Stress-induced increases in adrenaline further activate tonically presynaptic beta-adrenoceptors in renal arteries from prehypertensive rats of spontaneously hypertensive strain.

The effects of cumulatively applied doses (10(-8) M, 10(-7) M and 10(-6) M) of dl-carteolol, a nonselective beta-antagonist, on stimulation-evoked [3H] release at 5 Hz for 40 sec, were studied in renal arteries isolated from prehypertensive 4 weeks old spontaneously hypertensive rats unexposed and exposed to swimming stress for 1 hr, and then loaded with [3H]-noradrenaline. Carteolol, at 10(-8) M and 10(-7) M, produced no effect and at 10(-6) M it slightly inhibited the evoked [3H] release in the arteries from control spontaneously hypertensive rats. Carteolol, 10(-8) M to 10(-6) M, consistently inhibited the evoked [3H] release in renal arteries from spontaneously hypertensive rats exposed to stress and this inhibition differed from no effect, at 10(-8) M and 10(-7) M, and was greater than that at 10(-6) M in the arteries from control spontaneously hypertensive rats. Swimming stress increased the endogenous contents of adrenaline and dopamine in renal arteries without altering the level of noradrenaline. In conclusion, adrenaline appears to act as an endogenous agonist for tonically functioning presynaptic beta-adrenoceptors in renal arteries from prehypertensive young spontaneously hypertensive rats. Moreover, during and after a stressful situation, increased adrenaline appears to participate in further augmentation of vascular noradrenergic neurotransmission via further activation of these adrenoceptors to facilitate the release of noradrenaline.