A comparison of the haemodynamic and behavioural effects of moxonidine and clonidine in normotensive subjects.

Macphee, G. J. A.; Howie, Catherine A.; Elliott, Henry L.; Reid, JL

doi:10.1111/j.1365-2125.1992.tb04033.x

Cited by 32 publications

(12 citation statements)

References 27 publications

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“…The newer I 1 -imidazoline agonist moxonidine also leads to peripheral sympatho-inhibition but with less adverse reactions (189). However, information regarding its effect on MSNA is limited.…”

Section: Strategies To Combat Sympathetic Hyperactivitymentioning

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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Section: Strategies To Combat Sympathetic Hyperactivitymentioning

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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“…Clonidine is twice as potent as moxonidine at the I1 receptor but has a similar affinity for alpha-2 and I receptors. Moxonidine acts by decreasing systemic vascular resistance secondary to a reduction in central sympathetic tone, reducing plasma catecholamine and renin levels [51]. Moxonidine may also increase sodium and water excretion.…”

Section: Moxonidinementioning

confidence: 99%

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

Khan¹,

Ferguson²,

Jones³

1999

Anaesthesia

606

423

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SummaryClonidine has proved to be a clinically useful adjunct in clinical anaesthetic practice as well as in chronic pain therapy because it has both anaesthetic and analgesic-sparing activity. The more selective alpha-2 adrenoceptor agonists, dexmedetomidine and mivazerol, may also have a role in providing haemodynamic stability in patients who are at risk of peri-operative ischaemia. The side-effects of hypotension and bradycardia have limited the routine use of alpha-2 adrenoceptor agonists. Investigations into the molecular pharmacology of alpha-2 adrenoceptors have elucidated their role in the control of wakefulness, blood pressure and antinociception. We discuss the pharmacology of alpha-2 adrenoceptors and their therapeutic role in this review.

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“…4,5 Stimulation of imidazoline receptors seems to induce effects similar to those induced by stimulation of central ␣ 2 -adrenoreceptors; however, the pattern of adverse reactions seems to be more favorable. 6,7 The newly developed central antihypertensives, ie, moxonidine and rilmenidine, act mainly on imidazoline-1 receptors and less so on central ␣ 2 -adrenoreceptors in an agonistic fashion. 4,8,9 Indeed, affinity of moxonidine and rilmenidine for imidazoline-1 receptors is higher than that of clonidine; in contrast, other centrally acting antihypertensives, ie, ␣-methyldopa, guanfacine, or guanabenz, act mainly on central ␣ 2 -receptors.…”

mentioning

confidence: 99%

I ₁ -Imidazoline Agonist Moxonidine Decreases Sympathetic Nerve Activity and Blood Pressure in Hypertensives

Wenzel

Spieker

et al. 1998

Hypertension

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Abstract-Moxonidine is an I 1 -imidazoline receptor agonist that reduces blood pressure in hypertensives. Experimental data suggest that moxonidine inhibits central sympathetic activity. However, whether such a mechanism is involved in vivo in humans is still unclear. We investigated the effects of 0.4 mg moxonidine orally on muscle sympathetic nerve activity and heart rate in an open study in 8 healthy volunteers. Furthermore, we studied the effects of 0.4 mg moxonidine on muscle sympathetic nerve activity, heart rate, blood pressure, 24-hour blood pressure profile, and hormone plasma levels in 25 untreated hypertensives in a double-blind, placebo-controlled study. Moxonidine decreased muscle sympathetic nerve activity in both healthy volunteers (PϽ0.05 versus baseline) and hypertensives (PϽ0.02 versus placebo). Plasma norepinephrine also decreased (PϽ0.01), whereas plasma epinephrine and renin levels did not change (PϭNS). Furthermore, moxonidine decreased systolic (PϽ0.0001) and diastolic (PϽ0.001) blood pressure. Heart rate decreased after moxonidine in healthy subjects (PϽ0.05); in hypertensives, heart rate decreased during the night hours (PϽ0.05) but not during daytime (PϭNS). Plasma levels of LDL, HDL, and total cholesterol were not influenced by the drug (PϭNS). Moxonidine decreases systolic and diastolic blood pressure by inhibiting central nervous sympathetic activity. This makes this new drug suitable for the treatment of human hypertension and possibly for other cardiovascular diseases with increased sympathetic nerve activity, ie, ischemic heart disease and heart failure.

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A comparison of the haemodynamic and behavioural effects of moxonidine and clonidine in normotensive subjects.

Cited by 32 publications

References 27 publications

Sympathetic Hyperactivity in Chronic Renal Failure

Sympathetic Hyperactivity in Chronic Renal Failure

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

I ₁ -Imidazoline Agonist Moxonidine Decreases Sympathetic Nerve Activity and Blood Pressure in Hypertensives

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A comparison of the haemodynamic and behavioural effects of moxonidine and clonidine in normotensive subjects.

Cited by 32 publications

References 27 publications

Sympathetic Hyperactivity in Chronic Renal Failure

Sympathetic Hyperactivity in Chronic Renal Failure

Alpha‐2 and imidazoline receptor agonistsTheir pharmacology and therapeutic role

I 1 -Imidazoline Agonist Moxonidine Decreases Sympathetic Nerve Activity and Blood Pressure in Hypertensives

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Product

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I ₁ -Imidazoline Agonist Moxonidine Decreases Sympathetic Nerve Activity and Blood Pressure in Hypertensives