Role of vagal nerves and atrial natriuretic hormone in vasopressin release and a diuresis under hypertonic volume expansion

Abstract

of vagal nerves and atrial natriuretic hormone in vasopressin release and a diuresis under hypertonic volume expansion. Acta Endocrinol 1993:129:65-74. ISSN 0001-5598To assess whether increases in circulating atrial natriuretic hormone (ANH) in response to the plasma volume expansion, besides the volume receptor-mediated mechanisms, attenuate the arginine vasopressin (AVP) response to increased plasma osmolality and whether changes in plasma AVP and ANH affect renal solute excretion under hypertonic plasma volume expansion, hypertonic saline (0.95 mol/l saline) alone, hypertonic saline with 6% dextran (6D-HS) and hypertonic saline with 9% dextran (9D-HS) were administered into anesthetized dogs. In the control study, 0.15 mol/l NaCI alone was administered. Plasma AVP and ANH and cardiovascular and renal functions were determined.Hypertonic saline and 9D-HS also were administered into the vagotomized and sham operated dogs, and the same parameters were determined. Mean blood pressure and heart rate never changed in all the groups, but central venous pressure and plasma volume increased markedly in 6D-HS and 9D-HS groups. In the control and hypertonic saline groups, central venous pressure increased slightly but plasma volume never changed. Plasma AVP increased in the order of hypertonic saline, 6D-HS and 9D\ x=req-\ HS, but plasma ANH increased in reverse order. Vagotomy restored the AVP response to 9D-HS to 75% of its response to hypertonic saline, with a marked rise in plasma ANH. Urine sodium and potassium excretion and urine flow increased in hypertonic saline, 6D-HS and 9D-HS groups, but these increases were comparable among the groups. In the control group, these parameters never changed. These results suggest that the volume receptor-mediated vagal neural and ANH responses to the plasma volume expansion may have an effect on the suppression of the AVP response to osmotic stimuli, and increased plasma ANH release never potentiated the natriuresis under the hypertonic plasma volume expansion.It is well known that arginine vasopressin (AVP) plays an essential role in the regulation of body fluid metab¬ olism. The release of AVP is mainly regulated by the osmoreceptor, atrial volume receptor and aortic and carotid baroreceptors. Namely, a rise in plasma osmolality stimulates AVP release, but increased blood volume suppresses AVP release via the volume receptor and/or baroreceptor reflexes, which act via the afferent vagal and glossopharyngeal nerves (1-5). On the other hand, atrial natriuretic hormone (ANH), known to increase in response to the atrial stretch by the blood volume expansion (6), has been documented to interfere with AVP release (7-12) and AVP to stimulate ANH release (13-15).Thus, it is likely that the blood volume expansion may attenuate the AVP response to osmotic stimuli via both the volume receptor reflex and the increased plasma ANH. However, little is known about the mutual relationship between endogenous ANH release and the volume receptor reflex on AVP release under the hypertonic blood v...

Chlorpropamide-Induced ADH Release, Hyponatremia and Central Pontine Myelinolysis in Diabetes Mellitus.

“…On the other hand, it is also possible that diabetic neuropathy affects the CNS, thereby inappropriately secreting ADH and CPM potentiates peripherally the antidiuretic effect of ADH. Indeed, DM has been reported to give rise to SIADH associated with neuropathy (Sato et al 1993). In the present study, however, this is not the case, because plasma ADH decreased normally in response to decreases in Posm following an acute WL in the absence of CPM.…”