Effects of labetalol and methyldopa on renal function

Cruz, F.; OʼNeill, William M.; Clifton, Gil; Wallin, J. D.

doi:10.1038/clpt.1981.127

Cited by 20 publications

(5 citation statements)

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“…In general, the chronic use of propranolol for the management of hypertension is associated with 10%-20% decrements in RBF and GFR [21][22][23]. In contrast, labetalol, a [3-blocker with (z-blocking activity, spares renal haemodynamics [25,26]. Against this background, we found it of interest to study the effects of carvedilol on renal haemodynamics.…”

Section: Discussionmentioning

confidence: 94%

Effects of carvedilol on renal function

Dupont

1990

Eur J Clin Pharmacol

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A randomized, double-blind, placebo-controlled study was conducted to study the effects of acute and chronic administration of carvedilol in essential hypertension, with special emphasis on renal haemodynamics and function. Acute administration of a single dose of 50 mg carvedilol reduced systolic and diastolic blood pressure without inducing reflex tachycardia. Renal blood flow was preserved; accordingly, renal vascular resistance was significantly reduced. A significant reduction in the glomerular filtration rate and filtration fraction was observed. Plasma renin activity (PRA) and plasma aldosterone values were not changed. Chronic carvedilol treatment produced a significant fall in systolic and diastolic blood pressure, heart rate, PRA and plasma aldosterone. Renal blood flow, glomerular filtration rate and filtration fraction also remained unchanged; renal vascular resistance decreased significantly. It is concluded that carvedilol possesses definite antihypertensive and renal vasodilating properties, both acutely and after chronic treatment.

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Section: Discussionmentioning

confidence: 94%

Effects of carvedilol on renal function

Dupont

1990

Eur J Clin Pharmacol

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“…hemodynamic properties of several b-blockers that have been used to lower blood pressure in hypertensive patients with diabetic and nondiabetic renal impairment. [32][33][34][35][36][37][38][39][40][41][42] Lipophilic agents undergo extensive first-pass hepatic metabolism with relatively little being excreted unchanged in the urine. Hydrophilic agents are excreted primarily by the kidneys and require dose adjustment in patients with end-stage renal disease (ESRD).…”

Section: Pharmacologic Properties Of B-blockersmentioning

confidence: 99%

“…Presynaptic b 2 -receptors further augment the release of NE at synaptic junctions. Postsynaptic sympathetic neurons innervate the muscular layer of Sources: [32][33][34][35][36][37][38][39][40][41][42] resistance vessels controlling systemic and local circulations. NE stimulation of a 1 -adrenergic receptors in vascular smooth muscle results in an increase in renal as well as peripheral vascular resistance.…”

Section: Effects On Kidney Functionmentioning

confidence: 99%

“…84 By contrast, in 18 patients with essential hypertension labetalol diminished RBF and GFR by 20% 85 Two studies in patients with normal renal function, one including 17 patients and the other including 11 patients, found no significant effect of labetalol on GFR, RBF, or body fluid volumes. 36,86 The effects of labetalol on carbohydrate and lipid metabolism have also been evaluated in small studies. Labetalol administration resulted in a variable increase in serum glucose levels without a measurable effect on circulating insulin levels.…”

Section: Vasodilating B-blockersmentioning

confidence: 99%

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Beta blockers in the management of chronic kidney disease

Bakris

Hart

Ritz

2006

Kidney International

175

113

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The sympathetic nervous system modulates renal function through its receptors namely beta1 (cardiac output and renin release), alpha1 (systemic and renovascular constriction), and beta2 renovascular dilation. Sympathetic overactivity is commonly seen in chronic kidney disease (CKD) and is an important contributor to increasing the risk of cardiovascular events as well as increasing renal disease progression. Recent evaluations of drug use in people with CKD shows a remarkably low percentage of patients receiving beta-blockers, especially in more advanced stage CKD when cardiovascular risk is higher. This is in large part due to tolerability of these agents. Moreover, water-soluble beta-blockers such as atenolol and metoprolol are dialyzable and require supplementation to avoid exacerbation of arrhythmias following dialysis. Newer vasodilating beta-blockers have better tolerability and different effects on renal hemodynamics as well as metabolic variables. These effects are related to the relative alpha1-blocking effect of agents such as carvedilol and labetolol, with carvedilol having relatively greater alpha-blocking effects. Few studies evaluate beta-blockers on cardiovascular risk in CKD patients. Studies with carvedilol demonstrate attenuated increases in albuminuria as well as reduction in cardiovascular events in CKD patients with hypertension. This paper reviews the animal and clinical trial data that evaluate beta-blockers in CKD highlighting the vasodilating beta-blockers. It is apparent that greater use of this drug class for blood pressure control would further enhance reduction of risk of heart failure, the most common cause of death in the first year of starting dialysis.

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“…Grabie et al (23) and Cruz et al (24) reported studies assessing the effects of a-methyl dopa on renal hemodynamics in patients with normal baseline GFR. They both found a preservation of RPF, but with a reduction in GFR and filtration fraction (FF).…”

Section: Drugs Interacfing With A-adrenergic Receptorsmentioning

confidence: 99%

Antiadrenergic Antihypertensive Drugs: Their Effect on Renal Function

Bernstein¹,

O’Connor²

1984

Annu. Rev. Pharmacol. Toxicol.

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Peripheral alpha antagonists not only preserve renal hemodynamics, but decrease RVR and maintain renal perfusion autoregulation in the face of decreased systemic perfusion pressures. On the other hand, central alpha agonists appear to have variable effects. Clonidine preserves RBF and GFR both acutely and chronically, guanabenz decreases RBF acutely but not chronically, and alpha-methyl dopa preserved RBF but decreases GFR. Beta blockers also have variable effects on RBF: the most-often-studied beta blocker, propranolol, has reduced RBF by 10-20% while other commonly used beta blockers, such as nadolol and metoprolol, may preserve RBF. This may reflect propranolol's inability to maintain renal perfusion autoregulation in the face of decreased systemic blood pressure. This failure of propranolol is not completely understood but may be a function of its lack of cardioselectivity or ISA (49). It is also possible that inhibition of renal vasodilators such as the kallikrein-kinin system plays a role (49). Finally, it appears that patients with normal renal vascular tone may be at highest risk to suffer decrements in RBF with beta blockers. Perhaps most importantly, the clinical impact of propranolol's effect on renal function is unclear, since the reductions in GFR have not been sufficient to produce azotemia.

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Effects of labetalol and methyldopa on renal function

Cited by 20 publications

References 0 publications

Effects of carvedilol on renal function

Effects of carvedilol on renal function

Beta blockers in the management of chronic kidney disease

Antiadrenergic Antihypertensive Drugs: Their Effect on Renal Function

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