Parallel resetting of arterial baroreflex control of renal and cardiac sympathetic nerve activities during upright tilt in rabbits

2010 ◽  
Vol 298 (6) ◽  
pp. H1966-H1975 ◽  
Author(s):  
Atsunori Kamiya ◽  
Toru Kawada ◽  
Masaki Mizuno ◽  
Shuji Shimizu ◽  
Masaru Sugimachi
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Response Range ◽  
Sigmoidal Curve ◽  
Maximal Gain ◽  
Upright Tilt ◽  
Sinus Pressure

Since humans are under ceaseless orthostatic stress, the mechanisms to maintain arterial pressure (AP) against gravitational fluid shift are important. As one mechanism, it was reported that upright tilt reset baroreflex control of renal sympathetic nerve activity (SNA) to a higher SNA in anesthetized rabbits. In the present study, we tested the hypothesis that upright tilt causes a parallel resetting of baroreflex control of renal and cardiac SNAs in anesthetized rabbits. In anesthetized rabbits ( n = 8, vagotomized and aortic denervated) with 0° supine and 60° upright tilt postures, renal and cardiac SNAs were simultaneously recorded while isolated intracarotid sinus pressure (CSP) was increased stepwise from 40 to 160 mmHg with increments of 20 mmHg. Upright tilt shifted the reverse-sigmoidal curve of the CSP-SNA relationship to higher SNA similarly in renal and cardiac SNAs. Although upright tilt increased the maximal gain, the response range and the minimum value of SNA, the curves were almost superimposable in these SNAs regardless of postures. Scatter plotting of cardiac SNA over renal SNA during the stepwise changes in CSP was close to the line of identity in 0° supine and 60° upright tilt postures. In addition, upright tilt also shifted the reverse-sigmoidal curve of the CSP-heart rate relationship to a higher heart rate, with increases in the maximal gain and the response range. In conclusion, upright posture caused a resetting of arterial baroreflex control of SNA similarly in renal and cardiac SNAs in anesthetized rabbits.

Arterial baroreflex during pregnancy and renal sympathetic nerve activity during parturition in rabbits

1998 ◽  
Vol 274 (5) ◽  
pp. H1635-H1642 ◽  
Author(s):  
Kathleen P. O’Hagan ◽  
Susan M. Casey
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Reflex Gain ◽  
Maximal Gain ◽  
Renal Sympathetic

The arterial baroreflex control of renal sympathetic nerve activity (RSNA) was evaluated in nine term pregnant (P) and 12 nonpregnant (NP) conscious New Zealand White rabbits. In an additional four P rabbits, the RSNA response to spontaneous parturition was measured. The blood pressure (BP)-RSNA relationship was generated by sequential inflations of aortic and vena caval perivascular occluders. Rest BP (P: 61 ± 2 vs. NP: 73 ± 2 mmHg) and the centering point of the baroreflex (P: 57 ± 2 vs. NP: 70 ± 2 mmHg) were lower ( P < 0.05) in term pregnancy. Baroreflex range (P: 246 ± 14% vs. NP 263 ± 24% of rest RSNA) was not affected by pregnancy. However, maximal reflex gain was moderately depressed (−44%) in P rabbits (P: −15 ± 1 vs. NP: −27 ± 4% of rest RSNA/mmHg; P < 0.05) due to a significant reduction in the slope coefficient. Delivery of a fetus was associated with strong renal sympathoexcitation. Peak RSNA averaged 80 ± 37% of smoke-elicited RSNA or 1,221 ± 288% of rest RSNA (mean ± SD). These results suggest that, in contrast to rat pregnancy, depressed arterial baroreflex control of RSNA in rabbit pregnancy is due primarily to a reduction in maximal gain rather than a reduction in the maximal sympathetic response to hypotension.

