scholarly journals Adjustment of Reflex Bradycardia to Elevated Arterial Pressure in Conscious Rabbits

1962 ◽  
Vol 11 (4) ◽  
pp. 746-752 ◽  
Author(s):  
Natalie Alexander ◽  
Marjorie De Cuir
1998 ◽  
Vol 274 (5) ◽  
pp. R1283-R1294 ◽  
Author(s):  
Simon C. Malpas ◽  
Roger G. Evans ◽  
Geoff A. Head ◽  
Elena V. Lukoshkova

We have examined the role of the renal sympathetic nerves in the renal blood flow (RBF) response to hemorrhage in seven conscious rabbits. Hemorrhage was produced by blood withdrawal at 1.35 ml ⋅ min−1 ⋅ kg−1for 20 min while RBF and renal sympathetic nerve activity (RSNA) were simultaneously measured. Hemorrhage was associated with a gradual increase in RSNA and decrease in RBF from the 4th min. In seven denervated animals, the resting RBF before hemorrhage was significantly greater (48 ± 1 vs. 31 ± 1 ml/min intact), and the decrease in RBF did not occur until arterial pressure also began to fall (8th min); however, the overall percentage change in RBF by 20 min of blood withdrawal was similar. Spectral analysis was used to identify the nature of the oscillations in each variable. Before hemorrhage, a rhythm at ∼0.3 Hz was observed in RSNA, although not in RBF, whose spectrogram was composed mostly of lower-frequency (<0.25 Hz) components. The denervated group of rabbits had similar frequency spectrums for RBF before hemorrhage. RSNA played a role in dampening the effect of oscillations in arterial pressure on RBF as the transfer gain between mean arterial pressure (MAP) and RBF for frequencies >0.25 Hz was significantly less in intact than denervated rabbits (0.83 ± 0.12 vs. 1.19 ± 0.10 ml ⋅ min−1 ⋅ mmHg−1). Furthermore, the coherence between MAP and RBF was also significantly higher in denervated rabbits, suggesting tighter coupling between the two variables in the absence of RSNA. Before the onset of significant decreases in arterial pressure (up to 10 min), there was an increase in the strength of oscillations centered around 0.3 Hz in RSNA. These were accompanied by increases in the spectral power of RBF at the same frequency. As arterial pressure fell in both groups of animals, the dominant rhythm to emerge in RBF was centered between 0.15 and 0.20 Hz and was present in intact and denervated rabbits. It is speculated that this is myogenic in origin. We conclude that RSNA can induce oscillations in RBF at 0.3 Hz, plays a significant role in altering the effect of oscillations in arterial pressure on RBF, and mediates a proportion of renal vasoconstriction during hemorrhage in conscious rabbits.


1995 ◽  
Vol 269 (5) ◽  
pp. R1289-R1293 ◽  
Author(s):  
M. Fukuhara ◽  
T. Tsuchihashi ◽  
I. Abe ◽  
M. Fujishima

Adrenomedullin is a vasodilative peptide and shows slight homology with calcitonin gene-related peptide. In the present study, we investigated the effects of adrenomedullin on cardiovascular and neurohormonal responses in 13 conscious rabbits. The animals were chronically instrumented with bipolar electrodes on the left renal sympathetic nerve. Intravenous administration of human adrenomedullin (10, 100, 1,000, and 3,000 pmol/kg, n = 6) caused a dose-dependent reduction in mean arterial pressure (0 +/- 2, -1 +/- 2, -19 +/- 2, and -29 +/- 4 mmHg, respectively) concomitant with increases in heart rate, renal sympathetic nerve activity, plasma renin activity, and plasma norepinephrine. The significant reduction in mean arterial pressure induced by 1,000 pmol/kg of adrenomedullin occurred within 1 min after injection and lasted for 15 min (n = 7). In contrast, the significant increases in heart rate and renal sympathetic nerve activity lasted for more than 50 min. When mean arterial pressure was decreased by 15 mmHg by adrenomedullin, the increases in heart rate and renal sympathetic nerve activity were 53 +/- 8 beats/min and 78 +/- 13%, respectively, which were significantly smaller than those induced by intravenous injection of sodium nitroprusside (102 +/- 14 beats/min and 155 +/- 34%, respectively). These results suggest that intravenous adrenomedullin exerts a hypotensive action that is associated with the attenuated reflex-mediated sympathetic activation.


1983 ◽  
Vol 245 (2) ◽  
pp. H210-H217 ◽  
Author(s):  
F. J. Gordon ◽  
A. L. Mark

The purpose of this study was to examine baroreflex control of vascular resistance and heart rate in prehypertensive Dahl salt-sensitive (DS) and salt-resistant (DR) rats. Urethan-anesthetized normotensive DS rats demonstrated significantly impaired baroreflex control of both hindlimb vascular resistance and heart rate. This impairment was not secondary to elevated arterial pressure since blood pressure did not differ between DR and DS rats fed a low sodium diet. Vascular baroreflex responses were shown to depend on the integrity of efferent sympathetic innervation and to be mediated by the sinoaortic afferent arterial baroreceptors. No strain difference was observed for hindlimb vasodilation produced by papaverine or graded doses of nitroprusside, indicating that differences in resistance vessel vasodilator capacity or responsiveness could not account for differences in baroreflex responses. Since impaired baroreflex control was evident in DS rats prior to any elevation in arterial pressure, this abnormality may contribute to the DS rat's genetic propensity to develop hypertension.


