Increase in osmolality of venous blood from skeletal muscle during cholinergic vasodilatation.

The arterio-venous difference in the osmolality of blood plasma of cat m. triceps surae was studied during sympathetic cholinergic nerve excitation. The vasodilatation was induced by stimulation of hypothalamus or the sympathetic chain, the latter after alpha-adrenoceptor blockade. The vasodilator effect induced by intraarterial injection of acetylcholine was also tested. In all cases studied the vasodilatation was associated with an increase in osmolality (on the average by 10 mOsm/kg H2O with a maximum at the 30-40th s after the beginning of stimulation). Atropine (0.1 mg/kg) considerably decreased the vasodilator effect elicited by hypothalamic stimulation. The increase in osmolality was much smaller after atropine, a small peak remaining at the 50-60th s after the beginning of stimulation. The latter effect was blocked by propranolol (0.5 mg/kg). Atropine similarly almost completely abolished the vasodilator effect and the increase in osmolality produced by lumbar sympathetic stimulation and acetylcholine. The increase in osmolality was caused by a rise in the contents of Na+ (7.4%), lactate (8.2%) and K+ (13.2%); Ca2+, inorganic phosphate and total protein concentrations remained unchanged. Our data indicate that acetylcholine released by sympathetic endings activates muscle fibre metabolism via the muscarin-receptors. The increase in tissue osmolality resulting from activation of metabolism causes, at least partly, the vasodilator effect.