Stress-Induced Renin and Corticosterone Secretion Is Mediated by Catecholaminergic Nerve Terminals in the Hypothalamic Paraventricular Nucleus

Abstract

Cell bodies in the hypothalamic paraventricular nucleus (PVN) mediate stress-induced increases in renin and corticosterone secretion. Since the PVN has an extensive catecholaminergic innervation, we wanted to determine the role of catecholamines in the neuroendocrine response to stress. The stressor was a conditioned emotional (fear) response paradigm (CER). The catecholamine neurotoxin, 6-hydroxydopamine (6-OHDA), was injected into the PVN 14 days before the rats were subjected to the CER procedure. Damage to noradrenergic nerve terminals was verified immunocytochemically, using an antibody against dopamine β-hydroxylase. Injection of 6-OHDA into the PVN prevented the stress-induced increase in plasma renin activity (PRA), plasma renin concentration (PRC) and plasma corticosterone concentration, suggesting that intact catecholaminergic innervation of neurons in the PVN is necessary for the stress-induced increase in renin and corticosterone secretion. To determine if β-adrenoceptors in the PVN mediate the effect of stress on renin and corticosterone secretion, the β-adrenoceptor antagonist sotalol was injected into the PVN through chronically implanted bilateral cannulae. The injection was performed on the 4th day of the CER paradigm, just before the rats were placed into the CER chamber. Sotalol prevented the stress-induced increase in corticosterone concentration, but did not diminish the stress-induced increase in PRA and PRC. These results suggest that the stress-induced increase in corticosterone concentration is influenced by β-adrenoceptors in the PVN. The stress-induced increase in PRA and PRC is mediated by different receptors whose ligands might be catecholamines acting at non-β-receptors or other neuroactive substances colocalized in catecholaminergic nerve terminals.

Intravenous Delivery of PTH/PTHrP Type 1 Receptor cDNA to Rats Decreases Heart Rate, Blood Pressure, Renal Tone, Renin Angiotensin System, and Stress-Induced Cardiovascular Responses

“…As a rule, the animals react to stressful stimuli with a number of physiologic responses, including increases in BP, heart rate (59), and PRA (60). In the present studies, the rats underwent stressful manipulations, too, including tail-vein blood sampling, repeated stays in metabolic cages, and BP measurements.…”

The Ventral Ascending Noradrenergic Bundles Are Involved in the Stress Response to Immobilization in Rats

“…Catecholaminergic stimulation is involved in the stress-induced release of ACTH [22]. Furthermore, loss of noradrenergic innervation of the hypothalamus with local microinjection of 6-OHDA leads to strong inhibition of stress-induced activation of the HPA axis after ether inhalation [23], photic, acoustic, or sciatic nerve stimulation [24], or emotional stress [6]. Our current study indicates that the V-NAB input to the PVN is associated with a stimulatory role of immobilization stress-induced activation of the HPA axis, similar to the above stressors or stimulations.…”

“…Many studies have examined the role of the V-NAB in the response of the HPA axis to some types of stress [4]- [6]. For examples, medullary catecholamine innervation of the hypothalamus plays an important role in modulating the stimulatory effect of alcohol stress on the HPA axis [4].…”

“…For examples, medullary catecholamine innervation of the hypothalamus plays an important role in modulating the stimulatory effect of alcohol stress on the HPA axis [4]. And a conditioned emotional (fear) stressinduced increase in plasma corticosterone concentration is mediated by catecholaminergic nerves into the PVN [5] [6]. On the other hand, a differential involvement of the hypothalamic noradrenergic innervation upon the HPA axis according to the nature of stress conditions has been reported [7].…”

Neuroendocrine Evidence That (S)-2-(Chloro-5-fluoro-indol- l-yl)-1-methylethylamine Fumarate (Ro 60-0175) Is Not a Selective 5-Hydroxytryptamine2C Receptor Agonist

“…The ␣ 1 -adrenergic receptor antagonist prazosin and ␤-adrenergic receptor antagonist sotalol attenuate stress-induced increases in plasma ACTH and corticosterone levels (Feldman and Weidenfeld, 1996). Furthermore, catecholaminergic neurons mediate stress-induced oxytocin and corticosterone release (Richardson Morton et al, 1990;Knigge et al, 1999). Histamine (H 1 ) receptors are abundant within the paraventricular nucleus of the hypothalamus and histamine is also known to increase the secretion of ACTH and oxytocin (Kjaer et al, 1992).…”