Echocardiographic assessment of doxazosin on left ventricular mass in patients with essential hypertension

Monsalve, Pedro; Vera, Omaira; Acuña, Frank Pérez; Medina, Omar; Ostojich, Kasmir; López, Berardo; Torres, Nidia; Franco, Vicenta Lugo de; Fonseca, Ricardo; Fragachán, F.

doi:10.1016/0002-8703(91)90872-f

Cited by 14 publications

(9 citation statements)

References 19 publications

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“…29 A reduction of ventricular hypertrophy after doxazosin treatment was also observed in patients with essential hypertension. 30 Our results confirm a reduction in the diameter of cardiac muscle cells in rats with spontaneous hypertension treated with doxazosin compared to untreated SHR.…”

Section: Discussionsupporting

confidence: 81%

Influence of doxazosin on biosynthesis of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats

Kasacka

Piotrowska

Filipek

et al. 2015

Exp Biol Med (Maywood)

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Hypertension frequently results in severe complications in cardiovascular system and histopathological changes in the heart. To better understand the cellular processes and signaling pathways responsible for the proper functioning of the heart, we decided to check whether doxazosin affects the density of structures containing S100A6 and atrial natriuretic factor in the heart of spontaneously hypertensive rats. The aim of this study is to find differences in the density of the structures containing S100A6 and atrial natriuretic factor in the heart of spontaneously hypertensive rats treated with doxazosin compared to untreated animals. Fragments of heart were collected from five spontaneously hypertensive rats and five spontaneously hypertensive rats receiving doxazosin for six weeks (dose 0.1 mg per 1 kg of body weight). On the paraffin sections S100A6 and atrial natriuretic factor peptides were localized in the heart using immunohistochemistry. Positive immunohistochemical reaction for S100A6 was observed in atrial and ventricular cardiomyocytes and in the coronary vasculature. In the heart of hypertensive rats treated with doxazosin the S100A6 immunoreactivity was significantly lower compared to untreated animals. Immunodetection of atrial natriuretic factor in the heart of rats confirmed presence of peptide in atrial myocardium. Delicate atrial natriuretic factor-immunoreactivity was observed also in few ventricular cardiomyocytes. The atrial natriuretic factor-immunosignal was significantly weaker in hearts of hypertensive rats receiving doxazosin compared to spontaneously hypertensive rats untreated. Since we found that doxazosin reduces the levels of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats, it can be assumed that cardiovascular disorders that occur in hypertension may be associated with disturbances of cellular processes and signaling pathways.

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Section: Discussionsupporting

confidence: 81%

Influence of doxazosin on biosynthesis of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats

Kasacka

Piotrowska

Filipek

et al. 2015

Exp Biol Med (Maywood)

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“…Uncontrolled studies in small numbers of patients showed such an effect for the ␣ adrenergic blocker doxazosin (159,160), but the single-drug therapy study in patients with mild to moderate hypertension found reduction of left ventricular mass after ␤ blockade but not after the ␣ blocker prazosin or the central sympathicolytic agent clonidine (161). Again, it is difficult to say whether beneficial effects of adrenergic blockers occurred separate from their antihypertensive action.…”

Section: Sympathetic Hyperactivity and The Heartmentioning

confidence: 99%

Sympathetic Hyperactivity in Chronic Renal Failure

Koomans

Blankestijn

Joles

2004

Journal of the American Society of Nephrology

185

145

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Abstract. Sympathetic hyperactivity plays an important and distinct role in hypertension associated with chronic renal failure (CRF). Renal ischemia, elevated angiotensin II, and suppressed brain nitric oxide (NO) all stimulate sympathetic activity. Evidence is accumulating for a role of sympathetic hyperactivity in renal and cardiac damage in patients with CRF. Decreased NO availability and increased oxidative stress, characteristic in CRF patients, seem to sensitize target organs for damaging actions of sympathetic hyperactivity. Fortunately, sympatholytic agents can slow down progression of renal and cardiac dysfunction. Angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists suppress sympathetic activity, but complete elimination of the effect of sympathetic hyperactivity can be obtained only with specific adrenergic blockers. However, this important therapeutic option is grossly neglected, painfully illustrated by the unwillingness to treat CRF patients with ␤-blockers, even if they have had a myocardial infarction. After discussion of mechanisms and effects of the sympathetic hyperactivity, a case is made for increased application of specific adrenergic blockers in patients with CRF.Hypertension remains an important issue in patients with chronic renal failure (CRF). It plays a key role in progression of renal failure and forms the basis for the cardiovascular complications and mortality. Although this point is widely recognized, BP control in patients with CRF, whether in an early or advanced stage or when on dialysis, is often poor (1, 2).Hypervolemia and activated renin angiotensin system (RAS) have long been acknowledged as major determinants of hypertension in CRF, and in most patients, both need to be controlled to normalize BP. Besides, it has been shown in several trials that the renoprotective effect of RAS suppression extends beyond BP lowering only. This applies particularly to patients with diabetic (3-6) or nondiabetic (3, 5, 7) glomerulopathy.It has also become clear that many other factors cause renal hypertension. These include elevated levels of endothelin, sympathetic activity, and oxidant stress and reduced levels of NO and medullary vasodilating factors (8 -10). As is the case for angiotensin II, many of these factors probably damage the kidney and the cardiovascular system independent of their hypertensive effect. However, as long as their pathogenic role has not been proved in large clinical trials, it is understandable that these factors are still regarded as foot-soldiers compared with the well-accepted nobility of volume and RAS-understandable, but probably not right. Already several Cinderellas have been identified that relate CRF to cardiovascular disease, i.e., the underestimated role of renal dysfunction in cardiovascular risk profile (11) and of cardiac systolic dysfunction in dialysis patients (12). We can do without one more. In this review, we highlight the pathogenesis of sympathetic hyperactivity in CRF and the evidence for its role in organ damage...

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“…In contrast to ß-blockers and diuretics, which have adverse effects on the serum lipid Cardiac Hypertrophy LVH is an adaptive response to the additional after load caused by elevated blood pressure and is itself a major independent risk factor for CHD. A number of comparative and noncomparative studies have demon Eur Urol 1996;29(suppl l):31-39 Pool 36 strated that doxazosin decreases left ventricular mass in hypertensive patients [5,37], 6.1% with ACE inhibitors, 9.0% with calcium antago nists, and 14.1% with diuretics (p = 0.02 difference among active groups, p = 0.01 difference among all groups).…”

Section: Fibrinolysismentioning

confidence: 99%

Unique Aspects of Doxazosin: A Third-Generation Alpha-Blocker

Pool¹

1996

Eur Urol

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Echocardiographic assessment of doxazosin on left ventricular mass in patients with essential hypertension

Cited by 14 publications

References 19 publications

Influence of doxazosin on biosynthesis of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats

Influence of doxazosin on biosynthesis of S100A6 and atrial natriuretic factor peptides in the heart of spontaneously hypertensive rats

Sympathetic Hyperactivity in Chronic Renal Failure

Unique Aspects of Doxazosin: A Third-Generation Alpha-Blocker

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