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
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.