Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 293, Issue 4, Pages H2161-H2167Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00600.2007
Keywords
lasers; autonomic nervous system
Funding
- NHLBI NIH HHS [R01 HL087803, R01 HL074873, 5R01-HL-74873] Funding Source: Medline
- NIDDK NIH HHS [1R21-DK-071647, R21 DK071647] Funding Source: Medline
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Low flow postural tachycardia syndrome (POTS), is associated with reduced nitric oxide (NO) activity assumed to be of endothelial origin. We tested the hypothesis that cutaneous microvascular neuronal NO (nNO) is impaired, rather than endothelial NO (eNO), in POTS. We performed three sets of experiments on subjects aged 22.5 +/- 2 yr. We used laser-Doppler flowmetry response to sequentially increase acetylcholine (ACh) doses and the local cutaneous heating response of the calf as bioassays for NO. During local heating we showed that when the selective neuronal nNO synthase (nNOS) inhibitor N-omega-nitro-L-arginine-2,4-L-diaminobutyric amide (N-omega, 10 mM) was delivered by intradermal microdialysis, cutaneous vascular conductance (CVC) decreased by an amount equivalent to the largest reduction produced by the nonselective NO synthase (NOS) inhibitor nitro-L-arginine (NLA, 10 mM). We demonstrated that the response to ACh was minimally attenuated by nNOS blockade using N-omega but markedly attenuated by NLA, indicating that eNO largely comprises the receptor-mediated NO release by ACh. We further demonstrated that the ACh dose response was minimally reduced, whereas local heat-mediated NO-dependent responses were markedly reduced in POTS compared with control subjects. This is consistent with intact endothelial function and reduced NO of neuronal origin in POTS. The local heating response was highly attenuated in POTS [60 +/- 6 percent maximum CVC(%CVCmax)] compared with control (90 +/- 4 %CVCmax), but the plateau response decreased to the same level with nNOS inhibition (50 +/- 3 %CVCmax in POTS compared with 47 +/- 2 %CVCmax), indicating reduced nNO bioavailability in POTS patients. The data suggest that nNO activity but not NO of endothelial NOS origin is reduced in low-flow POTS.
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