Effects of adrenoceptor agonists and antagonists on smooth muscle cells and neuromuscular transmission in the guinea-pig renal artery and vein.

In the guinea-pig renal artery and vein, the membrane potential was -66.8 mV and -46.8 mV, the length constant 0.54 mm and 0.43 mm, and the time constant 240 ms and 98 ms, respectively. The maximum slope of the depolarization produced by a 10 fold increase [K]o was 46 mV in the renal artery and 39 mV in the renal vein. Noradrenaline (NA over 5 X 10(-7)M in the artery and over 10(-7)M in the vein) depolarized the membrane and slightly reduced the membrane resistance, assessed from relative changes in the amplitude of electrotonic potential. The action of NA was suppressed by prazosin in the artery but by yohimbine in the vein, i.e. the alpha 1-adrenoceptor is present in the extrajunctional muscle membrane in the renal artery while the alpha 2-adrenoceptor is present in the renal vein. Dopamine and isoprenaline did not modify the membrane properties. In the renal artery, repetitive perivascular nerve stimulation (0.1 ms, 50 Hz, 5 shocks) evoked excitatory junction potential (e.j.p.). Applications of guanethidine (10(-6) M) or tetrodotoxin (3 X 10(-7) M) abolished the generation of the e.j.p.. Low concentrations of phentolamine (5 X 10(-7) M), prazosin (10(-7) M) and yohimbine (5 X 10(-7) M) enhanced the e.j.p. amplitude, while high concentrations of phentolamine (10(-5) M) and prazosin (greater than 10(-5) M) reduced the amplitude of e.j.p.s. NA, dopamine and clonidine consistently suppressed the amplitude of e.j.ps, at any given concentration over 10(-7) M. Spontaneous generated miniature e.j.ps (m.e.j.ps) were recorded on rare occasions. Phentolamine and yohimbine both at 5 x 10(-7) M and prazosin 10(-7) M increased the appearance of m.e.j.ps. 5 In the renal vein, repetitive nerve stimulation failed to generate the e.j.p. Sympathetic innervation to this tissue seems to be sparse. 6 Specificity of innervation and adrenoceptors present on smooth muscle cells in both the renal artery and vein are discussed, and the presynaptic regulation ofNA release is compared with findings in other vascular tissues.