Lack of an effect of atrial natriuretic peptide on myogenic contraction of microvascular smooth muscle.

In previous studies we demonstrated that constriction of cremaster microvessels by occupation of alpha 1- but not alpha 2-adrenoceptors is inhibited by atrial natriuretic factor (ANF) at physiological concentrations (10(-11) to 10(-9) M). The present study examined the effect of ANF on "myogenic" constriction of arterioles induced by elevation of intravascular pressure. The cremaster skeletal muscle of anesthetized rats was denervated and extended with intact circulation into a tissue bath. Intravital microscopy was used to measure diameters of first- and second-order arterioles (80-150 microns diam). In group 1, propranolol and phentolamine (both at 10(-6) M) were added to the cremaster bath to block beta- and alpha-adrenoceptors, respectively. Norepinephrine was infused (3.51 micrograms.kg-1.min-1 iv) to raise arterial pressure by 30-35 mmHg. This induced a 30 +/- 3% (means +/- SE) decrease in arteriolar diameter (myogenic constriction). Thereafter, cumulative addition of ANF (10(-11) to 10(-7) M) to the tissue bath had no effect on microvessel diameter, except at the highest concentration wherein the myogenic constriction was reduced by approximately 40%. In a second study the rat's body, excluding the cremaster, was enclosed in an airtight Plexiglas box. Cremaster intravascular pressure was increased by elevating box (ambient) pressure by 10 and 20 mmHg, which caused arteriolar diameter to decrease to 81 +/- 5 and 73 +/- 8% control diameter, respectively, in the absence, and similar amounts 72 +/- 4 and 69 +/- 5%, in the presence of 10(-8) M ANF.(ABSTRACT TRUNCATED AT 250 WORDS)