Cell calcium concentration in glomerular afferent and efferent arterioles under the action of noradrenaline and angiotensin II.

The glomerular arterioles in the juxtaglomerular apparatus seem to function as effectors of the tubuloglomerular feedback mechanism. In this mechanism increased delivery of fluid to the distal nephron activates the macula densa cells through transport via an Na-2Cl-K cotransporter. This activation may lead to vasoconstriction of the afferent arteriole. Furthermore, vasoactive substances seem to affect both afferent and efferent arterioles. There are morphological differences along the afferent arteriole, some parts containing epithelioid cells with renin granules and others regular smooth muscle cells. The aim of the present experiments was to determine whether noradrenaline (10(-6) M) and angiotensin II (10(-6) M) had differential effects on the cell calcium concentration [Ca2+]i and on contraction in isolated perfused afferent and efferent arterioles and in the mesangial region. [Ca2+]i was measured with fura-2, an intensified videocamera and a digital imaging system. From the proximal to the distal part of the arteriole [Ca2+]i increased from about 100 to 250 nM. A [Ca2+]i increase and a contraction were caused by noradrenaline alone in the proximal part of the afferent arteriole and by angiotensin II alone in the distal part of this arteriole. In the mesangial region there was a high basal [Ca2+]i but no response to the vasoactive substances. In the efferent arteriole, application of both noradrenaline and angiotensin II led to an increase in [Ca2+]i and a contraction. The present experiments indicate that the two vasoactive substances tested act in a similar fashion along the whole length of the efferent arteriole, while in the afferent arteriole their actions are not equally distributed.