The role of supraspinal vasopressin and glutamate neurones in an increase in renal sympathetic activity in response to mild haemorrhage in the rat

Abstract

This study investigated the importance of supraspinal vasopressin and glutamate neurones in regulating renal sympathetic activity as part of the response to an acute reduction in blood volume. Wistar rats anaesthetized with chloralose and urethane were instrumented to record arterial blood pressure, heart rate and left renal sympathetic nerve activity. Pharmacological agonists and antagonists to glutamate and vasopressin were applied to the renal outflow of the spinal cord via an intrathecal catheter inserted at the foramen magnum and with the tip at the level of T10. Both glutamate and vasopressin increased renal sympathetic activity, and these actions were shown to be selectively blocked by their respective antagonists. Removing 1 ml of venous blood from a femoral venous catheter elicited an increase of 26 +/- 2% in renal sympathetic activity. This response to mild haemorrhage was halved to 13 +/- 4% by prior intrathecal application of a selective V1a antagonist. Similarly, prior intrathecal application of kynurenic acid reduced the response to the mild haemorrhage from 28 +/- 2 to 12.6 +/- 2.8%. Intrathecal application of both antagonists together reduced the haemorrhage response even further to 8 +/- 3%. All the changes were statistically significant at P < 0.01. It is concluded that a small reduction in blood volume induces an increase in renal sympathetic activity dependent on vasopressin and glutamate release from terminals of supraspinal neurones. It is suggested that the vasopressin neurones most probably originate from the paraventricular nucleus of the hypothalamus.

Regulation of Breathing and Autonomic Outflows by Chemoreceptors

“…Based on these projections, PVH may modulate a range of homeostatic functions, including cerebral and ocular blood flow, corneal and nasal hydration, ingestive behavior, sodium intake, and glucose metabolism, as well as cardiovascular, gastrointestinal, and respiratory activities [for references, see (136)]. Physiological studies have implicated these neurons in the regulation of blood volume and pressure and, more recently, in stress and appetite control (13, 26, 62, 398, 462). However, with few exceptions, the connectome of the PVH is largely deduced from light microscopic studies, that is, the nature of the cells directly contacted by these neurons is for the most part unknown.…”

Landmarks in understanding the central nervous control of the cardiovascular system

“…Furthermore, stimulation of volume receptors by distending the right atrial–caval junction with a balloon catheter or by plasma volume expansion activates the early gene c‐fos in PVN parvocellular neurones (Deng & Kaufman, 1995; Badoer et al 1997; Pyner et al 2002). Evidence that PVN–spinal vasomotor neurones transmit these afferent signals directly to spinal vasomotor neurones is provided by the demonstration that an increase in renal sympathetic nerve activity in response to a mild venous haemorrhage or to intracarotid hyperosmotic solution is significantly reduced by blocking the PVN–spinal vasopressin influence by application of V 1a antagonist to the spinal neurones (Coote & Yang, 2005; Yang & Coote, 2006; Antunes et al 2006).…”

In Vivo Discharge Properties of Hypothalamic Paraventricular Nucleus Neurons With Axonal Projections to the Rostral Ventrolateral Medulla

“…This is surprising given that sympathoexcitatory challenges such as water deprivation (Stocker et al 2004a(Stocker et al , 2006 and hemorrhage (Badoer and Merolli 1998;Badoer et al 1993) have been shown to induce c-fos expression in PVN-RVLM neurons. Moreover, hemorrhage increases RSNA by stimulating ionotropic glutamate and vasopressin V1a receptors in the spinal cord (Yang and Coote 2006), possibly via recruitment of PVN-RVLM/ IML neurons. Finally, PVN-RVLM neurons are largely glutamatergic (Stocker et al 2006) and activation of the PVN increases the discharge of RVLM vasomotor neurons (Yang et al 2001).…”