Amlodipine but Not Valsartan Increases Muscle Sympathetic Activity in Hypertensive Subjects

Dodt, Christoph; Struck, J.; Muck, Philip; Trübger, D.; Handrock, Renate; Weidinger, Gottfried; Fehm, Horst L.

doi:10.1097/00004872-200006001-00479

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“…Dodt et al [32] recently reported that in 18 hypertensive patients, amlodipine (5 mg/d) and the AT 1 receptor blocker valsartan (each for 7 days) decreased the BP to a similar extent, but muscle sympathetic nerve activity increased from 27.9 ± 2.4 bursts/ minute on placebo to 37.0 ± 2.5 bursts/minute on amlodipine (P < 0.05), and showed a minor (not significant) increase to 32.1 ± 3.0 on valsartan [32]. Similarly, in 10 hypertensive patients with chronic renal failure, treatment for 4 to 6 weeks with amlodipine (10 mg/d) decreased BP from 165 ± 10/94 ± 6 mm Hg to 143 ± 14/83 ± 8 mm Hg (P < 0.001), but increased muscle sympathetic nerve activity from 41 ± 19 bursts/minute to 56 ± 14 bursts/minute (P = 0.02) [33•].…”

Section: Dihydropyridines and Sympathetic Activity In Humans: Evidencmentioning

confidence: 99%

Central sympathoinhibitory effects of calcium channel blockers

Leenen

Ruzicka

Huang

2001

Current Science Inc

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It is generally assumed that the arterial vasodilation induced by inhibition of Ca(2+) influx into vascular smooth muscle cells represents the main mechanism for the hypotensive effect of dihydropyridine calcium channel blockers. Increases in sympathetic tone have been related to activation of the arterial baroreflex by rapid lowering of blood pressure. This review highlights new findings in two areas. First, in animal studies, direct central administration of dihydropyridines such as nifedipine or amlodipine lowers sympathetic nerve activity and thereby blood pressure. Peripheral administration of nifedipine or amlodipine at low rates appears to result in gradual accumulation of drug in the central nervous system, and also causes lowering of sympathetic nerve activity and thereby lowering of blood pressure (rather than by arterial vasodilation). Second, in hypertensive humans treated with long-acting dihydropyridines and presumably little activation of the arterial baroreflex, some studies have demonstrated lowering of sympathetic activity (as assessed by plasma norepinephrine), but others reported increases (as assessed by plasma norepinephrine or microneurography). This sympathoexcitatory response may be due to activation of the renin-angiotensin system, particularly at higher doses.

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Section: Dihydropyridines and Sympathetic Activity In Humans: Evidencmentioning

confidence: 99%