Antihypertensive Properties of Furosemide

Davidov, Michael; Kakaviatos, Nikos; Finnerty, Frank A.

doi:10.1161/01.cir.36.1.125

Cited by 46 publications

(14 citation statements)

References 10 publications

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“…already described by other investi gators [40,41], may influence peripheral re sistance and consequently cardiocirculatory balance, thus assuming the value of an addi tional functional test [12], This contributes to differentiating stages of 'borderline' hyper tension.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamics in Borderline Hypertension: Acute Effect of Furosemide

Franchi¹,

Pl²,

Scardi³

et al. 1984

Cardiology

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In order to identify the hemodynamics of borderline essential hypertension, radionuclide angiography was performed before and after bolus injection of furosemide (40 mg i.v.) both at 3 min (i.e. before diuretic effect) and at 30 min (i.e. after diuretic effect) in 16 borderline (B) patients and in 14 age-matched WHO classification I-II essential hypertensives (H) patients. 14 age-matched normotensive (N) subjects were used as controls. B patients were further subdivided into two subgroups according to a cardiac index under or above 3 liter/min/m2 in basal conditions. Baseline hemodynamic characteristics showed higher values of mean arterial pressure (MAP) and systemic vascular resistance index (SVRI) in both H and B patients when compared with N subjects (p < 0.001). Furthermore, B and H patients exhibited lower values of left ventricular peak filling rate (PFR) than seen in N subjects (p < 0.01 and p < 0.05, respectively). H patients demonstrated higher peak systolic blood pressure/end-systolic volume ratio (PSP/ESV) than seen in N subjects (p < 0.05). PFR positively correlated with peak emptying rate (PER) only in N and B patients (p < 0.05). After furosemide administration, even though differences were observed in the absolute values, B and H patients showed similar hemodynamic patterns. Only the B subgroup with cardiac index (CI) > 3 liter (‘volume-dependent’ patients) showed a decrease in left ventricular end-diastolic volume index (LVEDVI) at 30 min associated with a lowering of stroke index (SI; p < 0.005 for both), when compared with pre-drug values. In B patients with CI < 3 liter (‘afterload-dependent’ patients) no differences were observed either at 3 min or at 30 min in comparison with values obtained prior to drug administration. Moreover, in this subgroup, like in H patients, there was a negative correlation (p < 0.01) between 3-min percent change of SVRI and 3-min percent change of SI. Our data suggest that in ‘borderline’ hypertension: (a) there may be an increase in peripheral resistance, as in established hypertension, especially when age-matched groups are considered; (b) the earliest sign of compromised left ventricular function is the reduction in dia-stolic PFR but, unlike established hypertension, this index is still correlated with systolic function; (c) cardiac output might be even somewhat reduced and also negatively correlated with vascular resistance (‘afterload-dependent’ hearts); (d) furosemide (acute administration) might contribute to a better definition of hemodynamic behavior.

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Section: Discussionmentioning

confidence: 99%

Hemodynamics in Borderline Hypertension: Acute Effect of Furosemide

Franchi¹,

Pl²,

Scardi³

et al. 1984

Cardiology

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“…Similar or larger degrees of plasma volume reduction after diuresis have been described earlier. 8,35 Of particular interest in this study are the dynamic aspects of the plasma loss. As shown in table 8 the reduction of plasma volume takes place within the first 2 hr.…”

Section: Discussionmentioning

confidence: 99%

Dynamic Aspects of Volume and Osmoregulation in Congestive Heart Failure During Furosemide Diuresis

Olesen

1970

Angiology

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It is convenient to consider the regulation of extracellular fluid solute concentration and the control of extracellular fluid volume as relatively independent processes. Extracellular fluid solute concentration is regulated by alterations in the renal excretion of free water, and this in turn depends primarily upon changes in the secretion of antidiuretic hormone. Control of extracellular fluid volume depends upon the regulation of total extracellular solutes. Because of the great preponderance of sodium and its anions the problem resolves itself essentially to the control of body sodium which is regulated by adrenal, renal and other mechanisms not thus far elucidated. The distribution of extracellular water between plasma and interstitial fluid volume is determined by the balance between colloid osmotic and hydrostatic pressures in the intra-and extravascular phases. Control of intracellular solute concentration depends upon extracellular solute concentration as no osmotic gradient exists for most cells, and the control of intracellular fluid volume is closely related to the regulation of intracellular potassium content. These considerations are unified in the concept that the sum of osmotically active sodium and potassium is the major determinant of body water.1-5In patients with congestive heart failure a disturbance in volume regulation exists as indicated by the increase of intravascular and extracellular volumes, of total exchangeable sodium, total exchangeable chloride and body water.6, 7 Apparently, a retention of sodium is the primary event, and because the osmoregulation tends to adapt itself to the rise in solute content, a retention of water ensues.The objective of diuretic treatment is to remove the excess of body sodium and water, and clinical studies indicate that long-term treatment with diuretics is able to reduce plasma volume, extracellular water volume, body sodium and body water while serum sodium concentration is maintained at a normal level.8-11The alterations in body composition during diuretic treatment of congestive heart failure reflect the combined effects of the action of the drug on renal transport mechanisms and of the response of the patient in terms of homeostatic mechanisms involved in volume and osmoregulation. However, although the effects of diuretics on renal water and electrolyte excretion have been studied to a large extent, the homeostatic response to volume reduction caused by diuretics has received less attention.

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“…Thus, the rapid activation of compensatory volume-dependent Na and water retention during furosemide-induced volume contraction formed the basis for the hypothesis that neural mechanisms could be involved in the compensatory Na and water reabsorption during furosemide administration. In addition to its renal effects, substantial evidence suggests that furosemide has fast-acting extra-renal vasoactive actions which precede the diuretic effect and which are important for the therapeutic benefit of furosemide in the treatment of malignant hypertensive crisis and pulmonary edema (Davidov et al 1967;Dikshit et al 1967). However, little is known about the role of the sympathetic nervous system for these beneficial therapeutic actions.…”

Section: Introductionmentioning

confidence: 99%

Interactions Between Furosemide and the Renal Sympathetic Nerves

Petersen¹

1999

Pharmacology & Toxicology

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Antihypertensive Properties of Furosemide

Cited by 46 publications

References 10 publications

Hemodynamics in Borderline Hypertension: Acute Effect of Furosemide

Hemodynamics in Borderline Hypertension: Acute Effect of Furosemide

Dynamic Aspects of Volume and Osmoregulation in Congestive Heart Failure During Furosemide Diuresis

Interactions Between Furosemide and the Renal Sympathetic Nerves

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