Desynchronized sleep (DS) in the cat is accompanied by a long-lasting (tonic) constriction of muscle blood vessels (conductance decrease 5-30%), on which are superimposed short-lasting (phasic) vasoconstrictor waves that occur simultaneously with bursts of rapid eye movements and body twitches. Both the tonic and the phasic vasoconstrictions are abolished after regional sympathectomy (conductance increase 5-10%). Tonic vasoconstriction can also be prevented by hind-limb deafferentation (bilateral section of the dorsal roots from L5 down) or by transection of the spinal cord at L4 in such a way as to separate sympathetic innervation from afferent input from the hind limbs. These procedures do not affect the phasic vasoconstrictions. After lumbar sympathectomy or hind-limb deafferentation, iliac blood flow decreases during the tonic fall in blood pressure associated with DS by exactly the amount (1-2 ml/min) predicted by pressureflow relationships observed during artificial lowering of iliac blood pressure. We conclude that tonic and phasic vasoconstrictions are both due to sympathetic discharges. However, phasic sympathetic discharges are driven by central descending influences, and tonic sympathetic vasoconstriction depends on reflex influences originating from the limbs themselves. When tonic sympathetic vasoconstriction is prevented, muscle blood vessels exhibit autoregulatory behavior during DS. KEY WORDS hind-limb deafferentation spinal vasomotor reflexes muscle afferent fibers tonic and phasic vasoconstriction iliac blood flow autoregulation

1. Urinary kallikrein excreted by normal rats is significantly increased (P <0.001) 2 h after: (a) water loading, (b) water loading plus frusemide, 0.27 mmol (10 mg) per rat, (c) salt loading. In water-loaded rats, 5 i.u. of renin strikingly reduced kallikrein excretion (P < 0.01) but considerably increased sodium excretion (P150 mmHg) showed no increase of urinary kallikrein after water loading, although there was a marked natriuresis; in moderately hypertensive rats (blood pressure < 150 mmHg) urinary kallikrein was only one-third of that observed in control normotensive rats, after an equal degree of water loading.

SUMMARY Prerious studies have suggested that angiotensin II and sodium can act as alternative mechanisms in maintaining high blood pressure in chronic renovascular hypertension. In the present study, exchangeable sodium was measured in rats in which angiotensin II had been confirmed or excluded as the main cause of the hypertension. To determine the degree of participation of angiotensin II in the maintenance of the high blood pressure, we studied the mean blood pressure response to an angiotensin antagonist (l-Sar-8-Alaangiotensin II) and to a converting enzyme inhibitor (SQ20.881). Rats with a decrease hi blood pressure of less than 20 mm Hg, in response to both inhibitors, were classified as nonresponders; those with a decrease of 20 mm Hg or more, as responders. Fifty percent of the rats with two-kidney hypertension were nonrespooders, and they had lower blood pressure and plasma renin activity than the responders. Further, these two-kidney, hypertensive, nonresponder rats had normal exchangeable sodium. The two-kidney hypertensive responders, on the other hand, had significantly higher exchangeable sodium than both the two-kidney, hypertensive nonresponders and the two-kidney control rats. These results suggest that angiotensin II and exchangeable sodium do not play a major role in the maintenance of the high Mood pressure in the two-kidney hypertensive nonresponders. However, there appears to be an abnormal relationship between renin and exchangeable sodium in the two-kidney hypertensive responders that could contribute to the maintenance of the hypertension. differing roles in the pathogenesis of the maintenance of high blood pressure in oneas compared to two-kidney hypertensive rats (one renal artery constricted and the contralateral kidney removed or untouched, respectively). In one-kidney hypertensive rats, sodium retention appears to be the main pathogenetic factor in the chronic phase of the hypertension. In fact, Tobian et al. 1 have reported an increase in exchangeable sodium, and Swales et al. model of hypertension in rats. In the two-kidney model, angiotensin has been considered the most important pathogenetic factor.3 However, in previous work, we have found that in rats with moderate, chronic, two-kidney hypertension, the maintenance of high blood pressure does not always depend on the pressor effect of angiotensin II, since many rats do not respond to the administration of an angiotensin antagonist* or a converting enzyme inhibitor (CEI) with a decrease in blood pressure.8 Furthermore, MShring et al. 8 have reported a positive cumulative sodium balance and a positive correlation between the increase in blood pressure and sodium retention in rats with moderate two-kidney hypertension.It could be that the high blood pressure in the twokidney model is maintained by a dual mechanism: one related to sodium metabolism when the hypertension is moderate, and the other to the renin-angiotensin system when the hypertension is more severe. To further advance this hypothesis, in the present study we measu...

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