scholarly journals Relaxin in the subfornical organ (SFO) increases arterial pressure and lumbar sympathetic nerve activity in female rats: Role of Angiotensin II

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Randall J Brown ◽  
J. Glenn Phaup ◽  
Eileen M. Hasser ◽  
Cheryl M. Heesch
2002 ◽  
Vol 283 (2) ◽  
pp. R451-R459 ◽  
Author(s):  
Ling Xu ◽  
Alan F. Sved

Angiotensin II (ANG II) has complex actions on the cardiovascular system. ANG II may act to increase sympathetic vasomotor outflow, but acutely the sympathoexcitatory actions of exogenous ANG II may be opposed by ANG II-induced increases in arterial pressure (AP), evoking baroreceptor-mediated decreases in sympathetic nerve activity (SNA). To examine this hypothesis, the effect of ANG II infusion on lumbar SNA was measured in unanesthetized chronic sinoaortic-denervated rats. Chronic sinoaortic-denervated rats had no reflex heart rate (HR) responses to pharmacologically evoked increases or decreases in AP. Similarly, in these denervated rats, nitroprusside-induced hypotension had no effect on lumbar SNA; however, phenylephrine-induced increases in AP were still associated with transient decreases in SNA. In control rats, infusion of ANG II (100 ng · kg−1 · min−1 iv) increased AP and decreased HR and SNA. In contrast, ANG II infusion increased lumbar SNA and HR in sinoaortic-denervated rats. In rats that underwent sinoaortic denervation surgery but still had residual baroreceptor reflex-evoked changes in HR, the effect of ANG II on HR and SNA was variable and correlated to the extent of baroreceptor reflex impairment. The present data suggest that pressor concentrations of ANG II in rats act rapidly to increase lumbar SNA and HR, although baroreceptor reflexes normally mask these effects of ANG II. Furthermore, these studies highlight the importance of fully characterizing sinoaortic-denervated rats used in experiments examining the role of baroreceptor reflexes.


1991 ◽  
Vol 261 (3) ◽  
pp. R690-R696 ◽  
Author(s):  
T. Matsukawa ◽  
E. Gotoh ◽  
K. Minamisawa ◽  
M. Kihara ◽  
S. Ueda ◽  
...  

The effect of angiotensin II (ANG II) on the sympathetic outflow was examined in normal humans. The mean arterial pressure and muscle sympathetic nerve activity (MSNA) were measured before and during intravenous infusions of phenylephrine (0.5 and 1.0 micrograms.kg-1.min-1) or ANG II (5, 10, and 20 ng.kg-1.min-1) for 15 min at 30-min intervals. The baroreflex slope for the relationship between the increases in mean arterial pressure and the reductions in MSNA was significantly less acute during the infusions of ANG II than during the infusions of phenylephrine. When nitroprusside was infused simultaneously to maintain central venous pressure at the basal level, MSNA significantly increased during the infusions of ANG II (5 ng.kg-1.min-1 for 15 min) but not during the infusions of phenylephrine (1.0 micrograms.kg-1.min-1 for 15 min), with accompanying attenuation of the elevation in arterial pressure induced by these pressor agents. These findings suggest that ANG II stimulates the sympathetic outflow without mediating baroreceptor reflexes in humans.


1999 ◽  
Vol 276 (6) ◽  
pp. R1579-R1586 ◽  
Author(s):  
Karie E. Scrogin ◽  
Eugene T. Grygielko ◽  
Virginia L. Brooks

Acute infusion of hypertonic fluid increases mean arterial pressure (MAP) in part by elevating nonrenal sympathetic activity. However, it is not known whether chronic, physiological increases in osmolality also increase sympathetic activity. To test this hypothesis, MAP, heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured in conscious, 48-h water-deprived rats (WD) during a progressive reduction in osmolality produced by a 2-h systemic infusion (0.12 ml/min) of 5% dextrose in water (5DW). Water deprivation significantly increased osmolality (308 ± 2 vs. 290 ± 2 mosmol/kgH2O, P < 0.001), HR (453 ± 7 vs. 421 ± 10 beats/min, P < 0.05), and LSNA (63.5 ± 1.8 vs. 51.9 ± 3.8% baroreflex maximum, P < 0.01). Two hours of 5DW infusion reduced osmolality (−15 ± 5 mosmol/kgH2O), LSNA (−23 ± 3% baseline), and MAP (−10 ± 1 mmHg). To evaluate the role of vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist. The antagonist lowered MAP (−5 ± 1 mmHg) and elevated HR (32 ± 7 beats/min) and LSNA (11 ± 3% baseline) in WD ( P < 0.05), but not in water-replete, rats. 5DW infusion had a similar cumulative effect on all variables in V1-blocked WD rats, but had no effect in water-replete rats. Infusion of the same volume of normal saline in WD rats did not change osmolality, LSNA or MAP. Together these data indicate that, in dehydrated rats, vasopressin supports MAP and suppresses LSNA and HR and that physiological changes in osmolality directly influence sympathetic activity and blood pressure independently of changes in vasopressin and blood volume.


2003 ◽  
Vol 285 (4) ◽  
pp. R834-R841 ◽  
Author(s):  
Claude Julien ◽  
Bruno Chapuis ◽  
Yong Cheng ◽  
Christian Barrès

The role of arterial baroreceptors in controlling arterial pressure (AP) variability through changes in sympathetic nerve activity was examined in conscious rats. AP and renal sympathetic nerve activity (RSNA) were measured continuously during 1-h periods in freely behaving rats that had been subjected to sinoaortic baroreceptor denervation (SAD) or a sham operation 2 wk before study ( n = 10 in each group). Fast Fourier transform analysis revealed that chronic SAD did not alter high-frequency (0.75-5 Hz) respiratory-related oscillations of mean AP (MAP) and RSNA, decreased by ∼50% spectral power of both variables in the midfrequency band (MF, 0.27-0.74 Hz) containing the so-called Mayer waves, and induced an eightfold increase in MAP power without altering RSNA power in the low-frequency band (0.005-0.27 Hz). In both groups of rats, coherence between RSNA and MAP was maximal in the MF band and was usually weak at lower frequencies. In SAD rats, the transfer function from RSNA to MAP showed the characteristics of a second-order low-pass filter containing a fixed time delay (∼0.5 s). These results indicate that arterial baroreceptors are not involved in production of respiratory-related oscillations of RSNA but play a major role in the genesis of synchronous oscillations of MAP and RSNA at the frequency of Mayer waves. The weak coupling between slow fluctuations of RSNA and MAP in sham-operated and SAD rats points to the interference of noise sources unrelated to RSNA affecting MAP and of noise sources unrelated to MAP affecting RSNA.


Hypertension ◽  
2001 ◽  
Vol 38 (3) ◽  
pp. 384-388 ◽  
Author(s):  
Marcelo L.G. Correia ◽  
Donald A. Morgan ◽  
Jennifer L. Mitchell ◽  
William I. Sivitz ◽  
Allyn L. Mark ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document