Title:Role of Central and Peripheral Chemoreceptors in Vasopressin Secretion Control
Volume: 13
Issue: 3
Author(s): Michele Iovino, Edoardo Guastamacchia, Vito Angelo Giagulli, Giorgio Fiore, Brunella Licchelli, Emanuela Iovino and Vincenzo Triggiani
Affiliation:
Keywords:
Acid-base balance, blood pressure control, brain blood flow regulation, chemoreceptors, hypoxia, vasopressin,
ventilatory drive.
Abstract: In this review, we analyzed the role played by central and peripheral chemoreceptors (CHRs) in vasopressin
(AVP) secretion control. Central neural pathways subserving osmotic and non-osmotic control of AVP secretion are strictly
correlated to brain areas participating in chemoreception mechanisms. Among the different brain areas involved in central
chemoreception, the most important site has been localized in the retrotrapezoid nucleus of the rostral ventrolateral
medulla. These central CHRs are able to detect very small pH/CO2 fluctuations, participating in brain blood flow regulation,
acid-base balance and blood pressure control. Decreases in arterial pH and increases in arterial pCO2 stimulate AVP
release by the Supraoptic and Paraventricular Nuclei. Carotid CHRs transduce low arterial O2 tension into increased action
potential activity, leading to bradycardia and coronary vasodilatation via vagal stimulation, and systemic vasoconstriction
via catecholaminergic stimulation. Stimulation of carotid CHRs by hypoxia increases neurohypophyseal blood flow and
AVP release, an effect inhibited by CHRs denervation. Two renal CHRs have been identified: Type R1 CHRs do not have
a resting discharge but are activated by renal ischemia and hypotension; Type R2 CHRs have a resting discharge and
respond to backflow of urine into the renal pelvis. Signals arising from renal CHRs modulate the activity of hypothalamic
AVPergic neurons: activation of R1 and R2 CHRs, following increased intrapelvic pressure with solutions of mannitol,
NaCl and KCl, produces a significant increase of AVP secretion and the same effect has been obtained by the intrarenal
infusion of bradykinin, which excites afferent renal nerves, as well as by the electrical stimulation of these nerves.
