There is evidence of increased oxidative stress and acute-phase inflammation in patients with stage 3-5 chronic kidney disease compared to healthy subjects that does not closely correlate with estimates of GFR. Among CKD patients, inflammatory biomarkers correlate with known CVD and inversely correlate with the use of angiotensin II inhibitors and statins. A further increase in oxidative stress was noted in diabetic and hypercholesterolemic patients. Inflammation and oxidative stress may contribute to cardiovascular risk in CKD patients.

Impulse activity in vagal afferent fibres and changes in heart rate were simultaneously recorded during rapid hemorrhage or blood pooling in cats in order to elucidate whether the sudden reflex bradycardia, sometimes evoked with the mentioned interventions, was correlated to an increased activity in any type of heart receptors. The results show that the slowing of the heart, resulting from an emptying of the central blood reservoirs was correlated to, and preceded by, an increased activity in receptors located in the left ventricle and signalling in non‐medullated afferents. The receptors were found to be activated also by obstructions of the ascending aorta and mechanical stimulation of the heart, and therefore seem to operate as mechanorecepton, stimulated by a “distortion” of the myocardium. ‐ It is conceivable that with rapid bleeding or pooling of blood, the receptors are excited by an improper squeezing of the myocardium when the ventricles contract vigorously around an almost empty chamber, and then induce a reflex bradycardia. This reflex mechanism, resembling the so‐called vaso‐vagal syncope reaction in man, may therefore serve as a protective system causing a break on the heart and allowing for an improved diastolic filling in situations when venous return is critically reduced.

MELLANDER, S., B. BERG and H. O n E L u M . Vascular adjustments to increased transmural pressure in cat and man with special reference to shifts in capillaiyjfuid transfer. Acta physiol. scand. 1964. 61. 34-48. -When a vascular bed is exposed to an increased transmural pressure, as occurs in the lower extremities in man on standing, adjustments of the vascular tone take place which tend to protect the organism against excessive transcapillary loss of circulating fluid into the extravascular space. Thus, first, by closure of a number of the precapillary sphincter vessels, the size of the capillary surface

The vasoconstrictor fibre influence on veins, exposed to varying distending pressures, was analysed with respect to the relative contribution of active venoconstruction and passive venous recoil, respectively, to total venous blood mobilization. The results indicate that active venoconstriction can produce only a minor reduction of venous capacity when venous transmural pressure is low but a considerable diminution of the capacity at higher venous pressures, provided the pressure is not so high as to “overstretch” the muscle elements. — The passive emptying of blood at vasoconstrictor fibre stimulation is very pronounced in the low pressure range, but becomes small at higher pressures, in accordance with the pressure‐volume characteristics of the veins, demonstrating an apparently very high distensibility at low pressures. This high “distensibility” is mainly due to changes of vessel geometry, associated with the collapse, and does not reflect true wall distensibility. … Consequently, when venous pressure is low, venous function is primarily governed by passive factors, while active shortening of venous smooth muscles will play a dominant role first when the vessels are kept well distended. — The implications of these findings for venous control is discussed, with special respect to man, where venous pressure varies greatly with body position. Some methods earlier used for assessing venous tone changes are critically analysed.

OBERG, B. and P. THOR~N. Studies on left ventricular receptors, signalling in nonmedullated vagal afferents. Acta physiol. scand. 1972. 85. 145-163. Left ventricular receptors, signalling in non-medullated vagal fibres and displaying a low, irregular spontaneous activity, have been analysed by recordings of impulse activity in cardiac afferent nerves. The receptors were distributed diffusely all over the ventricle and in both superficial and deep layers of the myocardium. They were activated by occlusions of the ascending aorta, by substantial elevations of arterial blood pressure and by rapid infusions of saline or dextran, whenever these procedures produced a clearcut increase of intraventricular diastolic pressure and end-diastolic volume. The endings were also excited by veratrum alkaloids, nicotine and digitalis alkaloids. When activated, the receptors usually displayed a cardiac rhytm, but with intense stimulation the activity usually became continuous. The receptors evidently function as mechanoor deformation receptors, responding primarily to a distension of the ventricle. Activation of the receptors causes a reflex bradycardia and, in all probability, vasodilatation and blood pressure fall. They may contribute to the homeostatic control of blood pressure and blood volume, but their main function seems to be to protect the heart from e.g. imminent overloading. The endings are probably of main importance for the emergence of the Bezold-Jarisch reflex.

