We found that coronary vasodilation in response to dipyridamole infusion was significantly diminished in SHR and that antihypertensive therapy restored vasodilatory response of coronary vasculature. This report concerns the effects of dipyridamole on the other regional circulations of normotensive Wistar-Kyoto (WKY) rats and SHR. Our purpose was to determine whether there were differences between WKY and SHR in the hemodynamic responses of various vascular beds to the systemic administration of dipyridamole, an agent commonly used ...

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“…Achieving target blood pressure is of utmost importance for improving renal outcomes, as reduction in blood pressure is known to exert a nephroprotective effect. 3,15,16 In these patients with renal dysfunction, mean trough plasma aliskiren concentrations increased with dose and reached steady state 2-4 weeks after the start of dosing or up-titration of the dose. The results from an earlier study assessing the effects of renal impairment on pharmacokinetics of aliskiren (300 mg once daily) in patients with mild-to-moderate renal dysfunction and healthy volunteers showed that although exposure is increased by renal impairment, the increase in exposure does not correlate with the severity of renal impairment.…”

Section: Discussionmentioning

confidence: 99%

Efficacy and safety of aliskiren in Japanese hypertensive patients with renal dysfunction

et al. 2009

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This 12-week, multicenter, open-label study assessed the efficacy, pharmacokinetics and safety of a once-daily aliskiren in Japanese hypertensive patients with renal dysfunction. Patients (n¼40, aged 20-80 years) with mean sitting diastolic blood pressure (msDBP) X95 and o110 mm Hg and serum creatinine between X1.3 and o3.0 mg per 100 ml in males or between X1.2 and o3.0 mg per 100 ml in females were eligible. Patients began therapy with a once-daily morning oral dose of 75 mg of aliskiren. In patients with inadequate blood pressure control (msDBP X90 or mean sitting systolic blood pressure [msSBP] X140 mm Hg) and without safety concerns (serum potassium 45.5 mEq l -1 or an increase in serum creatinine X20%), the aliskiren dose was increased to 150 mg and then to 300 mg in sequential steps starting from Week 2. Efficacy was assessed as change in msSBP/msDBP from baseline to the Week 8 endpoint (with the last observation carried forward). The mean reduction from baseline to Week 8 endpoint was 13.9 ± 16.6 and 11.6 ± 9.7 mm Hg for msSBP and msDBP, respectively. At the Week 8 endpoint, 65% patients had achieved blood pressure response (msDBP o90 or a 10 mm Hg decrease or msSBP o140 or a 20 mm Hg decrease) and 30% had achieved blood pressure control (msSBP o140 mm Hg and msDBP o90 mm Hg). Aliskiren was well tolerated with no new safety concerns in Japanese hypertensive patients with renal dysfunction.

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Nephroprotective effect of antihypertensive drugs in essential hypertension

Cited by 22 publications

References 141 publications

Arterial Stiffness and Plasma Creatinine in Untreated Hypertensive Patients

Arterial Stiffness and Plasma Creatinine in Untreated Hypertensive Patients

Abnormal Renal Vascular Responses to Dipyridamole-Induced Vasodilation in Spontaneously Hypertensive Rats

Efficacy and safety of aliskiren in Japanese hypertensive patients with renal dysfunction

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