1999 ◽  
Vol 277 (3) ◽  
pp. R675-R681 ◽  
Author(s):  
Virginia L. Brooks ◽  
Colleen M. Kane ◽  
Lisa S. Welch

Late pregnant (P) conscious rabbits are less able to maintain arterial pressure during hemorrhage than nonpregnant (NP) animals. This study tested the hypothesis that the difference is due in part to less reflex vasoconstriction when the rabbits are P. Rabbits ( n = 14) were instrumented with arterial and venous catheters as well as ultrasonic flow probes around the superior mesenteric, renal, and/or terminal aortic arteries. Pregnancy increased ( P < 0.05) blood volume [235 ± 5 (P) vs. 171 ± 3 (NP) ml], terminal aortic conductance [1.88 ± 0.11 (P) vs. 0.98 ± 0.06 (NP) ml ⋅ min−1 ⋅ mmHg−1], mesenteric conductance [1.20 ± 0.19 (P) vs. 0.80 ± 0.05 (NP) ml ⋅ min−1 ⋅ mmHg−1], and heart rate [191 ± 4 (P) vs. 162 ± 3 (NP) beats/min] and decreased arterial pressure [59 ± 1 (P) vs. 67 ± 2 (NP) mmHg; P < 0.05]. Renal conductance was unaltered. The rabbits were bled in both the NP and P states at 2% of the initial blood volume per minute until arterial pressure fell below 45 mmHg. Arterial pressure fell with less blood loss in P rabbits [28 ± 2% (P) vs. 39 ± 2% (NP) of initial blood volume; P < 0.001]. Terminal aortic conductance decreased ( P < 0.001) before the pressure fall in both groups, but the response was reduced in P rabbits. Mesenteric and renal conductances did not change in either group before the blood pressure fall. During the pressure fall, terminal aortic conductance increased ( P < 0.05) only in NP rabbits. Mesenteric conductance increased in both groups. In summary, rabbits in late gestation are less able to maintain arterial pressure during hemorrhage, at least in part because of reduced vasoconstriction in tissues perfused by the terminal aorta.


1997 ◽  
Vol 272 (1) ◽  
pp. R208-R216 ◽  
Author(s):  
Y. H. Yu ◽  
W. W. Blessing

We determined whether alerting stimuli cause cutaneous vasoconstriction in conscious rabbits. We compared ear blood flow with renal, mesenteric, and femoral flows at rest and in response to nonnoxious alerting stimuli, which induced theta-rhythm (4-9 Hz) in the simultaneously recorded hippocampal electroencephalogram (EEG). theta-Inducing stimuli (e.g., whistles and fur touches) reduced ear flow by 95 +/- 6%, commencing 1-2 s after the EEG change and lasting 45 s. Renal flow did not significantly change with alerting stimuli, mesenteric and femoral flows slightly decreased, arterial pressure transiently rose (+10 +/- 3 mmHg), and heart rate fell (+43 +/- 9 beats/min). At rest, the coefficient of variation for ear flow (62 +/- 6%) was greater than for other flows (P < 0.01). Phentolamine (1 mg/kg iv) reduced this coefficient to 29 +/- 4% (P < 0.01). Our study demonstrates that alerting responses in conscious rabbits are associated with selective cutaneous vasoconstriction, without increase in flow to skeletal muscle.


Hypertension ◽  
2001 ◽  
Vol 38 (5) ◽  
pp. 1096-1100 ◽  
Author(s):  
Kiyoshi Matsumura ◽  
Takuya Tsuchihashi ◽  
Isao Abe

1981 ◽  
Vol 61 (1) ◽  
pp. 97-105 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin

1. Systemic and regional vascular changes were measured in conscious rabbits after intravenous sodium meclofenamate, captopril and phentolamine. These drugs were used respectively to inhibit prostaglandin synthesis and angiotensin-converting enzyme, and to block α-adrenoceptors. 2. Meclofenamate reduced renal and adrenal blood flow by 11 and 28% respectively, and doubled hepatic artery flow. The effect on renal and adrenal flow persisted in the presence of phentolamine. 3. Captopril decreased estimated peripheral resistance and increased cardiac output without changing arterial pressure. Kidney and adrenal flow increased by 70 and 21% respectively. 4. Phentolamine reduced arterial pressure and doubled flow to skeletal muscle and increased hepatic artery flow to the liver. 5. Splenic blood flow was unaffected by meclofenamate, captopril or phentolamine alone. Meclofenamate given after captopril caused a halving of splenic flow and a rise in arterial pressure; these effects were prevented by phentolamine. 6. The results point to a continuing effect of prostaglandin synthesis in maintaining blood flow to the kidney and adrenal gland independent of α-adrenoceptor activation in resting conscious rabbits. An important modulating effect of prostaglandins on sympathetic vascular tone in the spleen is suggested.


1990 ◽  
Vol 39 (4) ◽  
pp. 565-569
Author(s):  
Shin-ichiro KATSUDA ◽  
Shiro TAJI ◽  
Hiroshi HOSOMI

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