18 June 1999
Prostacyclin, Nitric oxide, Microvascular permeability, Hydraulic permeability, Capillary filtration coefficient, <italic>L</italic>-Arginine, L-NAME, Tranylcypromine, Beta-2-receptor stimulation, Cat skeletal muscle, Permeability regulation
The effects of prostacyclin, nitric oxide (NO) and β<sub>2</sub>-receptor stimulation on capillary filtration coefficient (CFC) and vascular tone were analyzed in an autoperfused cat skeletal muscle in vivo preparation, to evaluate if these substances are involved in regulation of basal microvascular hydraulic permeability. CFC was increased from control (100%) to 124% with the prostacyclin-synthase inhibitor tranylcypromine and restored by simultaneous infusion of prostacyclin at 0.1 ng·kg<sup>–1</sup>· min<sup>–1</sup>, with further reduction to 76% at 1 ng· kg<sup>–1</sup>·min<sup>–1</sup>. Prostacyclin at these doses did not influence vascular tone. NO inhibition by L-NAME increased CFC to 116% of control, with a vascular resistance increase of 45%. CFC was restored by simultaneous 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·kg<sup>–1</sup>·min<sup>–1</sup> with no significant further reduction by adding L-arginine. Adrenaline alone, in a vasodilating dose verifying β<sub>2</sub> stimulation, or when followed by simultaneous β-blockade with propranolol, did not influence CFC. We conclude that NO and especially prostacyclin are involved in bi-directional regulation of basal microvascular hydraulic permeability and can account for up to 30–40% increase or decrease from a basal value. Physiological β<sub>2</sub> 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.