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Agostino Virdis, Fabio Monzani, Nadia Caraccio, Lorenzo Ghiadoni, Heloise Cardinal, Simona Buralli, Guido Salvetti, Stefano Taddei, Antonio Salvetti, P-106: Patients with subclinical hypothyroidism are characterized by endothelial dysfunction caused by an impairment in the L-arginine-nitric oxide pathway, American Journal of Hypertension, Volume 14, Issue S1, April 2001, Page 65A, https://doi.org/10.1016/S0895-7061(01)01657-0
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Abstract
In this study we evaluated whether patients with subclinical hypothyroidism are characterized by a reduced endothelium (END)-dependent vasodilation (VD) and whether this putative alteration is caused by a defect in the L-arginine-NO pathway. In n=12 healthy control women (C, age: 41.4±9.8 years; blood pressure (BP) 116.9±8.5 /79.±4.4 mmHg; TSH: 1.92±0.4 μU/ml; FT3: 3.62±0.7 pg/ml; FT4: 11.4±0.7 pg/ml) and n= 12 women with subclinical hypothyroidism (H, 40.8±9.4 years; 120.3±9.6/77.8±6.5 mmHg; TSH: 8.7±6.5* μU/ml; FT3: 3.8±2.3 pg/ml; FT4: 8.0±2 pg/ml; *p<0.05 vs C) we studied the forearm blood flow changes (FBF: strain-gauge venous plethysmography) induced by intra-arterial acetylcholine (ACH, 0.15, 0.45, 1.5, 4.5, 15 μg/100 ml/min), an END-dependent vasodilator, or sodium nitroprusside (SNP, 0.5, 1, 2 μg/100 ml/min), an END-independent vasodilator. ACH was repeated during NG-monomethyl-L-arginine (L-NMMA, 100 μg/100 ml/min), an NO-synthase inhibitor. Finally, the minimal forearm vascular resistances (MFVR), an integrated index of vascular structural changes, were also evaluated. VD to ACH was significantly (*p<0.05) reduced in H (FBF % increase above baseline: 15±16, 71±39, 146±47, 249±61*, 364±81*) as compared to C (FBF %: 12±6, 63±25, 225±32, 454±45, 639±56), while response to SNP was similar in the two groups (FBF %: H: 123±26, 258±42, 398±57; C: 109±19, 328±38, 546±64, p=N.S.). L-NMMA blunted (*p<0.05) VD to ACH in C (FBF %: 3±6, 31±11, 125±24*, 249±31*, 318±42*), while was ineffective in H (FBF %: 12±13, 46±37, 118±57, 201±64, 322±71;p=N.S). The MFVR values were similar in both groups (C: 2.0±0.2 SU; H: 2.2±0.3 SU; p=N.S.).
In conclusions, this study indicate that patients with subclinical hypothyroidism are characterized by endothelial dysfunction and this alteration is caused by an alteration in the L-Arginine-NO pathway.