Cardiovagal regulation during combined hypoxic and orthostatic stress: fainters vs. nonfainters

2005 ◽  
Vol 98 (3) ◽  
pp. 1050-1056 ◽  
Author(s):  
John R. Halliwill ◽  
Christopher T. Minson
Keyword(s):  
Heart Rate ◽  
Individual Differences ◽  
Acute Hypoxia ◽  
Orthostatic Stress ◽  
Orthostatic Tolerance ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Hypoxic Conditions ◽  
Normotensive Subjects ◽  
Upright Tilt

We tested the hypothesis that individual differences in the effect of acute hypoxia on the cardiovagal arterial baroreflex would determine individual susceptibility to hypoxic syncope. In 16 healthy, nonsmoking, normotensive subjects (8 women, 8 men, age 20–33 yr), we assessed orthostatic tolerance with a 20-min 60° head-upright tilt during both normoxia and hypoxia (breathing 12% O2). On a separate occasion, we assessed baroreflex control of heart rate (cardiovagal baroreflex gain) using the modified Oxford technique during both normoxia and hypoxia. When subjects were tilted under hypoxic conditions, 5 of the 16 developed presyncopal signs or symptoms, and the 20-min tilt had to be terminated. These “fainters” had comparable cardiovagal baroreflex gain to “nonfainters” under both normoxic and hypoxic conditions (normoxia, fainters: −1.2 ± 0.2, nonfainters: −1.0 ± 0.2 beats·min−1·mmHg−1, P = 0.252; hypoxia, fainters: −1.3 ± 0.2, nonfainters: −1.0 ± 0.1 beats·min−1·mmHg−1, P = 0.208). Furthermore, hypoxia did not alter cardiovagal baroreflex gain in either group (both P > 0.8). It appears from these observations that hypoxic syncope results from the superimposed vasodilator effects of hypoxia on the cardiovascular system and not from a hypoxia-induced maladjustment in baroreflex control of heart rate.

Baroreflex control of renal sympathetic nerve activity and heart rate in near-term fetal sheep

2011 ◽  
Vol 96 (8) ◽  
pp. 736-744 ◽  
Author(s):  
Lindsea C. Booth ◽  
Alistair J. Gunn ◽  
Simon C. Malpas ◽  
Carolyn J. Barrett ◽  
Joanne O. Davidson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Fetal Sheep ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Near Term ◽  
Renal Sympathetic

scholarly journals Arterial baroreflex control of sympathetic nerve activity and heart rate in patients with type 2 diabetes

2016 ◽  
Vol 311 (5) ◽  
pp. H1170-H1179 ◽  
Author(s):  
Seth W. Holwerda ◽  
Lauro C. Vianna ◽  
Robert M. Restaino ◽  
Kunal Chaudhary ◽  
Colin N. Young ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Group Differences ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control

Despite greater blood pressure reactivity to acute cardiovascular stressors and a higher prevalence of hypertension in type 2 diabetes (T2D) patients, limited information is available regarding arterial baroreflex (ABR) control in T2D. We hypothesized that ABR control of muscle sympathetic nerve activity (MSNA) and heart rate (HR) are attenuated in T2D patients. Seventeen T2D patients (50 ± 2 yr; 31 ± 1 kg/m2), 9 weight-matched controls (WM-CON, 46 ± 2 yr; 32 ± 2 kg/m2) and 10 lean controls (Lean-CON, 49 ± 3 yr; 23 ± 1 kg/m2), underwent bolus infusions of sodium nitroprusside (100 μg) followed 60 s later by phenylephrine (150 μg) and weighted linear regression performed. No group differences in overall sympathetic baroreflex gain were observed (T2D: −2.5 ± 0.3 vs. WM-CON: −2.6 ± 0.2 vs. Lean-CON: −2.7 ± 0.4 arbitrary units·beat·mmHg−1, P > 0.05) or in sympathetic baroreflex gain when derived separately during blood pressure (BP) falls (nitroprusside) and BP rises (phenylephrine). In contrast, overall cardiac baroreflex gain was reduced in T2D patients compared with Lean-CON (T2D: 8.2 ± 1.5 vs. Lean-CON: 15.6 ± 2.9 ms·mmHg−1, P < 0.05) and also tended to be reduced in WM-CON (9.3 ± 1.9 ms·mmHg−1) compared with Lean-CON ( P = 0.059). Likewise, during BP rises, cardiac baroreflex gain was reduced in T2D patients and weight-matched controls compared with lean controls ( P < 0.05), whereas no group differences were found during BP falls ( P > 0.05). Sympathetic and cardiac ABR gains were comparable between normotensive and hypertensive T2D patients ( P > 0.05). These findings suggest preserved ABR control of MSNA in T2D patients compared with both obese and lean age-matched counterparts, with a selective impairment in ABR HR control in T2D that may be related to obesity.

