Factors correlated with plasma renin activity in general Japanese population

Abiko, Hiroshi; Konta, Tsuneo; Hao, Zhimei; Takasaki, Satoshi; Suzuki, Kazuko; Ichikawa, Kazunobu; Ikeda, Ami; Shibata, Yoko; Takeishi, Yasuchika; Kawata, Satoshi; Kato, Takeshi

doi:10.1007/s10157-008-0114-x

Cited by 7 publications

(7 citation statements)

References 28 publications

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“…6b). Considering that plasma renin levels change in response to changes in dietary salt to sustain blood pressure, 3,34,36) it is reasonable that the forms of hypertension, renin activity-dependent or volumedependent, are determined by the statuses of both renin activity and UNaV. Although UNaV was not selected as a significant covariate on drug effect in the present study, this finding indicates a possibility that UNaV, in combination with pre-treatment PRA, may be a predictor of responsiveness to azelnidipine.…”

Section: Discussioncontrasting

confidence: 52%

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Comparative Pharmacodynamics of Olmesartan and Azelnidipine in Patients with Hypertension: a Population Pharmacokinetic/Pharmacodynamic Analysis

Yoshihara

Kuramoto

Arakawa

2009

Drug Metabolism and Pharmacokinetics

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The objectives of this study were to identify the factors influencing antihypertensive response to the angiotensin receptor blocker, olmesartan medoxomil, or the calcium channel blocker, azelnidipine, and to discuss the possibility of utilizing them as predictors for drug selection prior to therapy. A two-way crossover study of olmesartan medoxomil and azelnidipine was conducted in 29 patients with mild to moderate essential hypertension. The 24-hour ambulatory blood pressure measurements (ABPM) and plasma drug concentrations were obtained on the first and at the end of each treatment period, and were analyzed using population pharmacokinetic/pharmacodynamic (PK/PD) modeling approach. The population PK/PD models considering circadian variations in baseline blood pressure well described the observed plasma drug concentrations and 24-hour ABPM profiles. Pre-treatment plasma renin activity (PRA) was identified as a significant covariate on the maximum drug effect (E(max)) of olmesartan, whereas azelnidpine E(max) was independent of patient background characteristics investigated. No patient was found to have a high E(max) to one agent who also had a high E(max) to the other. In conclusion, the effects of olmesartan medoxomil and azelnidipine were modestly correlated with pharmacokinetic profiles, and the pre-treatment PRA level could be a useful determinant of responsiveness in selecting olmesartan medoxomil and azelnidipine.

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Section: Discussioncontrasting

confidence: 52%

“…[35][36][37] The Japanese patients in the current study exhibited pre-treatment PRA values which were relatively low and were categorized as having a normal or low renin profile in the classification of hypertensive patients defined by Laragh et al 3,34) (Fig. 6b).…”

Section: Discussionmentioning

confidence: 99%

Comparative Pharmacodynamics of Olmesartan and Azelnidipine in Patients with Hypertension: a Population Pharmacokinetic/Pharmacodynamic Analysis

Yoshihara

Kuramoto

Arakawa

2009

Drug Metabolism and Pharmacokinetics

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“…Thus, the acute infusion of Ang II at 8 ng/min/kg over 120 min results in (a) a drop in fractional excretion of urate from 9.3 ± 1.3% to 4.5 ± 1.0% and (b) a drop in urate excretion from 0.16 ± 0.03 mmol/h to 0.07 ± 0.02 mmol/h (166). Hyperuricemia also predicts a blunted renal vascular response to infused Ang II, indicative of an activated intrarenal renin-angiotensin system (168), and plasma renin activity correlates with SUA (169).…”

Section: The Role Of Pdz Domain Proteinsmentioning

confidence: 84%

The Molecular Physiology of Uric Acid Homeostasis

Mandal

Mount²

2015

Annu. Rev. Physiol.

403

331

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Uric acid, generated from the metabolism of purines, has proven and emerging roles in human disease. Serum uric acid is determined by production and the net balance of reabsorption or secretion by the kidney and intestine. A detailed understanding of epithelial absorption and secretion of uric acid has recently emerged, aided in particular by the results of genome-wide association studies of hyperuricemia. Novel genetic and regulatory networks with effects on uric acid homeostasis have also emerged. These developments promise to lead to a new understanding of the various diseases associated with hyperuricemia and to novel, targeted therapies for hyperuricemia.

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“…In addition to regulating blood pressure, high dietary sodium suppresses the renin angiotensin system (RAS), while restricted sodium intake activates the RAS, as well-documented in both human and animal studies [8–10]. Activation of the RAS increases blood pressure and contributes to the development of atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Differential effects of dietary sodium intake on blood pressure and atherosclerosis in hypercholesterolemic mice

Lü

Howatt

et al. 2013

The Journal of Nutritional Biochemistry

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The amount of dietary sodium intake regulates the renin angiotensin system (RAS) and blood pressure, both of which play critical roles in atherosclerosis. However, there are conflicting findings regarding the effects of dietary sodium intake on atherosclerosis. This study applied a broad range of dietary sodium concentrations to determine the concomitant effects of dietary sodium intake on the RAS, blood pressure, and atherosclerosis in mice. Eight-week-old male low-density lipoprotein receptor −/− mice were fed a saturated fat-enriched diet containing selected sodium concentrations (Na 0.01%, 0.1%, or 2% w/w) for 12 weeks. Mice in these three groups were all hypercholesterolemic, although mice fed Na 0.01% and Na 0.1% had higher plasma cholesterol concentrations than mice fed Na 2%. Mice fed Na 0.01% had greater abundances of renal renin mRNA than those fed Na 0.1% and 2%. Plasma renin concentrations were higher in mice fed Na 0.01% (14.2±1.7 ng/ml/30 min) than those fed Na 0.1% or 2% (6.2±0.6 and 5.8±1.6 ng/ml per 30 min, respectively). However, systolic blood pressure at 12 weeks was higher in mice fed Na 2% (138±3 mm Hg) than those fed Na 0.01% and 0.1% (129±3 and 128±4 mmHg, respectively). In contrast, mice fed Na 0.01% (0.17±0.02 mm2) had larger atherosclerotic lesion areas in aortic roots than those fed Na 2% (0.09±0.01 mm2), whereas lesion areas in mice fed Na 0.1% (0.12±0.02 mm2) were intermediate between and not significantly different from those in Na 0.01% and Na 2% groups. In conclusion, while high dietary sodium intake led to higher systolic blood pressure, low dietary sodium intake augmented atherosclerosis in hypercholesterolemic mice.

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Factors correlated with plasma renin activity in general Japanese population

Abstract: This study revealed that PRA was higher in men than women and was associated negatively with blood pressures and urine sodium excretion, and positively with total protein, smoking and HDL-C in Japanese population.

Cited by 7 publications

References 28 publications

Comparative Pharmacodynamics of Olmesartan and Azelnidipine in Patients with Hypertension: a Population Pharmacokinetic/Pharmacodynamic Analysis

Comparative Pharmacodynamics of Olmesartan and Azelnidipine in Patients with Hypertension: a Population Pharmacokinetic/Pharmacodynamic Analysis

The Molecular Physiology of Uric Acid Homeostasis

Differential effects of dietary sodium intake on blood pressure and atherosclerosis in hypercholesterolemic mice

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