Effects of Losartan and Chlorthalidone on Blood Pressure and Renal Vascular Resistance Index in Non-Diabetic Patients with Essential Hypertension and Normal Renal Function

Abstract

Antihypertensive drugs can differ in target organ protection despite similar blood pressure (BP) control. We compared the effects of losartan (L) and chlorthalidone (C) on renal vascular resistance index (RVRI) in 194 grade I to II, non-diabetic hypertensive patients with increased RVRI (>0.68 m/s by echo-Doppler) but normal renal function. Patients were randomly allocated to C 25 mg/d or L 50 mg/d according to a single blind, PROBE study design. After 4 weeks of treatment, 92 patients (48 L/44 C) with BP <140/90 mm Hg were enrolled in the long-term phase of the study. After 12 months a normalization of RVRI was observed in 47 of 48 patients treated with L (97.5%) and only in 14 of 44 of those treated with C (25.8%) despite no differences in BP control. Patients whose RVRI remained elevated during C therapy underwent a 2-week washout period and then were treated with L 50 mg/d for 12 additional months. After that period 28 of 30 (95%) of patients who were nonresponders to C showed a normalization of RVRI despite no differences in BP control. In conclusion, our data suggest that treatment with L can improve renal hemodynamic and exert a protective renal effect beyond BP control in patients with hypertension.

The Link Between Adipose Tissue Renin-Angiotensin-Aldosterone System Signaling and Obesity-Associated Hypertension

“…This is at least partially attributable to increased AngII levels stimulating sodium transport in multiple nephron segments, altering tubuloglomerular feedback and constricting efferent arterioles (13,28,36,83,84,113,160) (FIGURE 2), which may be reinforced by upregulation of the renal AT1R, as has been demonstrated in obese Zucker rats (221). Accordingly, both enalapril and candesartan produced greater increases in urinary sodium excretion in obese compared with lean Zucker rats (202), whereas losartan reduced renovascular resistance in essential hypertensive patients with a relatively high BMI (30). Interestingly, renal AT2R upregulation has been reported as well in obese rats (82), and chronic AT2R activation has been shown to both promote urinary sodium excretion, probably via effects on proximal tubule Na ϩ -pump activity (4), and lower blood pressure in these rats.…”

HbA1c is an Independent Determinant of Renal Vascular Resistance Estimated by Doppler Sonography in Non-Diabetic Hypertensive Patients

“…During 24 months of treatment, despite similar blood pressure reduction, lisinopril was associated with a significant decrease in renal RI, whereas the nifedipine gastrointestinal therapeutic system did not influence RI significantly [26]. In a further study on non-diabetic hypertensive patients with increased RI (>0.68), Caruso reported that 12 months of treatment with either losartan 50mg/day or chlorthalidone 25mg/day caused a normalization of RI in 97.5% of patients treated with losartan compared to only 25.8% in those treated with chlorthalidone, despite there being no difference in blood pressure control with the two agents [27]. These findings indicate that blockade of the renin-angiotensin axis has the potential to decrease RI and improve arteriolosclerosis in hypertensive patients with elevated HbA1c levels in the upper limit of the normal range, as well as in patients with diabetes mellitus.…”

Effect of the Combined Antihypertensive Therapy With Target Blood Pressure Achievement on Intrarenal Blood Flow in Patients With Type 2 Diabetes

“…По данным Leoncini G., у па-циентов с эссенциальной АГ лечение нифедипином GITS не приводило к улучшению показателей ВПСС, в отли-чие от терапии лизиноприлом, при сопоставимом снижении АД [34]. Терапия ИАПФ и АРА II сопровож-дается существенным уменьшением ВПСС на фоне 2-24 месяцев лечения [5,12,[34][35][36][37]. Снижение ин-дексов периферического сопротивления кровотоку на уровне ПА и ВПА при лечении цилазаприлом имело связь с исходным состоянием сосудистого тонуса [35] и сопровождалось достоверным возрастанием ско-ростных показателей на всех уровнях ренального кро-вотока при терапии нолипрелом [36].…”