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In anesthetized and immobilized rats, an hour-long continuous intravenous injection of dl-propranolol (PR; 3 mg/kg), pindolol (PI; 1 mg/kg), oxprenolol (OX; 3 mg/kg) or atenolol (AT; 3 mg/kg) invariably resulted in moderate hypotension. When the drug-induced hypotension was plotted against the control arterial pressure (AP), two types of correlation were found. The hypotension induced by PR or PI, both known to accumulate in the brain at a high concentration was positively correlated to the control AP, whereas the hypotension produced by OX or AT, both known to penetrate the blood-brain-barrier poorly, was not. To test the hypothesis that the observed difference was attributable to the presence or lack of sympathoinhibitory action of the drug, the effect of these agents on the renal nerve activity (RNA) was examined. PR or PI diminished the tonic and reflexly evoked RNA, when the evoked RNA was elicited by sciatic nerve stimulation. No such changes were induced by OX or AT. These results demonstrate a modulatory role of sympathoinhibitory effect of beta-blocking agents in their hypotensive action.

1. In the guinea pig, the central projections of somatic and visceral C-afferent fibers were compared by tracing arborizations labeled through injection of Phaseolus vulgaris leucoagglutinin (PHA-L) intracellularly into single neurons of the 13th thoracic dorsal root ganglia (DRG). 2. Two of 27 somatic C-afferent neurons that responded to electrical stimulation of the 13th thoracic (subcostal) nerve (conduction velocity: 0.69 +/- 0.14 m/s, mean +/- SD) were well enough marked to allow delineation of their central processes. In both cases, the entering axon ran rostrally, giving off branches that converged on a single terminal field located in the substantia gelatinosa (lamina II) with some extension in lamina I. The terminal field in each case extended approximately 400 microns rostrocaudally and 100 microns mediolaterally. 3. Intracellular recordings were obtained from 31 afferent units that responded to electrical stimulation of the celiac ganglion. Units with onset latencies of greater than 15 ms were classified as having visceral C-afferent fibers because the shortest course from the celiac ganglion stimulation electrodes to the DRG was greater than 7 mm (i.e., a conduction velocity of less than 0.5 m/s). 4. Seven visceral C-afferent fibers were labeled well enough to follow their central trajectories. Each had a main ascending and a descending central branch. Each main branch in turn issued several collaterals that terminated in the superficial dorsal horn (laminae I and II), laminae IV, V, and X, and occasionally in the dorsal and lateral funiculi. A few collaterals reached the contralateral laminae V and X.(ABSTRACT TRUNCATED AT 250 WORDS)

In urethane-anesthetized and vagotomized rabbits, activation of C-fibers of renal afferents resulted in a reflex change in multifiber renal nerve activity (RNA) which consisted of inhibitory (I) and excitatory (E) components, either alone or in combination. The I and E components were individually and reversibly blocked by bilateral application of bicuculline and kynurenic acid, respectively, to the ventral surface of medulla. Bicuculline further eliminated the sympathoinhibiton produced by stimulation of the aortic nerve. Within the subjacent rostral ventrolateral medulla (RVLM), we recorded 23 spontaneously active single units that responded to electrical stimulation of renal afferents and were antidromically activated by stimulation of the dorsolateral funiculus at the C2 level.

Simultaneous recording of activity in the vagal and sympathetic supplies to the heart has revealed that in reflexly and centrally evoked activity these two "antagonists" do not necessarily change action reciprocally. Coactivation occurs in chemoreceptor reflexes and related reactions, upon stretching of the sinoatrial nodal region of the right atrium and when certain hypothalamic regions are stimulated. The objective of the present work was to assay the physiological importance of coactivation of the two potentially antagonistic cardiac nerves in anesthetized dogs. Output from the heart was monitored by recording volume flow in the thoracic aorta just below the aortic arch; cardiac contractility was measured as left ventricular dp/dt. Tape recordings of vagus and sympathetic nerve activity during chemoreceptor and baroreceptor reflexes, during reciprocal and nonreciprocal changes produced by hypothalamic stimulation, and during hypoxia and hypercapnia were used to trigger stimulators feeding a stimulus per action potential to cardiac vagus and sympathetic nerves after central connections were cut. The vagus stimulation alone produced a decrease in aortic blood flow; stimulation of the sympathetic nerve alone resulted in increased aortic blood flow. Simultaneous stimulation of vagus and sympathetic, however, produced an even greater cardiac output (measured by aortic blood flow). Intermediate degrees of heart rate and strength of myocardial contraction were maintained in coactivation. Obviously, an association of increased vagus and sympathetic actions, which can be effected reflexly or by action of higher centers, is of physiological benefit. In control reactions that relate cardiac function to body need, both reciprocal and synergistic actions (coactivation) of cardiac nerves are used.