OBERG, B. and S. WHITE. Circulatory effects of interruption and stimulation of cardiac uagal afferents. Acta physiol. scand. 1970. 80. 383-394.The influence of the rhythmic activity in cardiac vagal afferents on the circulation was analyzed in chloralose-anrsthetized cats by observing the cardiovascular responses to sudden interruption of this activity 2nd to afferent stimulation of the cardiac nerves. The evoked responses were compared with those produced by "unloading" and stimulation of arterial baroreceptors. -Elimination of the impulse traffic in vagal afferents produced a blood pressure rise, a tachycardia and vasoconstrictions in skeletal muscle, intestine and kidney, indicating a tonic restraint of these afferents on the medullary vasomotor centre. The responses were generally moderate in the presence of normally functioning arterial baroreceptors but were pronounced after elimination of "buffering" influences from these receptors. -Comparisons of the inhibitory influences from vaKal cardiac afferents and baroreceptor afferents, respectively, on the vasomotor centre indicated that the former were preferentially directed to neurons controlling the efferent discharge to the heart and the renal vessels. There was no evidence for a particularly strong engagement of the capacitance vessels in reflex patterns mediated through cardiac afferents. -Low frequency afferent stimulation of the cardiac nerves generally induced a profound bradycardia, which was probably due to stimulation of fibres not normally tonically active. 7-70303'3. Act4 phyrid. s c a d VoE. 80: 3

OBERG: B. and S. WHITE. T h e role of vagal cardiac nerves and arterial baroreceptors in the circulatory adjustments to hemorrhage in the cat. Acta physiol. scand. 1970. 80. 395-403.The relative importance of arterial baroreceptors and receptors with afferent fibres in the cardiac nerves, respectively, in producing compensatory circulatory adjustments in moderate hemorrhage was analyzed in chloralose-anesthetized cats. -The effects of standardized hemorrhage on blood pressure, heart rate and renal and skeletal muscle blood flows were observed before and after section of respective receptor afferents. Both groups of receptors, when operating in the absence of the other, were capable of producing tachycardia and vasoconstriction during a blood loss, but the pattern of response, elicited via the two sets of afferents, differed. Compensation via cardiac nerve afferents thus implied a particularly strong engagement of vasomotor neurons, controlling the heart and the renal vessels, while the arterial baroreceptor adjustments seemed to involve a more uniform exitation of all vasomotor centre neurons. Very rapid hemorrhages often produced a pronounced bradycardia, resembling that seen in the "vaso-vagal" syncope in man. This response was found to he mediated through a vago-vagal reflex arch, and probably constitutes a protective mechanism, causing a break on the heart in situations of extremely poor diastolic filling.

DJOJOWGITO,A. M., B. FOLKOW, B. UBERG and S. W. WHITE. A comparison of blood viscosity measured in vitro and in a vascular bed. Acta physiol. scand. 1970. 78. 70-84.Blood viscosity in vivo ("apparent viscosity") and its variations with flow rate was analyzed in the maximally dilated calf muscle vascular bed of the cat by comparing pressure-flow relationships for blood and a Newtonian fluid (dextran-Tyrode) over a flow range between 60 and 0.2 ml/min x 100 g tissue. Viscosity in vitro for the same perfusates was measured in a cone-plate viscometer.-Apparent viscosity was much lower (approximately 50 76 ) than iii vitro values at high shear rates, with less variation between animals. I t increased with decreased flow but was as a maximum only doubled, which occurred at flows around 0.5 ml/min x 100 g. Since such small flows normally occur in constricted vessels with higher flow velocities than at maximal dilatation, the range of viscosity changes with flow in the intact circulation is probably decidedly smaller. The steep rise of viscosity in vitro at quite low shear rates had no counterpart in vivo; in fact, viscosity then tended to fall again. The discrepancies between blood viscosity in vivo and in vitro seem to be related to vascular dimensions, favour-