Forebrain pathways mediating stress-induced renin secretion.
1. All stressors tested so far increase plasma renin levels; among these are exposure to foot-shock, immobilization, forced swimming, head-up tilt, exercise, hypotension haemorrhage and conditioned fear. 2. In old rats (22 months old), conditioned fear stress fails to increase plasma renin concentrations to the same level as in young rats (7 months old). 3. Destruction of cells in the paraventricular hypothalamic nucleus (PVH), either electrolytically or with the cell-selective neurotoxin ibotenic acid, prevents the effect of conditioned fear stress, but not of immobilization, on plasma renin concentration. 4. Ibotenic acid-induced lesions in the central amygdaloid nucleus inhibit conditioned fear stress-induced increases in plasma renin concentrations, but do not reduce the renin response to immobilization. Lesions in lateral amygdaloid nuclei do not reduce the renin response to stressors. 5. Although lesions in the bed nucleus of the stria terminalis (BNST) reduce the adrenocortical response to conditioned fear stress, they do not reduce the effect of stress on plasma renin concentration. 6. Destruction of catecholaminergic terminals in the PVH prevents the effect of conditioned fear stress on plasma renin concentration. 7. Electrolytic lesions in the dorsal raphe nucleus, which is a major site of origin of ascending serotonergic pathways, also inhibit the effect of conditioned fear stress on plasma renin concentration. 8. Activation of serotonin1A (5HT1A) receptors with the anti-anxiety drugs buspirone and ipsapirone reduces the firing rate of serotonergic neurons in the dorsal raphe nucleus in the midbrain and decreases the effect of stress on plasma renin concentrations. In contrast, the benzodiazepine anxiolytic drugs, chlordiazepoxide and midazolam, are ineffective in inhibiting the renin response to stress. 9. Chemical sympathectomy combined with adrenal medullectomy does not prevent the effect of conditioned fear stress on plasma renin concentration, suggesting that the sympathetic system is not the sole mediator of the message from the brain to the kidneys. 10. Combined, these observations suggest that aversive information from the cortex is transmitted via the amygdala to catecholaminergic cells in the medulla and to serotonergic cells in the dorsal raphe that stimulate the PVH to increase the release of renin.
Van de Kar
L D
LD
Loyola University of Chicago, Stritch School of Medicine, Department of Pharmacology, Maywood, Illinois 60153, USA.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000378:metabolism; D002065:Buspirone / Q000494:pharmacology; D007668:Kidney / Q000378:metabolism; D016548:Prosencephalon / Q000502:physiology*; D051381:Rats; D012083:Renin / Q000097:blood / Q000378:metabolism*; D017366:Serotonin Receptor Agonists / Q000494:pharmacology; D013312:Stress, Physiological / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*
D000318:Adrenergic beta-Agonists; D017366:Serotonin Receptor Agonists; D012083:Renin; D002065:Buspirone