Central alpha-adrenergic receptors and corticotropin releasing factor mediate hemodynamic responses to acute cold stress.
Behavioral stress is likely to contribute to the development of hypertension in susceptible individuals. We reported that hemodynamic response patterns to acute startle vary and that those patterns predict the predisposition of rats to sustained stress-induced elevations in arterial pressure. Since considerable evidence suggests that central catecholamines and corticotropin releasing factor (CRF) contribute to the regulation of arterial pressure and the development of hypertension, we investigated the role of central alpha-adrenergic receptors and CRF in mediating different hemodynamic response patterns to acute cold water stress in conscious rats. Rats were instrumented for arterial pressure, heart rate and cardiac output determination and for intracerebroventricular (icv) administration of selective antagonists. After acclimation to a water tight cage, ice water (1 cm deep) was rapidly added then drained 1 min later. Although the early startle response to cold water stress elicited a pressor response in all rats, the hemodynamic response pattern varied between rats. Vascular responders (n=19) had an initial considerable increase in systemic vascular resistance and a decrease in cardiac output. In contrast, mixed responders (n=11) had a smaller increase in vascular resistance and an increase in cardiac output. Pretreatment with phentolamine (30 microgram/5 microliter, icv, n=8), prazosin (10 microgram/5 microliter, icv, n=12) or alpha-helical CRF(9-41) (10 microgram/5 microliter, icv, n=9) prevented the decrease in cardiac output elicited by acute cold water stress in vascular responders without affecting mixed responders. Yohimbine (3 microgram/5 microliter, icv, n=8) pretreatment did not alter hemodynamic responses. Therefore, we conclude that central alpha(1)-adrenoceptors and CRF mediate the specific hemodynamic response patterns to acute startle and may be responsible for the predisposition to develop hypertension in vascular responders.
Tan
Yun
Y
Department of Pharmacological Science, Saint Louis University School of Medicine, 1402 S. Grand Blvd, 63104, Saint Louis, MO, USA.
Gan
Qi
Q
Knuepfer
Mark M
MM
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000704:Analysis of Variance; D000818:Animals; D003080:Cold Temperature / Q000009:adverse effects; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology / Q000502:physiology*; D006439:Hemodynamics / Q000187:drug effects* / Q000502:physiology; D006727:Hormone Antagonists / Q000494:pharmacology; D008297:Male; D010446:Peptide Fragments / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011941:Receptors, Adrenergic / Q000502:physiology*; D013312:Stress, Physiological / Q000503:physiopathology*; D013997:Time Factors; D015016:Yohimbine / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D006727:Hormone Antagonists; D010446:Peptide Fragments; D011941:Receptors, Adrenergic; D015016:Yohimbine; D003346:Corticotropin-Releasing Hormone; C045089:corticotropin releasing hormone (9-41); D011224:Prazosin; D010646:Phentolamine