SUMMARY1. The responses of mesenteric microcirculation ofthe rat to circulating noradrenaline were studied by in vivo microscopy, using a photo-electric device placed on a television monitor to measure changes in diameter of individual vessels. Blood flow was measured in the anterior mesenteric artery with an electromagnetic flow transducer, mesenteric vascular conductance was computed on-line from mesenteric artery flow and arterial pressure. 3. The diameter increases of small and principal arteries were not reflex dilator responses initiated by the rise in systemic arterial pressure, nor due to /J-adrenoreceptor stimulation. However, local application ofphentolamine abolished responses of all sections of the vascular tree indicating that they all depended on activation of a-adrenoreceptors.4. During i.v. infusion of noradrenaline small arteries showed a maintained increase in diameter which began at the peak of the pressor response, while arterioles initially decreased in diameter but then relaxed, often attaining resting diameter before infusion ceased. Meanwhile mesenteric flow and conductance decreased transiently, but then returned to near control levels, i.e. 'autoregulatory escape' occurred.5. It is argued that noradrenaline induced a-mediated contraction of all sections of the vascular tree; the tendency of arteries to constrict was counteracted by the rise in intravascular pressure caused by arteriolar constriction, active constriction of venous vessels may have been augmented by passive collapse secondary to arteriolar constriction. The secondary relaxation of arterial vessels reflects an inherent property of their smooth muscle to relax from the constrictor influence of noradrenaline and is more marked in proximal than distal vessels.6. It is proposed that the initial decrease in mesenteric vascular conductance in M. T. HEBERT AND J. M. MARSHALL response to circulating noradrenaline may be attributed to active constriction of distal arterioles and the secondary increase in conductance ('escape') to secondary relaxation of more proximal arterial vessels.

SUMMARY1. In anaesthetized rats, supramaximal baroreceptor stimulation by carotid sinus inflation evoked a reflex fall in arterial pressure and an increase in vascular conductance and flow of muscles of the hindquarters.2. Simultaneously, main arteries, primary and secondary arterioles (13-90 /sm, internal diameter (i.d.)) and terminal arterioles (7-13 ,sm) of the spinotrapezius muscle all showed a diameter increase that reached a peak as arterial pressure neared its zenith; terminal arterioles then showed a diameter decrease to below control level. These responses were abolished by local application of phentolamine or guanethidine to the spinotrapezius, or by crushing the paravascular nerve supply.3. It is suggested that the diameter increases were mediated by reflex inhibition of sympathetic tone, while the secondary diameter decrease in terminal arterioles was induced by a fall in local concentrations of vasodilator metabolites, caused by an increase in muscle blood flow.4. But after sympathetic blockade 25% of all arterial vessesl showed a diameter increase beginning as the fall in arterial pressure neared its zenith. These responses may be attributed to vasodilator metabolites accumulating as a consequence of a reduction in muscle blood flow secondary to the reflex reduction in perfusion pressure.5. No venous vessels, from venules (9-18,m) to main veins (65-130 /sm) that drain the muscle, showed a diameter change in response to baroreceptor stimulation, in accord with evidence that they have no sympathetic supply.6. These results accord with and can provide explanation for changes in blood flow, regional blood volume and capillary filtration evoked by baroreceptor stimulation in studies on whole-limb muscle. They support suggestions that active changes in capacity of venous vessels of muscle play a minor role in the baroreceptor reflex; both active and passive changes in vascular capacity may be due to large veins outside of muscle proper.

In a malnutrition setting, this subpopulation should be given personalized health care, including a strengthened refeeding program. Thus, catalase genotyping could enable earlier recovery of satisfactory nutritional status and thus avoid the consequences of malnutrition, which are especially deleterious in the elderly.