VAGAL AND SYMPATHETIC COMPONENTS OF THE HEART-RATE REFLEX IN CHRONIC PORTAL-VEIN STENOSIS

Citation
Hd. Battarbee et al., VAGAL AND SYMPATHETIC COMPONENTS OF THE HEART-RATE REFLEX IN CHRONIC PORTAL-VEIN STENOSIS, American journal of physiology: Gastrointestinal and liver physiology, 32(6), 1995, pp. 892-901
Citations number
48
Categorie Soggetti
Physiology
ISSN journal
01931857
Volume
32
Issue
6
Year of publication
1995
Pages
892 - 901
Database
ISI
SICI code
0193-1857(1995)32:6<892:VASCOT>2.0.ZU;2-2
Abstract
The effects of portal hypertension and portosystemic shunting on auton omic components of the heart rate (HR) baroreflex and on skeletal musc le blood flow changes were investigated using the chronic portal vein- stenosed rat. Phenylephrine- and sodium nitroprusside-induced changes in mean arterial pressure (MAP), HR, and skeletal muscle conductance ( SMC) were assessed before and after muscarinic or beta-adrenoceptor bl ockade. Stenosed rats had lower MAP than sham-operated rats (90 +/- 3 vs. 81 +/- 2 mmHg, P < 0.05), and their portal pressure was higher (7. 4 +/- 0.5 vs. 13.9 +/- 1.0 mmHg, P < 0.005). Phenylephrine presser res ponses were reduced in stenosed animals, their associated bradycardic responses were enhanced [-1.912 +/- 0.109 vs. -1.427 +/- 0.148 beats p er minute (bpm)/mmHg, P < 0.01], and their SMC responses were diminish ed. Methylatropine abolished bradycardic responses and enhanced presse r responses without affecting SMC. After propranolol, reflex bradycard ic responses in stenosed rats were less than in shams (-0.492 +/- 0.08 5 vs. -0.738 +/- 0.058 bpm/mmHg, P < 0.01), and their pressor SMC resp onses became indistinguishable from shams. In contrast, tachycardic re sponses to nitroprusside-induced hypotension before propranolol were i mpaired in stenosed rats (-1.492 +/- 0.114 vs. -2.225 +/- 0.347 bpm/mm Hg, P < 0.05), and their SMC responses were reduced. Muscarinic blocka de did not affect HR or SMC responses to hypotension in either stenose d or sham rats. beta-Adrenoceptor blockade, however, prevented hypoten sion-induced tachycardia, enhanced nitroprusside depressor responses, and eliminated the between-group differences in SMC responses. These s tudies indicate that increased gain of the parasympathetic limb of the cardiac baroreflex was responsible for attenuated presser responses t o phenylephrine in portal vein-stenosed animals and that beta-adrenoce ptors contributed to skeletal muscle vascular hyporesponsiveness to ph enylephrine in portal-vein stenosed animals. Altered beta-adrenoceptor function also appears to contribute to impaired chronotropic and skel etal muscle conductance responses to hypotension.