scholarly journals Reflex Inhibition of Renal Sympathetic Nerve Activity during Myocardial Ischemia Mediated by Left Ventricular Receptors with Vagal Afferents in Dogs

1979 ◽  
Vol 63 (3) ◽  
pp. 395-402 ◽  
Author(s):  
Marc D. Thames ◽  
Francois M. Abboud
1987 ◽  
Vol 253 (1) ◽  
pp. H1-H7
Author(s):  
B. N. Gupta ◽  
A. L. Abboud ◽  
J. S. Floras ◽  
P. E. Aylward ◽  
F. M. Abboud

We measured the effect of vasopressin (8 mU X kg-1 X min-1) on reflex inhibition of renal sympathetic nerve activity induced by volume expansion in 13 sinoaortic-denervated anesthetized rabbits. Volume expansion increased left ventricular end-diastolic pressure (LVEDP) from 5.1 +/- 0.7 to 14.1 +/- 1.4 mmHg and decreased renal nerve activity (RNA) from 57.4 +/- 6.9 to 30.2 +/- 5.6 impulses/s. Infusion of vasopressin elevated LVEDP from 6.0 +/- 1.0 to 7.3 +/- 1.1 mmHg and decreased RNA from 61.8 +/- 7.2 to 47.1 +/- 6.3 impulses/s. Heart rate fell from 243 +/- 7 to 231 +/- 9 beats/min; no other significant hemodynamic changes were seen. During the infusion of vasopressin, volume expansion increased LVEDP to 13.7 +/- 1.2 mmHg and decreased RNA to 17.0 +/- 4.2 impulses/s. The slopes relating the percent decrease in RNA to the rise in LVEDP were calculated from values of RNA recorded at several levels of LVEDP. The slope averaged -6.2 +/- 1.1%/mmHg before vasopressin and nearly doubled (-11.9 +/- 1.8%/mmHg) during vasopressin. Infusion of placebo (saline) instead of vasopressin did not alter the reflex inhibition of nerve activity. Bilateral vagotomy abolished the decrease in resting nerve activity that occurred during infusion of vasopressin as well as the reflex inhibition of RNA. These data demonstrate that vasopressin facilitates the reflex inhibition of renal sympathetic nerve activity associated with increases in LVEDP and mediated through vagal afferents.


1998 ◽  
Vol 275 (4) ◽  
pp. H1115-H1121 ◽  
Author(s):  
Kanji Matsukawa ◽  
Jun Murata ◽  
Tetsuya Wada

We examined whether the cerebrum is essential for producing the rapid autonomic adjustment at the onset of spontaneous overground locomotion. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP), heart rate (HR), and electromyogram of the forelimb triceps brachialis were measured when freely moving, decerebrate cats spontaneously produced overground locomotion, supporting body weight. Decerebration was performed at the level of the precollicular-premammillary body. RSNA increased 95 ± 14 impulses/s (68 ± 10% of baseline value) at the onset of spontaneous locomotion, which was followed by rises in MAP and HR (7 ± 1 mmHg and 18 ± 2 beats/min, respectively). Concomitantly with the MAP rise, RSNA declined toward control values and then increased again during the subsequent period of locomotion. The same rapid increase in RSNA at the onset of locomotion was observed after sinoaortic denervation and vagotomy. It is concluded that some central site(s), other than the cerebrum and the rostral part of the diencephalon, can generate the centrally induced autonomic adjustment at the onset of spontaneous overground locomotion, which is independent of arterial baroreceptor and vagal afferents.


1994 ◽  
Vol 266 (2) ◽  
pp. R537-R545 ◽  
Author(s):  
J. S. Petersen ◽  
G. F. DiBona

To examine the relative role of cardiopulmonary and sinoaortic baroreceptor afferents in reflex changes in efferent renal sympathetic nerve activity (ERSNA) during furosemide diuresis, ERSNA was measured before and after administration of a maximal diuretic dose of furosemide (300 mg/kg iv) in four groups (n = 8 each) of pentobarbital sodium-anesthetized rats: animals with intact baroreflexes, sinoaortic denervation (SAD), bilateral vagotomy, or SAD plus bilateral vagotomy. In addition, measurements of left ventricular end-diastolic pressure (LVEDP), mean arterial pressure (MAP), heart rate, and afferent vagal nerve activity were performed. Furosemide administration produced an early increase in MAP (+40 mmHg) and ERSNA (+50%) that was maintained in rats with SAD plus vagotomy, suggesting that this effect is not of sinoaortic or cardiopulmonary baroreflex origin. The early pressor response was due to the vehicle, 2% ethanolamine, whereas the early renal sympathoexcitation was due to furosemide. Whereas MAP remained unchanged in rats with intact arterial baroreflexes, MAP gradually decreased along with a reduction in LVEDP during progressive diuresis-related volume depletion in animals with SAD. With progressive diuresis-related volume depletion and falling LVEDP, ERSNA increased in intact animals (delta ERSNA/delta LVEDP = 46.0 +/- 1.5%/mmHg). This late increase in ERSNA was inhibited by bilateral vagotomy or SAD, suggesting that vagal and sinoaortic baroreceptor afferents are both essential for expressing the reflex increase in ERSNA observed during furosemide-induced volume depletion. There were no significant differences among furosemide groups in urinary flow rate and sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)


2002 ◽  
Vol 97 (2) ◽  
pp. 99-102 ◽  
Author(s):  
Akira Niijima ◽  
Tomoko Okui ◽  
Yasuo Matsumura ◽  
Toshihiko Yamano ◽  
Nobuo Tsuruoka ◽  
...  

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