Abstract
Recent studies have suggested that the central nervous system is responsible for activation of sympathetic nerve activity (SNA) and the renin-angiotensin system in heart failure (HF). The aim of this study was to determine whether activation of the renin-angiotensin system within the nucleus of the solitary tract (NTS) plays a role in enhanced SNA in HF. High-output HF was induced by an aortocaval (A-V) shunt with some modifications in the rat. These rats exhibited a left ventricular dilatation and hemodynamic signs of high-output HF. Urinary catecholamine excretion and maximal renal SNA (RSNA) were greater in the A-V shunted rats than in the control rats. Microinjection of an angiotensin II type 1-receptor antagonist, CV11974, into the NTS was performed. The arterial pressure and RSNA were reduced by CV11974 to a greater degree in the A-V shunted rats than in the control rats. The expression of angiotensin-converting enzyme mRNA in the medulla was greater in the A-V shunted rats than in the control rats. These results suggest that activation of the renin-angiotensin system within the NTS contributes to an enhanced SNA in this model.
| Original language | English |
|---|---|
| Pages (from-to) | R1665-R1673 |
| Journal | American Journal of Physiology - Regulatory Integrative and Comparative Physiology |
| Volume | 280 |
| Issue number | 6 49-6 |
| Publication status | Published - Jul 3 2001 |
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All Science Journal Classification (ASJC) codes
- Physiology
- Physiology (medical)
Cite this
Endogenous angiotensin II in the NTS contributes to sympathetic activation in rats with aortocaval shunt. / Shigematsu, Hideaki; Hirooka, Yoshitaka; Eshima, Kenichi; Shihara, Miwako; Tagawa, Tatsuya; Takeshita, Akira.
In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 280, No. 6 49-6, 03.07.2001, p. R1665-R1673.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Endogenous angiotensin II in the NTS contributes to sympathetic activation in rats with aortocaval shunt
AU - Shigematsu, Hideaki
AU - Hirooka, Yoshitaka
AU - Eshima, Kenichi
AU - Shihara, Miwako
AU - Tagawa, Tatsuya
AU - Takeshita, Akira
PY - 2001/7/3
Y1 - 2001/7/3
N2 - Recent studies have suggested that the central nervous system is responsible for activation of sympathetic nerve activity (SNA) and the renin-angiotensin system in heart failure (HF). The aim of this study was to determine whether activation of the renin-angiotensin system within the nucleus of the solitary tract (NTS) plays a role in enhanced SNA in HF. High-output HF was induced by an aortocaval (A-V) shunt with some modifications in the rat. These rats exhibited a left ventricular dilatation and hemodynamic signs of high-output HF. Urinary catecholamine excretion and maximal renal SNA (RSNA) were greater in the A-V shunted rats than in the control rats. Microinjection of an angiotensin II type 1-receptor antagonist, CV11974, into the NTS was performed. The arterial pressure and RSNA were reduced by CV11974 to a greater degree in the A-V shunted rats than in the control rats. The expression of angiotensin-converting enzyme mRNA in the medulla was greater in the A-V shunted rats than in the control rats. These results suggest that activation of the renin-angiotensin system within the NTS contributes to an enhanced SNA in this model.
AB - Recent studies have suggested that the central nervous system is responsible for activation of sympathetic nerve activity (SNA) and the renin-angiotensin system in heart failure (HF). The aim of this study was to determine whether activation of the renin-angiotensin system within the nucleus of the solitary tract (NTS) plays a role in enhanced SNA in HF. High-output HF was induced by an aortocaval (A-V) shunt with some modifications in the rat. These rats exhibited a left ventricular dilatation and hemodynamic signs of high-output HF. Urinary catecholamine excretion and maximal renal SNA (RSNA) were greater in the A-V shunted rats than in the control rats. Microinjection of an angiotensin II type 1-receptor antagonist, CV11974, into the NTS was performed. The arterial pressure and RSNA were reduced by CV11974 to a greater degree in the A-V shunted rats than in the control rats. The expression of angiotensin-converting enzyme mRNA in the medulla was greater in the A-V shunted rats than in the control rats. These results suggest that activation of the renin-angiotensin system within the NTS contributes to an enhanced SNA in this model.
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UR - http://www.scopus.com/inward/citedby.url?scp=0034977003&partnerID=8YFLogxK
M3 - Article
C2 - 11353669
AN - SCOPUS:0034977003
VL - 280
SP - R1665-R1673
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 6 49-6
ER -