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Study on antihypertensive efficacy of slow-release verapamil: pharmacokinetic and noninvasive hemodynamic profile.
No full textL-type calcium channels modulate the regression of left ventricular hypertrophy after ace-inhibition in genetic hypertension.
No full textThe aim of this study was to investigate the possible link between the regression of the left ventricular mass induced by ACE-inhibition and L-type calcium channels. For this purpose, an evaluation of both L-type calcium channels and AT1 receptor patterns in the left ventricular tissue of adult spontaneously hypertensive rats (SHR) was made before and after long-term treatment with ramipril. An abnormal density of both dihydropyridine and AT1 receptors was observed in SHR at 24 weeks, compared to age-matched control Wistar-Kyoto (WKY) rats (dihydropyridine receptor Bmax: 1. 30+/-0.09 vs 1.14+/-0.06 pmol mg-1 proteins, P<0.001; AT1 receptor Bmax: 1.35+/-0.07 vs 2.62+/-0.08, P<0.001 pmol mg-1 proteins). A treatment for 10 weeks with ramipril induced a significant decrease in the left ventricular mass index of SHR, as well as a significant decrease in dihydropyridine receptor density (Bmax: 0.96+/-0.01 vs 1. 39+/-0.08 pmol mg-1 proteins, P<0.001) and a significant increase in AT1 receptor density (Bmax: 3.08+/-0.26 vs 2.78+/-0.09 pmol mg-1 proteins, ramipril-treated SHR vs vehicle-treated SHR, P<0.001). These results suggest that the decrease in left ventricular mass after treatment with ramipril may be dependent on changes in L-type calcium channels other than the direct effect on circulating and tissue angiotensin II (ang II) levels: involvement of calcium channels and subsequent calcium influx into cardiac cells could be proposed as an additional mechanism for the regression of left ventricular mass after ACE-inhibitio
Total blood pressure reactivity to laboratory tasks, but not absolute changes, is associated to the hypertensive state and vascular damage
No full textThe functional blood pressure changes in different hypertensive states: ambulatory monitoring and total cardiovascular reactivity
No full textL’alterazione strutturale microcircolatoria è associata all’insulinoresistenza indipendentemente dallo stato ipertensivo
No full textCapillary rarefaction is associated with arterial stiffness independently by age and hypertensive state
No full textEffects of Mineralocorticoid and AT1 Receptor Antagonism on The Aldosterone-Renin Ratio In Primary Aldosteronism-the EMIRA Study
Full text linkAbstract
Context
While current guidelines recommend the withdrawal of mineralocorticoid receptor antagonist (MRA) and renin-angiotensin system blockers for the screening and detection of primary aldosteronism (PA), this can worsen hypokalemia and control of high blood pressure (BP) values.
Objective
To investigate whether aldosterone/renin ratio (ARR) values were affected by the MRA canrenone and/or by canrenone plus olmesartan treatment in patients with PA.
Design
Within-patient study.
Setting
The European Society of Hypertension center of excellence at the University of Padua.
Patients
Consecutive patients with an unambiguous diagnosis of PA subtyped by adrenal vein sampling.
Interventions
Patients were treated for 1 month with canrenone (50–100 mg orally), and for an additional month with canrenone plus olmesartan (10–20 mg orally). Canrenone and olmesartan were up-titrated over the first 2 weeks until BP values and hypokalemia were controlled. Patients with unilateral PA were adrenalectomized; those with bilateral PA were treated medically.
Main Outcome Measures
BP, plasma levels of sodium and potassium, renin and aldosterone.
Results
Canrenone neither lowered plasma aldosterone nor increased renin; thus, the high ARR and true positive rate remained unaffected. Addition of the angiotensin type 1 receptor blocker raised renin and slightly lowered aldosterone, which reduced the ARR and increased the false negative rate.
Conclusions
At doses that effectively controlled serum potassium and BP values, canrenone did not preclude an accurate diagnosis in patients with PA. Addition of the angiotensin type 1 receptor blocker olmesartan slightly raised the false negative rate. Hence, MRA did not seem to endanger the accuracy of the diagnosis of P
Non-invasive haemodynamic study in hypertensive subjects after treatment with verapamil slow release.
No full textAim of this study is to investigate the haemodynamic effects, after the short and long-term antihypertensive treatment. After a wash-out period and a placebo treatment period, 30 hypertensive patients received verapamil SR (slow release, 240 mg o.d.) for 30 days. A significant decrease in systolic and diastolic blood pressure was obtained already 4 h after the first administration of verapamil; it was more evident and persistent throughout the study. No significant changes of heart rate or PR interval in ECG were observed. A significant decrease in total vascular resistances, both supine and upright, was evident already 4 h after the drug intake and observed throughout the study. The major effect was obtained after one month. No significant changes of cardiac output, cardiac index and stroke volume were recorded. Furthermore, plasma verapamil levels were measured to confirm that the haemodynamic effects are obtained by low drug concentrations. The present study provides evidence that the antihypertensive effect of verapamil, whose mechanism is the reduction of total vascular resistances, is progressive, long acting and achieved by low plasma levels, when slow release formulation is considered
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