Influence of nitric oxide on vascular resistance and muscle mechanics during tetanic contractions in situ

Abstract

Studies of the effect of nitric oxide (NO) synthesis inhibition were performed in the isometrically contracting blood-perfused canine gastrocnemius-plantaris muscle group. Muscle blood flow (Q˙) was controlled with a pump during continuous NO blockade produced with either 1 mMl-argininosuccinic acid (l-ArgSA) or N G-nitro-l-arginine methyl ester (l-NAME) during repetitive tetanic contractions (50-Hz trains, 200-ms duration, 1/s). PumpQ˙ was set to match maximal spontaneousQ˙ (1.3–1.4 ml ⋅ min−1 ⋅ g−1) measured in prior, brief (3–5 min) control contraction trials in each muscle. Active tension and oxygen uptake were 500–600 g/g and 200–230 μl ⋅ min−1 ⋅ g−1, respectively, under these conditions. Within 3 min ofl-ArgSA infusion, vascular resistance across the muscle (Rv) increased significantly (from ∼100 to 300 peripheral resistance units; P < 0.05), whereas Rv increased to a lesser extent with l-NAME (from ∼100 to 175 peripheral resistance units; P < 0.05). The increase in Rv withl-ArgSA was unchanged by simultaneous infusion of 0.5–10 mMl-arginine but was reduced with 1–3 μg/ml sodium nitroprusside (41–54%). The increase in Rv withl-NAME was reversed with 1 mM ofl-arginine. Increased fatigue occurred with infusion ofl-ArgSA; active tension and intramuscular pressure decreased by 62 and 66%, whereas passive tension and baseline intramuscular pressure increased by 80 and 30%, respectively. These data indicate a possible role for NO in the control of Rv and contractility within the canine gastrocnemius-plantaris muscle during repetitive tetanic contractions.