The distribution of renal cortical blood flow was studied in seven Nembutal anesthetized dogs in control periods, during hemorrhagic hypotension and after retransfusion. Local cortical blood flow was measured as hydrogen clearance recorded simultaneously from 3 to 6 platinum electrodes inserted into inner and outer half of the cortex. Total renal blood flow (RBF) was measured by electromagnetic flowmeter. In control periods flow averaged 3.47 ± 0.83 ml/min×g in outer cortex and 3.61 ± 0.86 ml/min × g in inner cortex. Bleeding to mean arterial pressure of 50 mm Hg in the course of 5–36 min in 5 expts. caused a proportional reduction of RBF and average flow in outer and inner cortex to 40–60 % of control, with further reduction to 10–30 % with maintenance of hypotension for 2 h. Bleeding to 70 mm Hg in 2 expts. gave princpially the same response. All electrodes showed a similar response and the percentual deviation between electrodes did not increase during hypotension. Thus no evidence was obtained for patchy or segmental ischemia or for regional redistribution of cortical blood flow. Retransfusion gave only incomplete restoration of flow.

K I I I . I-. .. J . K J E K~W -~ and E. L~~Y S I N G . K c i i d n~rtor~~grtlntion duritig infusion of ~O T -i r i i i t jioliric. n,igiott,rtsiii nrid nccty/c/io/itir. -Acts phyhiol. scand. 1969. 76. 10-1 .i .l'o t,\aiiliiie \vlirtlier i.elral aiitoreg~ila~iori was almlislied by \-asoconstriction and vasodilatation, t ' \ p ( ' i iniriit* \\ere pcrlol-iried on anesthetized dogs tvith intact renal rirc.iilation arid nervous S l l l J [ > l > . ~\iieioterisin oi' noradrenaline \vas infused into the I-erial artcry at a constant rate that I -C~U C (d iriial Iilood ilotv lKBF to less than half of control \ a l u m By riiec.hanical constriction ol tlic I t w a l artery. perfusion pressure could be reduced to averages of 69 and SO mm I-ig >ct,ti\e!>. 1 i 4 nini 135 during control conditions), before KBF dropped more than 5 % . Lo1 mrii ;iutoicgiilatiori \\as also obtained dui-ing intravenous infusion of angiotensin and nor-.icli-c.~i:iIiiic~. during stirnrilatioii of renal nerves, and after development of tachyphylaxis to 11. .It Irornial a r i d low arterial pressures. Init at similar RBF, noradrenaline or angiotcil.;iii irijrcted into tlie renal artery. RBF \vas least reduced a t low perfusion pressure, iiiclicatirie that autoregiilatiori did not cornpensate for the vasoconstrictive effect of noradrenalirir arid aiiqioterisiri. By acetylcholine infiision. KBF could be doubled, and a curviliriear relalioiidiip l)et\\ eel1 KBF arid perfusion pressure was obtained. Similar curves could I x constructed h y tlic ;tpplication of Poiseuille's law on the premise that vaqoacti\-e agents act mairily on 1 1 1~b c [v c!crrients othey than those participating in autoregulation. I t is coricliicled that autontially inclcpcndent of iiervnus and humoral stimuli.Rciial I~lcod flow I KBF I and glornerular filtration rate (GFR) remain constant when w11a1 pvrfrision pressure is lowered to 70-80 rnni Hg by mechanical constriction of thc. rcnal artery or aorta above the renal artery. Autoregulating mechanisms which tiilatc the afferent arterioles are then maximally activated, and the resistance in the prcglonicwilar vessel probab1)-remains tinchanged when perfusion pressure is further ~d u c c d .U'hether nervous and humoral stimuli interfere with renal autoregulation in the i n t a c~ organisiii has not yet hcen established. and it is accordingly undecided \dwtlicr rcrial autorcgrilation is of any significance in circulatory homeostasis. PI-?\ iom studies of the effects of 1,asoactit.e agents on rerial autoregulation have