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Selective Peripheral Regulation Of Noradrenaline And Adrenaline Release By Nitric Oxide
Author(s) -
Elayan Hamzeh H,
Kennedy Brian P,
Ziegler Michael G
Publication year - 2002
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2002.03693.x
Subject(s) - prazosin , endocrinology , medicine , stimulation , sympathoadrenal system , catecholamine , nitric oxide , chemistry , sympathetic nervous system , baroreflex , norepinephrine , antagonist , blood pressure , heart rate , dopamine , receptor
SUMMARY 1. Nitric oxide (NO) has complex effects on the sympathoadrenal and cardiovascular systems and may act at both central and peripheral loci. Nitric oxide appears to act directly on blood vessels and indirectly by modulating the sympathoadrenal system. In the present study, we investigated the contribution of catecholamine release from peripheral vascular and adrenal sympathetic nerves to the cardiovascular effects of the NO synthesis inhibitor N G ‐nitro‐ L ‐arginine methyl ester ( L ‐NAME; 10 mg/kg). Our experiments were perfomed in pithed vagotomized rats to remove the influence of central and baroreflex pathways. 2. Spinal cord stimulations for 30 s periods at 1, 2, 5 and 10 Hz using pulses of 1 msec at 10 V caused marked increases in plasma adrenaline and noradrenaline. N G ‐Nitro‐ L ‐arginine methyl ester did not alter resting plasma catecholamine concentrations. However, L ‐NAME generally more than doubled stimulation‐evoked release of adrenaline while reducing the extent of noradrenaline release relative to vehicle (saline)‐treated controls. 3. N G ‐Nitro‐ L ‐arginine methyl ester significantly enhanced the vasopressor responses to spinal cord stimulation. The α 1 ‐adrenoceptor antagonist prazosin (0.2 mg/kg) reduced the pressor responses of electrically stimulated L ‐NAME‐treated rats to levels below those of vehicle‐treated control rats. 4. In the absence of electrical stimulation, L ‐NAME raised the blood pressure of pithed rats without altering plasma catecholamines and the pressor effect was briefly attenuated by L ‐arginine, but was unaffected by prazosin. 5. We conclude that the augmented pressor response to sympathetic stimulation in L ‐NAME‐treated pithed rats is due largely to enhanced adrenal adrenaline release mediated by a peripheral mechanism. Stimulation of α 1 ‐adrenoceptors plays a major role in the pressor response to electrical stimulation of L ‐NAME‐treated rats, but this is not due to L ‐NAME augmentation of noradrenaline release from vascular sympathetic nerves.