Stress‐induced changes in epinephrine expression in the adrenal medulla in vivo

Abstract

Immobilization (IMMO) stress was used to examine how stress alters the stress hormone epinephrine (EPI) in the adrenal medulla in vivo. In rats subjected to IMMO for 30 or 120 min, adrenal corticosterone increased to the same extent. In contrast, EPI changed very little, suggesting that EPI synthesis replenishes adrenal pools and sustains circulating levels for the heightened alertness and physiological responses of the 'flight or fight' response. In part, stress activates EPI via the phenylethanolamine N-methyltransferase (PNMT) gene as single or repeated IMMO elevated PNMT mRNA. The rise in PNMT mRNA was preceded by induction of the PNMT gene activator, Egr-1, with increases in Egr-1 mRNA, protein, and protein-DNA binding complex apparent. IMMO also evoked changes in Sp1 mRNA, protein, and Sp1-DNA complex formation, although for chronic IMMO changes were not entirely coincident. In contrast, glucocorticoid receptor and AP-2 mRNA, protein, and protein-DNA complex were unaltered. Finally, IMMO stress elevated PNMT protein. However, with seven daily IMMOs for 120 min and delayed killing, protein stimulation did not attain the highly elevated levels expected based on mRNA changes. The latter may perhaps suggest initiation of adrenergic desensitization to prolonged and repeated IMMO stress and/or dissociation of transcriptional and post-transcriptional regulatory mechanisms.

Prenatal glucocorticoid exposure programs adrenal PNMT expression and adult hypertension

“…GCs are key regulators of PNMT, and we have previously demonstrated that the induction of PNMT gene expression in vitro upon GC administration is mediated by GC response elements (GRE) within the PNMT promoter . Further, altered activity of the transcription factors regulate PNMT not only in vitro (Tai et al , 2010a, but also in immobilization stress (Tai et al 2007, Wong et al 2008 as well as in a genetic model of hypertension, the SHR (Nguyen et al 2009). …”

Effects of lycium barbarum polysaccharides on neuropeptide Y and heat-shock protein 70 expression in rats exposed to heat

“…This activation increases the release of catecholamines and the release of co-located substances, including neuropeptides at the sympathetic neuroeffector juncture into the blood. For a number of years, it has been known that stress induces a cascade of adaptive neuroendocrine responses, which generally includes the synthesis and release of Cor and EPI from the adrenal gland (44,45). Melin et al showed that when rats were exposed to heat stress followed by exhaustive exercise, the levels of EPI and norepinephrine were increased (46).…”

Genetic and Functional Evidence Supports LPAR1 as a Susceptibility Gene for Hypertension

“…Previously, it has been shown that stresses induce the release of epinephrine into the circulation and elevate blood pressure, 5,23,24 indicating a psychophysiological link between stress, adrenomedullary activation, and hypertension. 25 We demonstrated that the arteries from LPAR1-deficient mice became less responsive to phenylephrine stimulation in contraction, Two hundred seventy-eight healthy individuals were randomly recruited, and rs531001 was genotyped by direct sequencing.…”

“…Finally, we demonstrated that mice lacking the LPAR1 gene presented an attenuated response to sleep deprivation-induced blood pressure elevation and phenylephrine-induced vasoconstriction, dependent on the dosages of LPAR1 gene. These genetic and functional evidences suggest that LPAR1 is an EH susceptibility gene.Previously, it has been shown that stresses induce the release of epinephrine into the circulation and elevate blood pressure, 5,23,24 indicating a psychophysiological link between stress, adrenomedullary activation, and hypertension. 25 We demonstrated that the arteries from LPAR1-deficient mice became less responsive to phenylephrine stimulation in contraction, Figure 2.…”