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 approximate to 550 nM), but maximum effects were greater in the proximal than in the distal vessel segments (approximate to 10 and 6 mN, respectively). 3 The noradrenaline-induced contraction was inhibited by low prazosin concentrations (3-10 nM) but not by 1 mu M yohimbine indicating involvement of alpha(1)- but not alpha(2)-adrenoceptors. The alpha(1A)- adrenoceptor-selective antagonists, 5-methylurapidil and tamsulosin, had high potency (apparent affinities of approximate to 8 nM and 57 pM, respectively) while the alpha(1D)-adrenoceptor-selective antagonist, BMY 7378, had only low potency (apparent affinity approximate to 300 nM). The alpha(1B)-adrenoceptor-alkylating agent, chloroethylclonidine (10 mu M 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(1A)-adrenoceptor; its cotransmitter, neuropeptide Y, affects the response only marginally in this vascular bed.