Contrasting effects of moderate vagal stimulation on heart rate and carotid sinus baroreflex-mediated sympathetic arterial pressure regulation in rats

This study tests the hypothesis that conscious rabbits late in pregnancy (P), but not at midgestation (MP), are less able to maintain arterial pressure during hemorrhage. Blood volume (BV) was elevated ( P < 0.05) by an average of 13 ± 4 (MP) and 35 ± 3% (P). Rabbits were bled in both the nonpregnant (NP) and P state at 2% of the initial BV per minute. The hemorrhage was stopped after arterial pressure decreased. In NP rabbits, arterial pressure was well maintained near control pressures of 70 ± 2 mmHg until 38 ± 2% of the initial BV was removed and then rapidly fell to reach a nadir at 35 ± 2 mmHg. In contrast, in P rabbits, basal arterial pressure was lower (61 ± 2 mmHg; P < 0.05) and gradually decreased to below control after <25% of the initial BV was removed. Moreover, the rapid hypotensive phase was triggered with a lower percent BV removal (33 ± 2%; P < 0.05). Basal heart rate was higher during P (149 ± 5 vs. 189 ± 9 beats/min; P < 0.05), and reflex increases were delayed. The slope of the relationship between arterial pressure and vasopressin was not modified during P, although the line was shifted to a lower pressure ( P < 0.05). Larger increases in plasma renin activity and ANG II concentration were produced during hemorrhage in P rabbits. In contrast, no differences in the changes in arterial pressure, heart rate, and vasopressin were found between NP and MP rabbits during hemorrhage, although increases in renin and ANG II were greater at MP ( P < 0.05). In summary, although P conscious rabbits are less able to maintain blood pressure during hemorrhage, this change is not evident at MP. These data suggest that the factors that mediate the P-induced alterations in arterial pressure regulation are not operative until late in gestation.

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Effect of vasopressin blockade on blood pressure during water deprivation in intact and baroreceptor-denervated conscious dogs

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1988.254.4.e490 ◽

1988 ◽

Vol 254 (4) ◽

pp. E490-E495 ◽

Cited By ~ 1

Author(s):

L. C. Gregory ◽

E. W. Quillen ◽

L. C. Keil ◽

D. Chang ◽

I. A. Reid

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Pressure ◽

Plasma Renin Activity ◽

Water Deprivation ◽

Carotid Sinus ◽

Plasma Renin ◽

Renin Activity ◽

Pressure Regulation ◽

Marked Contrast

Previous studies have provided evidence that vasopressin plays an important role in blood pressure regulation during water deprivation. However, these investigations have been complicated by reflex compensatory increases in cardiac output and renin secretion. The aim of the present study was to investigate the effect of blockade of the vasoconstrictor action of vasopressin in conscious water-deprived dogs in which the low- and/or high-pressure baroreceptors were denervated to minimize reflex responses. Vasopressin blockade in sham-operated dogs (n = 7) did not change arterial pressure. Heart rate rose from 78 +/- 9 to 119 +/- 13 beats/min (P less than 0.01), and plasma renin activity increased from 10.9 +/- 2.1 to 21.6 +/- 4.6 ng.ml-1.3 h-1 (P less than 0.01). In carotid sinus-denervated dogs (n = 6), vasopressin blockade again failed to decrease arterial pressure. Heart rate increased from 105 +/- 10 to 132 +/- 10 beats/min (P less than 0.01), and plasma renin activity rose from 6.8 +/- 1.7 to 15.5 +/- 2.4 ng.ml-1.3 h-1 (P less than 0.01). The antagonist also failed to change blood pressure in cardiac-denervated dogs (n = 5). Heart rate increased from 111 +/- 9 to 119 +/- 1 beats/min (P less than 0.01), but plasma renin activity did not increase significantly. In marked contrast, vasopressin blockade in sinoaortic/cardiac-denervated dogs (n = 7) promptly decreased arterial pressure from 115 +/- 8 to 94 +/- 7 mmHg (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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Center of arterial pressure regulation during rotation of normal and abnormal dogs

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1963.204.6.979 ◽

1963 ◽

Vol 204 (6) ◽

pp. 979-982 ◽

Cited By ~ 8

Author(s):

Edward E. Smith ◽

Arthur C. Guyton

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Arterial Pressure ◽

Carotid Sinus ◽

Regulatory Mechanisms ◽

Pressure Regulation ◽

Transverse Axis ◽

Total Spinal Anesthesia ◽

Axis Of Rotation ◽

Arterial Pressure Regulation

Dogs were rotated about a horizontal transverse axis. By shifting the axis of rotation along the length of the animal's body it was possible to find a point at which arterial pressure remained almost constant in all positions of rotation. In most normal dogs such an axis lay in the neck a few centimeters cephalad to the sternum. Denervation of carotid sinus and aortic pressoreceptors caused a caudal shift of the axis; total spinal anesthesia did also, and to a much greater degree. This study demonstrates that pressure regulatory mechanisms operate to maintain a constant arterial pressure in the neck, probably for the minimizing of postural alterations of cerebral blood flow

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Effects of calcium channel antagonists on carotid sinus baroreflex control of arterial pressure and heart rate in anesthetized dogs.

