SUMMARY. This study compares the effect of arginine-vasopressin with phenylephrine on arterial pressure, heart rate, and renal sympathetic nerve activity in conscious rabbits with and without functional arterial baroreflexes and in rabbits with lesions of the area postrema. In intact rabbits, progressive infusions of arginine-vasopressin result in large decreases in renal sympathetic nerve activity and heart rate for a given increase in blood pressure as compared to progressive infusions of phenylephrine. In sinoaortic-denervated rabbits, the responses of arterial pressure on heart rate and renal sympathetic nerve activity to both arginine-vasopressin and phenylephrine are markedly attenuated, indicating the necessity for afferent baroreceptor activity in this response. This observation indicates that arginine-vasopressin is acting centrally to enhance the baroreflex. A central site of action of circulating vasopressin may be the area postrema, since it is the only circumventricular organ in the hindbrain. Lesioning the region of the area postrema resulted in a normalization of the responses evoked with arginine-vasopressin and phenylephrine. There was no difference in the phenylephrine responses of arterial pressure on renal sympathetic nerve activity or heart rate in area postrema-lesioned animals, compared to control rabbits. Therefore, we conclude that the area postrema or its surrounding tissue is either a site of action of circulating arginine-vasopressin or contains fibers of passage from another site where arginine-vasopressin acts to enhance baroreflex activity. (CircRes 56: 410-417, 1985) ALTHOUGH arginine-vasopressin (AVP) has been shown to be a potent vasoconstrictor agent (Alrura and Alrura, 1977;Cowley et al., 1974), increases in mean arterial pressure (MAP) have often been shown to be less than those observed with other vasoconstrictor agents when administered to animals with intact reflexes. A number of studies (Cowley et al., 1974;Montani et al., 1980;liard et al., 1981;Guo et al., 1982) have indicated that AVP interacts in the central nervous system to modify arterial baroreflexes. It has been postulated that the central action of AVP results in increases in the gain of the arterial baroreflexes (Cowley et al., 1974;Montani et al., 1980). The resulting enhanced inhibition would result in a greater fall in sympathetic activity for any given increase in MAP. On the other hand, microinjections of AVP into the nucleus rractus solitarius results in increases in arterial pressure and heart rate (Matsuguchi et al., 1982), while administration of AVP into the 4th cerebral ventricle causes bradycardia (Varma et al., 1969). Although the effects of AVP appear to be dependent upon the site or route of administration, data from these studies suggest that AVP can act centrally to alter the control of the circulation. Liard et al. (1981) bral infusions of AVP, in concentrations which do not exert a peripheral effect, result in a decrease in cardiac output and heart rate, suggesting that the hindbrain is ...
The purpose of this study was to assess the effect of rapid baroreceptor resetting on the baroreflex control of renal sympathetic nerve activity in conscious rabbits. Renal sympathetic nerve activity was recorded and used as an index of the efferent limb of the baroreflex. Heart rate and arterial pressure were also recorded. Arterial pressure was raised with either phenylephrine or angiotensin II to a level that eliminated renal sympathetic nerve activity and was maintained at this level for periods of time ranging from 1 to 60 min. On returning pressure to control levels, renal sympathetic nerve activity remained suppressed for up to 90 min, with the duration of the suppression dependent on the magnitude and duration of the pressure stimulus. During this period of suppressed nerve activity, baroreflex curves were generated. The curves produced at this time were also suppressed as compared with control baroreflex curves. With time, the suppressed baroreflex curves returned to control. Further studies were performed to show that the suppression of renal sympathetic nerve activity was mediated via the prolonged increase in baroreceptor afferent activity during the pressure stimulus and was not due to a central effect of phenylephrine. This study indicates that although baroreceptor afferent activity may reset rapidly, there does not appear to be an augmentation of renal sympathetic nerve activity as would be expected.
Effects of arginine vasopressin (AVP) on inhibition of renal sympathetic nerve activity (RSNA) during activation of cardiopulmonary reflexes by volume expansion were examined in conscious sinoaortic-denervated rabbits. The role of the area postrema in mediating these effects was also evaluated in rabbits subjected to area postrema lesion. Animals were subjected to 12% volume expansion with whole blood alone or during infusion of AVP (0.6 mU . kg-1 . min-1). Volume expansion in area postrema-intact animals caused a progressive reflex inhibition of RSNA (maximum = -36.5 +/- 3.3% delta RSNA). Vasopressin infusion did not significantly alter resting arterial pressure, right atrial pressure, heart rate, or RSNA. However, maximum inhibition of RSNA during volume expansion (-62.6 +/- 3.2% delta RSNA) was significantly augmented during AVP infusion, and the augmentation was reversed by a specific vascular (V1) AVP receptor antagonist. Vagotomy eliminated RSNA responses to volume expansion with or without AVP. In area postrema-lesioned animals, the RSNA response to volume expansion was similar to that of intact animals (-31.8 +/- 2.3% delta RSNA). However, AVP did not augment the RSNA response to volume expansion in lesioned animals (-30.4 +/- 2.5% delta RSNA). Thus exogenous AVP augmented cardiopulmonary reflex-mediated inhibition of RSNA due to volume expansion. This effect appeared to be mediated by the V1 AVP receptor and to require the presence of an intact area postrema.
The effect of increased arterial pressure on aortic depressor nerve activity was studied in the conscious rabbit. Aortic baroreceptor resetting was observed following 15 min of sustained pressure elevation. At 15 min, there was a significant increase in the threshold arterial pressure for aortic nerve activity, but peak nerve activity did not change. This resulted in an increase in the slope of the pressure-nerve activity relationship. Therefore, except for peak nerve activity, aortic nerve activity was reduced at all pressures following 15 min of sustained pressure elevation. At 30 min, peak nerve activity also increased, resulting in a parallel shift in the pressure-activity curve. The early increase in slope of the pressure-activity relationship may be due to an early resetting of low threshold fibers with a high pressure differential between their threshold pressure and the sustained pressure elevation used to induce resetting. A late resetting of high threshold fibers with a low pressure differential between their threshold pressures and the pressure used to cause resetting of baroreceptors results in a parallel shift in the curve observed at 30 min. These data obtained from multiunit recordings provide unexpected evidence about baroreceptor resetting, which is not apparent from single-unit recordings.
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