Changes in Plasma Vasopressin Levels and Cardiovascular Function due to Postural Changes in Diabetic Neuropathy.

Abstract

Decreases in blood pressure are well known to increase the release of vasopressin. Studies were carried out to investigate whether vasopressin responses to postural changes in blood pressure are maintained in diabetic patients with orthostatic hypotension [DM-OH( +)] as well as non-diabetic patients with orthostatic hypotension [nonDM-OH( +)] and these responses were compared with them observed in normal subjects and diabetic patients without orthostatic hypotension [DM-OH( -)] . After 30 min in the supine position, the upright posture for 40 min was maintained and then the supine for 10 min. Blood pressure and heart rate (HR) were measured every 5 min and plasma vasopressin levels (plasma AVP) were determined every 10 min. In normal subjects and DM-OH( -), mean arterial blood pressure (MABP) did not change, but HR increased significantly by the upright position. Plasma AVP did not change in these group. On the other hand, in DM-OH( +) MABP fell abruptly and remained to decrease during the upright posture. The HR responses in this group, however, were similar to those in normal control and DM-OH( -). Plasma AVP in DM-OH( + ) significantly increased only at 30 min during upright. These increases were significantly greater than those in normal and DM-OH( -). There were significant correlation in changes in MABP (JMAP) and plasma AVP (zJAVP) in DM-OH( +) p<0.01).Relationship between aMABP and QAVP in nonDM-OH( +) was similar to that in DM-OH( +). It is concluded that AVP responses to orthostatic hypotension in diabetic and nondiabetic neuropathies were attenuated, but heart rate responses in these patients ware well reserved. hypotension; diabetes mellitus; blood pressure; heart rate; baroreflex

Serum Vasopressin Response in Patients With Intradialytic Hypotension

“…AVP has been shown to increase in the setting of hypotension in septic or hypovolemic shock (14 -16). In patients with autonomic insufficiency, however, AVP levels are inappropriately low to the level of hemodynamic compromise and likely related to baroreceptor dysfunction leading to decreased endogenous AVP synthesis and secretion (4,5,17). Thus, vasopressin insufficiency is thought to underlie or at the very least contribute to hypotension in these patients.…”

Vasopressin and Prevention of Hypotension during Hemodialysis

“…In addition, in a study conducted in animals with hemorrhagic shock demonstrated that using V1 receptor antagonist increases hypotension ( 58 ). The results of Sato et al ( 59 ) and Cignarelli et al studies also supported the important role of vasopressin in the maintenance of blood pressure. They showed in two separate studies that vasopressin concentrations do not increase in the setting of orthostatic hypotension among diabetic patients with severe diabetic neuropathy ( 60 ).…”

“…Therefore, it is suggested that the vasopressin insufficiency due to decreased synthesis and or secretion may have an important role in the pathogenesis of hemodynamic instability during HD. In addition, as diabetes mellitus is the most common cause of ESRD, the results of Sato et al and Cignarelli et al studies also supported that the inappropriately low vasopressin concentrations may be a part of the underlying mechanism for IDH in diabetic patients ( 59 ). Shimizu et al examined whether vasopressin is a part of the mechanism of blood pressure control in ESRD patients receiving hypertonic solution for IDH ( 61 ).…”

“…Vasopressin is a well-recognized vasoconstrictor by increment of peripheral vascular resistance via V1a receptors activation on vascular smooth muscle, but it appears that this effect is negligible in healthy individuals. However, in the setting of hypotension and hypovolemia, the hemodynamic response to vasopressin becomes an important compensatory mechanism in maintaining arterial pressure and tissue perfusion ( 56 - 59 ). For instance, in patients with septic shock, release of vasopressin (together with other vasoconstrictors) usually increases systemic vascular resistance and elevates blood pressure ( 57 ).…”

Gene Network Analysis in Amygdala following Taste Aversion Learning in Rats

“…The recent studies on EGR2 knockout mice showed that deletion of this gene in mice does not impair any CTA learning and memory; in fact these knockout mice were found to have improved motor learning and object recognition memory [ 34 ]. Earlier reports also suggest that the EGR2 is one of the downstream targets of CREB transcriptional factor [ 35 ]. The downregulation of this gene in the amygdala of long-term CTA in mice suggests its possible role in developing object recognition memory and motor learning as part of the aversion learning paradigm.…”