[Origin and role of circulating catecholamines in the normotensive sympathectomized rat]

Early chronic treatment with guanethidine destroys peripheral sympathetic nerves while sparing the adrenal medulla, and does not lower blood pressure (BP) in conscious normotensive rats (Julien et al. Am J Physiol 1990; 259: H1337). Therefore, the origin and role of circulating catecholamines (CAs) in BP maintenance were examined in conscious normotensive control, sympathectomized (SNX)--daily s.c. injections of guanethidine from 1 to 13 weeks of age--and sympathectomized-adrenalectomized (SNX-A) rats by measuring i) their plasma CAs (norepinephrine, NE and epinephrine, E) and 3,4-dihydroxyphenylglycol (DHPG) by HPLC-FD, and ii) their mean BP (MBP) responses to phenylephrine and phentolamine (5 mg/kg i.v.). The doses of phenylephrine that produced similar MBP rises were 3 micrograms/kg in controls (44 +/- 4 mmHg) and 1.5 micrograms/kg in SNX (47 +/- 3 mmHg) and SNX-A (48 +/- 2 mmHg) rats. Results are as follows: [table: see text] In conclusion, in conscious normotensive SNX rats: (1) most of the circulating NE is of adrenomedullary origin and plasma DHPG derives from neuronal NE; (2) due to supersensitivity of the cardiovascular system, stimulation of alpha-adrenoreceptors by circulating CAs play a significant role in BP maintenance.