Vasoconstriction of rat renal interlobar arteries by noradrenaline and neuropeptide Y

1. We have studied the contractile effects of noradrenaline and neuropeptide Y given alone and in combination on isolated rat renal interlobar arteries. 2. Noradrenaline contracted proximal and distal intrarenal microvessels in a concentration dependent manner, with similar potency (EC50 approximately equal to 550 nM), but maximal effects were greater in the proximal than in the distal vessel segments (approximately equal to 10 and 6 nM, respectively). 3. The noradrenaline-induced contraction was inhibited by low prazosin concentrations (3-10 nM) but not by 1 microM yohimbine indicating involvement of alpha(1)-but not alpha(2)-adrenoceptors. The alpha(1)A-adrenoceptor-selective antagonist, 5-methylurapidil and tamsulosin, had high potency (apparent affinities of approximately equal to 8 nM and 57 pM, respectively) while the alpha(1)D-adrenoceptor-selective antagonist, BMY 7378, had only low potency (apparent affinity approximately equal to 300 nM). The alpha(1)B-adrenoceptor-alkylating agent, chloroethylclonidine (10 microM for 30 min at 37 degrees C), had no inhibitory effects. The Ca2+ entry blocker, nitrendipine (300 nM), reduced the potency and maximal effects of noradrenaline. 4. Neuropeptide Y (1-100 nM) also contracted interlobar arteries in a concentration dependent manner, with greater effects in the proximal than in the distal segments, but maximal effects were only small in either segment (< 2 mN). In addition, neuropeptide Y also potentiated the response to noradrenaline, i.e. lowered its EC50 but this enhancement was also small. 5. We conclude that noradrenaline contracts rat interlobar arteries by an alpha(1)A-adrenoceptor; its co-transmitter, neuropeptide Y, affects the response only marginally in this vascular bed.