Changes in plasma catecholamines and plasma renin activity during hypotension in conscious rats with lesions of the nucleus tractus solitarii.
The purpose of the present study was to examine the effects of lesions of the nucleus tractus solitarii on the reflex control of sympathetic activity and renin release in the conscious rat. Two doses of the arteriolar vasodilator hydralazine (0.3 and 1 mg/kg, i.v.) were used to activate reflexively the sympathetic nervous system in nucleus tractus solitarii lesion and control rats. Administration of 1 mg/kg of hydralazine to the control rats caused mean arterial pressure to fall from 120 +/- 2 mm Hg to 84 +/- 2 mm Hg and elicited an 11.2-fold increase in plasma renin activity and a 2.7-fold increase in plasma norepinephrine concentration. Administration of 0.3 mg/kg of hydralazine caused the arterial pressure of the lesion group to fall from 118 +/- 3 mm Hg to a comparable value of 85 +/- 4 mmg Hg, but plasma renin activity and plasma norepinephrine concentration did not rise significantly. However, administration of 1 mg/kg of hydralazine to the lesion group caused arterial pressure to fall from 128 +/- 6 mm Hg to 64 +/- 2 mm Hg, in association with a 12.4-fold increase in plasma renin activity and a 1.6-fold elevation in plasma norepinephrine concentration. Atenolol, a beta 1-adrenoceptor antagonist, blocked 70% of the rise in plasma renin activity caused by 1 mg/kg of hydralazine in both groups of rats. In addition, prior renal denervation also markedly attenuated the rise in plasma renin activity caused by hydralazine in the lesion group. Finally, electrical stimulation of the vagus nerves, which caused a large vasodepressor response in the control group, failed to lower the arterial pressure of the lesion group. Based on these observations, we conclude that in the conscious rat (1) nucleus tractus solitarii lesions eliminate the arterial baroreflexes as well as the cardiopulmonary baroreflex, and (2) severe hypotension induces sympathetically mediated renin release in the apparent absence of arterial and cardiopulmonary baroreflex function.
Hubbard
J W
JW
Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284.
Buchholz
R A
RA
Reed
K
K
Nathan
M A
MA
Keeton
T K
TK
D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001794:Blood Pressure; D002319:Cardiovascular System / Q000187:drug effects; D003243:Consciousness; D003714:Denervation; D004558:Electric Stimulation; D006830:Hydralazine / Q000494:pharmacology; D007022:Hypotension / Q000097:blood* / Q000378:metabolism / Q000503:physiopathology; D007668:Kidney / Q000294:innervation / Q000378:metabolism; D008297:Male; D008526:Medulla Oblongata / Q000502:physiology*; D009490:Neurosecretory Systems / Q000187:drug effects; D009638:Norepinephrine / Q000097:blood* / Q000378:metabolism; D011311:Pressoreceptors / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012018:Reflex / Q000502:physiology; D012083:Renin / Q000097:blood*
D006830:Hydralazine; D001262:Atenolol; D012083:Renin; D009638:Norepinephrine