Central mechanisms of acute ANG II modulation of arterial baroreflex control of renal sympathetic nerve activity

2002 ◽  
Vol 282 (5) ◽  
pp. H1592-H1602 ◽  
Author(s):  
Max G. Sanderford ◽  
Vernon S. Bishop
Keyword(s):  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Short-term intravenous infusion of angiotensin II (ANG II) into conscious rabbits reduces the range of renal sympathetic nerve activity (RSNA) by attenuating reflex disinhibition of RSNA. This action of ANG II to attenuate the arterial baroreflex range is exaggerated when ANG II is directed into the vertebral circulation, which suggests a mechanism involving the central nervous system. Because an intact area postrema (AP) is required for ANG II to attenuate arterial baroreflex-mediated bradycardia and is also required for maintenance of ANG II-dependent hypertension, we hypothesized that attenuation of maximum RSNA during infusion of ANG II involves the AP. In conscious AP-lesioned (APX) and AP-intact rabbits, we compared the effect of a 5-min intravenous infusion of ANG II (10 and 20 ng · kg−1 · min−1) on the relationship between mean arterial blood pressure (MAP) and RSNA. Intravenous infusion of ANG II into AP-intact rabbits resulted in a dose-related attenuation of maximum RSNA observed at low MAP. In contrast, ANG II had no effect on maximum RSNA in APX rabbits. To further localize the central site of ANG II action, its effect on the arterial baroreflex was assessed after a midcollicular decerebration. Decerebration did not alter arterial baroreflex control of RSNA compared with the control state, but as in APX, ANG II did not attenuate the maximum RSNA observed at low MAP. The results of this study indicate that central actions of peripheral ANG II to attenuate reflex disinhibition of RSNA not only involve the AP, but may also involve a neural interaction rostral to the level of decerebration.

Arterial baroreceptor reflex control of renal sympathetic nerve activity following chronic myocardial infarction in male, female, and ovariectomized female rats

2015 ◽  
Vol 309 (2) ◽  
pp. R169-R178 ◽  
Author(s):  
Maximilian I. Pinkham ◽  
Gillian A. Whalley ◽  
Sarah-Jane Guild ◽  
Simon C. Malpas ◽  
Carolyn J. Barrett
Keyword(s):  
Myocardial Infarction ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sham Group ◽  
Chronic Myocardial Infarction ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

There is controversy regarding whether the arterial baroreflex control of renal sympathetic nerve activity (SNA) in heart failure is altered. We investigated the impact of sex and ovarian hormones on changes in the arterial baroreflex control of renal SNA following a chronic myocardial infarction (MI). Renal SNA and arterial pressure were recorded in chloralose-urethane anesthetized male, female, and ovariectomized female (OVX) Wistar rats 6–7 wk postsham or MI surgery. Animals were grouped according to MI size (sham, small and large MI). Ovary-intact females had a lower mortality rate post-MI (24%) compared with both males (38%) and OVX (50%) ( P < 0.05). Males and OVX with large MI, but not small MI, displayed an impaired ability of the arterial baroreflex to inhibit renal SNA. As a result, the male large MI group (49 ± 6 vs. 84 ± 5% in male sham group) and OVX large MI group (37 ± 3 vs. 75 ± 5% in OVX sham group) displayed significantly reduced arterial baroreflex range of control of normalized renal SNA ( P < 0.05). In ovary-intact females, arterial baroreflex control of normalized renal SNA was unchanged regardless of MI size. In males and OVX there was a significant, positive correlation between left ventricle (LV) ejection fraction and arterial baroreflex range of control of normalized renal SNA, but not absolute renal SNA, that was not evident in ovary-intact females. The current findings demonstrate that the arterial baroreflex control of renal SNA post-MI is preserved in ovary-intact females, and the state of left ventricular dysfunction significantly impacts on the changes in the arterial baroreflex post-MI.

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