Serotonin and stress-induced increases in renin secretion are not blocked by sympathectomy/adrenal medullectomy but are blocked by beta antagonists.
The present study examined the role of the sympathetic nervous system as a mediator of the message from the CNS to the kidneys to stimulate the secretion of renin. Two procedures that increase the secretion of renin were tested: administration of the serotonin releaser fenfluramine, which increases renin release without altering blood pressure [53], and subjecting the rats to the 'psychological' stressor of conditioned emotional response (CER) stress. Pretreatment of rats with either the beta antagonist sotalol or the beta 1-selective antagonist atenolol completely prevented the increase in plasma renin activity and concentration caused by fenfluramine (5 mg/kg i.p.) injection. However, chemical sympathectomy with 6-hydroxydopamine (6-OHDA) combined with surgical adrenal medullectomy did not prevent the increase in plasma renin activity and concentration following fenfluramine injection. Since beta-antagonists have been previously shown to prevent the renin response to CER stress, we also tested whether the sympathetic nervous system mediates the renin response to CER stress. Chemical sympathectomy combined with adrenal medullectomy did not prevent the effect of CER stress on renin release. The completeness of the sympathectomy/adrenal medullectomy was verified biochemically by measuring plasma epinephrine and both plasma and renal norepinephrine concentrations. Plasma epinephrine and renal norepinephrine levels were reduced to below 1% of control while plasma norepinephrine was reduced to below 8% of control values. In conclusion, our data support previous reports suggesting that activation of CNS pathways increases the secretion of renin. However, the message from the brain to release renin from the kidneys does not exclusively involve either the sympathetic innervation of the kidneys or adrenal epinephrine. Although beta 1 receptors are involved in mediating this phenomenon, their location or mechanism remains unknown and will be discussed.
Morton
K D
KD
Department of Pharmacology, Loyola University Chicago Stritch School of Medicine, Maywood, IL 60153, USA.
Johnson
M D
MD
Van de Kar
L D
LD
D000313:Adrenal Medulla / Q000502:physiology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000704:Analysis of Variance; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D005277:Fenfluramine / Q000494:pharmacology*; D008297:Male; D016627:Oxidopamine; D051381:Rats; D017207:Rats, Sprague-Dawley; D012083:Renin / Q000378:metabolism*; D012701:Serotonin / Q000502:physiology*; D013015:Sotalol / Q000494:pharmacology; D013312:Stress, Physiological / Q000503:physiopathology*; D013563:Sympathectomy, Chemical
D000319:Adrenergic beta-Antagonists; D005277:Fenfluramine; D012701:Serotonin; D001262:Atenolol; D016627:Oxidopamine; D013015:Sotalol; D012083:Renin