156 Rilmenidine sympatholytic activity preserves mental and orthostatic sympathetic response and epinephrine secretion

2003 ◽  
Vol 24 (5) ◽  
pp. 15
Author(s):  
M ESLER
Keyword(s):  
Diabetes ◽  
1994 ◽  
Vol 43 (8) ◽  
pp. 1052-1060 ◽  
Author(s):  
M. Hamilton-Wessler ◽  
R. N. Bergman ◽  
J. B. Halter ◽  
R. M. Watanabe ◽  
C. M. Donovan
Keyword(s):  

2021 ◽  
Author(s):  
Marcus K. Taylor ◽  
Nikki E. Barczak‐Scarboro ◽  
D. Christine Laver ◽  
Lisa M. Hernández

2013 ◽  
Vol 155 (8) ◽  
pp. 1501-1510 ◽  
Author(s):  
Michael Moussouttas ◽  
Meghna Bhatnager ◽  
Thanh T. Huynh ◽  
Edwin W. Lai ◽  
John Khoury ◽  
...  

1973 ◽  
Vol 160 (4) ◽  
pp. 317-320 ◽  
Author(s):  
R. Kullmann ◽  
H. G. Junk

2011 ◽  
Vol 301 (6) ◽  
pp. R1831-R1837 ◽  
Author(s):  
Jian Cui ◽  
Urs A. Leuenberger ◽  
Zhaohui Gao ◽  
Lawrence I. Sinoway

We recently showed that a fixed volume (i.e., 40 ml) of saline infused into the venous circulation of an arterially occluded vascular bed increases muscle sympathetic nerve activity (MSNA) and blood pressure. In the present report, we hypothesized that the volume and rate of infusion would influence the magnitude of the sympathetic response. Blood pressure, heart rate, and MSNA were assessed in 13 young healthy subjects during forearm saline infusions (arrested circulation). The effects of different volumes of saline (i.e., 2%, 3%, 4%, or 5% forearm volume at 30 ml/min) and different rates of infusion (i.e., 5% forearm volume at 10, 20, or 30 ml/min) were evaluated. MSNA and blood pressure responses were linked with the infusion volume. Infusion of 5% of forearm volume evoked greater MSNA responses than did infusion of 2% of forearm volume (Δ11.6 ± 1.9 vs. Δ3.1 ± 1.8 bursts/min and Δ332 ± 105 vs. Δ38 ± 32 units/min, all P < 0.05). Moreover, greater MSNA responses were evoked by saline infusion at 30 ml/min than 10 ml/min ( P < 0.05). Sonographic measurements confirmed that the saline infusions induced forearm venous distension. The results suggest that volume and rate of saline infusion are important factors in evoking sympathetic activation. We postulate that venous distension contributes to cardiovascular autonomic adjustment in humans.


1989 ◽  
Vol 67 (5) ◽  
pp. 2095-2100 ◽  
Author(s):  
V. K. Somers ◽  
A. L. Mark ◽  
D. C. Zavala ◽  
F. M. Abboud

The sympathetic response to hypoxia depends on the interaction between chemoreceptor stimulation (CRS) and the associated hyperventilation. We studied this interaction by measuring sympathetic nerve activity (SNA) to muscle in 13 normal subjects, while breathing room air, 14% O2, 10% O2, and 10% O2 with added CO2 to maintain isocapnia. Minute ventilation (VE) and blood pressure (BP) increased significantly more during isocapnic hypoxia (IHO) than hypocapnic hypoxia (HHO). In contrast, SNA increased more during HHO [40 +/- 10% (SE)] than during IHO (25 +/- 19%, P less than 0.05). To determine the reason for the lesser increase in SNA with IHO, 11 subjects underwent voluntary apnea during HHO and IHO. Apnea potentiated the SNA responses to IHO more than to HHO. SNA responses to IHO were 17 +/- 7% during breathing and 173 +/- 47% during apnea whereas SNA responses to HHO were 35 +/- 8% during breathing and 126 +/- 28% during apnea. During ventilation, the sympathoexcitation of IHO (compared with HHO) is suppressed, possibly for two reasons: 1) because of the inhibitory influence of activation of pulmonary afferents as a result of a greater increase in VE, and 2) because of the inhibitory influence of baroreceptor activation due to a greater rise in BP. Thus in humans, the ventilatory response to chemoreceptor stimulation predominates and restrains the sympathetic response. The SNA response to chemoreceptor stimulation represents the net effect of the excitatory influence of the chemoreflex and the inhibitory influence of pulmonary afferents and baroreceptor afferents.


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