Role of prostacyclin and nitric oxide in regulation of basal microvascularhydraulic permeability in cat skeletal muscle

The effects of prostacyclin, nitric oxide (NO) and beta(2)-receptor stimula tion on capillary filtration coefficient (CFC) and vascular tone were analy zed in an autoperfused cat skeletal muscle in vivo preparation, to evaluate if these substances are involved in regulation of basal microvascular hydr aulic permeability. CFC was increased from control (100%) to 124% with the prostacyclin-synthase inhibitor tranylcypromine and restored by simultaneou s infusion of prostacyclin at 0.1 ng.kg(-1).min(-1), with further reduction to 76% at 1 ng.kg(-1).min(-1). Prostacyclin at these doses did not influen ce vascular tone. NO inhibition by L-NAME increased CFC to 116% of control, with a vascular resistance increase of 45%. CFC was restored by simultaneo us infusion of the NO precursor L-arginine. L-arginine given alone reduced CFC to 86% of control. Tranylcypromine and L-NAME given together increased CFC to 141% of control and CFC was reduced to 86% by prostacyclin at 1 ng.k g(-1).min(-1) with no significant further reduction by adding L-arginine. A drenaline alone, in a vasodilating dose verifying beta(2) stimulation, or w hen followed by simultaneous beta-blockade with propranolol, did not influe nce CFC. We conclude that NO and especially prostacyclin are involved in bi -directional regulation of basal microvascular hydraulic permeability and c an account for up to 30-40% increase or decrease from a basal value. Physio logical beta(2) stimulation has no effect on basal hydraulic permeability. The permeability-reducing effects of prostacyclin and NO are additive. NO, but not prostacyclin, is involved in regulation of basal vascular tone.