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1. The effect of physical exercise on blood pressure, plasma catecholamines and plasma renin activity was studied in fourteen patients with essential hypertension and in eight healthy subjects. 2. Resting plasma noradrenaline and adrenaline and plasma renin activity of the hypertensive patients did not differ from those of the control subjects. 3. In response to graded exercise producing successive heart rates of 120, 140 and 160 beats/min, significantly greater increases of blood pressure were found in the patients than in the control subjects. 4. Plasma noradrenaline increased significantly in both groups at all levels of exercise, the responses being significantly greater in the hypertensive patients. 5. The mean arterial blood pressure was significantly correlated with plasma noradrenaline concentration in the control subjects but not in the hypertensive patients. 6. In the hypertensive group plasma adrenaline increased significantly after exercise at all work loads whereas, in the control group, significant increase occurred only at the highest work load. The differences in the response of the two groups were significant at each work load. 7. Plasma renin activity increased significantly after exercise at the heart rate of 120 beats/min, both in the hypertensive patients and in the control subjects. The magnitude of the response was similar in the two groups.

SUMMARY In 3 of 10 anesthetized dogs with aortic nerves sectioned and renal arterial pressure maintained constant, reduction to 40 mm Hg of the pressure in the vascularly isolated carotid sinuses resulted in an increase in renin secretion. After section of the vagus nerves, carotid sinus hypotension resulted in an increase in renin secretion in 9 of the 10 dogs. Vagal nerve section in these 10 dogs with carotid sinuses vascularly isolated and maintained at a pressure equal to existing aortic pressure resulted in significant increases in basal levels of plasma renin activity and renin secretion. The increase in renin secretion found during carotid sinus hypotension in vagotomized dogs was totally or substantially inhibited when renal arterial pressure was not maintained constant but allowed to increase equally with systemic arterial pressure. The increase in renin secretion observed during carotid hypotension in vagotomized dogs with renal arterial pressure held constant was abolished by renal denervation. We conclude that the carotid baroreflex is involved in the neural control of renin release. However, a concomitant activation of cardiopulmonary receptors and/or a substantial rise in renal arterial pressure can suppress the reflex increase in the secretion of renin induced by carotid sinus hypotension. have shown that the release of renin in such diverse situations as suprarenal aortic stenosis, administration of the diuretic furosemide, and tilting to the upright position is dependent on neural mechanisms in considerable degree. In view of these observations, it is surprising to find disagreement regarding the role of the carotid baroreflex in the control of renin secretion. Three studies"*" 12 reported an increase in renin secretion during carotid occlusion and three studies 13 " 15 reported that renin secretion was not affected by changes in carotid sinus pressure. IN THE LAST FEW YEARS increasing attention hasIn a recent study it was shown that, when the carotid sinus was free to exert its buffering influence, complete interruption of afferent vagal nerve traffic from cardiopulmonary receptors did not result in an increase in renin secretion in 17 of 20 dogs. 16 Because it has been shown that the inhibitory influence of vagally innervated cardio- pulmonary receptors becomes more pronounced as that of the carotid baroreceptors is reduced," it seemed possible that this interaction between the two receptor systems might act to inhibit the release of renin during carotid sinus hypotension. The following studies were carried out to investigate this question. MethodsDogs weighing 16-20 kg were maintained on a daily intake of 65 mEq of Na + and 55 mEq of K + for 5 days before study. Anesthesia was induced with sodium thiopental (30 mg/kg, intravenously) followed by a-chloralose (80 mg/kg dissolved in 5% dextrose in water and administered intravenously). Supplemental doses of chloralose (5-10 mg/kg) were given hourly. Gallamine triethiodide (Flaxedil; 3 mg/kg, iv) was used to obtain muscle relaxation during the su...

Arterial ketone body ratio (AKBR), which reflects hepatic intramitochodrial redox potential, was measured in 20 patients with Carcinoma hepatis metastaticum and good circulatory condition (group A), and 16 patients with Carcinoma hepatis metastaticum and chronic cardiogenic circulatory insufficiency (group B). Total ketone body concentration (TKB) and arterial oxygen tension (PaO2) was simultaneously determined. We have stated that AKBR values in both groups of patients were decreased below the normal level. AKBR values in group B were significantly lower than in group A. At the same time TKB values in both groups were statistically equal and significantly increased above the normal level. The levels of arterial oxygen tension (PaO2) in group A were physiologically high, whereas in group B were significantly decreased. Furthermore arterial oxygen tension of patients in group B correlated with AKBR values significantly. In group A we found statistically significant negative correlation between TKB and AKBR values. Our study indicate that the main mechanism which may explain the decrease of intrahepatic mitochondrial redox potential in patients with liver metastatic cancers and good circulatory condition, is the enhanced beta-oxidation of fatty acids, when the efficiency of NAD+ to NADH reduction in beta-oxidation pathway and tricarboxylic acid cycle is higher than re-oxidation of NADH to NAD+ in the oxidative phosphorylation. In patients with coexisting chronic cardiogenic circulatory insufficiency deprivation of blood oxygen supply initiate the irreversible dysfunction of oxidative phosphorylation.