Circulation Research ◽

10.1161/01.res.64.2.276 ◽

1989 ◽

Vol 64 (2) ◽

pp. 276-286 ◽

Cited By ~ 8

Author(s):

D F Rigel ◽

R W Millard

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Calcium Channel ◽

Carotid Sinus ◽

Calcium Channel Antagonists ◽

Baroreflex Control ◽

Carotid Sinus Baroreflex ◽

Anesthetized Dogs

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Enhanced carotid sinus baroreflex responses in dogs with chronic A-V block

Journal of Applied Physiology ◽

10.1152/jappl.1975.38.1.1 ◽

1975 ◽

Vol 38 (1) ◽

pp. 1-4 ◽

Cited By ~ 1

Author(s):

J. DiSalvo ◽

R. Reynolds ◽

J. L. Robinson ◽

G. Grupp

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Carotid Sinus ◽

Ventricular Rate ◽

Vagus Nerves ◽

Atrial Rate ◽

Carotid Sinus Baroreflex ◽

Sinus Pressure

Effects of carotid sinus pressure on arterial pressure, atrial rate, and ventricular rate were examined in anesthetized normal dogs and in dogs with chronic complete A-V block. Change in arterial pressure per mmHg change in sinus pressure was 0.8 plus or minus 0.2 mmHg for controls but increased (P is less than 0.001) to 1.6 plus or minus 0.1 mmHg in A-V blocked dogs. Arterial pressure was 140–145 mmHg at low sinus pressure in both groups, but at high sinus pressure arterial pressure was significantly lower in A-V blocked dogs (44 plus or minus 4 mmHg) than in controls (92 plus or minus 8 mmHg). These differences were virtually abolished after vagotomy. Heart rate increased in normal dogs as sinus pressure was increased before vagotomy, but decreased after vagotomy. In blocked dogs atrial and ventricular rates decreased at high sinus pressure either before or after vagotomy. The results show that reflex circulatory responses to changes in carotid sinus pressure are enhanced in dogs with A-V block. This enhancement may involve attenuation of buffering influences exerted from other baroreceptors whose afferents are in the vagus nerves.

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Plasma hyperosmolality and arterial pressure regulation during heating in dehydrated and awake rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.275.5.r1703 ◽

1998 ◽

Vol 275 (5) ◽

pp. R1703-R1711 ◽

Cited By ~ 15

Author(s):

Yasufumi Nakajima ◽

Hiroshi Nose ◽

Akira Takamata

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Skin Blood Flow ◽

Plasma Osmolality ◽

Cardiovascular Responses ◽

Pressure Regulation ◽

Highly Correlated ◽

Arterial Pressure Regulation

To gain better insights into the effect of dehydration on thermal and cardiovascular regulation during hyperthermia, we examined these regulatory responses during body heating in rats under isosmotic hypovolemia and hyperosmotic hypovolemia. Rats were divided into four groups: normovolemic and isosmotic (C), hypovolemic and isosmotic [L, plasma volume loss (ΔPV) = −20% of control], hypovolemic and less hyperosmotic [HL1, increase in plasma osmolality (ΔPosm) = 23 mosmol/kgH2O, ΔPV = −16%], and hypovolemic and more hyperosmotic (HL2, ΔPosm = 52 mosmol/kgH2O, ΔPV = −17%). Hyperosmolality was attained by subcutaneous injection of hypertonic saline and hypovolemia by intra-arterial injection of furosemide before heating. Then rats were placed in a thermocontrolled box (35°C air temperature, ∼20% relative humidity) for 1–2 h until rectal temperatures (Tre) reached 40.0°C. Mean arterial pressure in L decreased with rise in Tre( P < 0.001), whereas mean arterial pressure remained constant in the other groups. Maximal tail skin blood flow in L, HL1, and HL2 was decreased to ∼30% of that in C ( P < 0.001). Tre threshold for tail skin vasodilation (TVD) was not changed in L, whereas the threshold shifted higher in the HL groups. Trethreshold for TVD was highly correlated with Posm( r = 0.94, P < 0.001). Heart rate in the HL groups increased with rise in Tre( P < 0.001), whereas it remained unchanged in C and L. Cardiovascular responses to heating were not influenced by V1 antagonist in C, L, and HL2. Thus isotonic hypovolemia attenuates maximal tail skin blood flow, whereas hypertonic hypovolemia causes an upward shift of Tre threshold for TVD and an increase in heart rate during hyperthermia. These results suggest that plasma hyperosmolality stimulates pressor responses in the hypovolemic condition that subsequently contribute to arterial pressure regulation during heat stress.

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Neural arc of baroreflex optimizes dynamic pressure regulation in achieving both stability and quickness

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.3.h882 ◽

1996 ◽

Vol 271 (3) ◽

pp. H882-H890 ◽

Cited By ~ 52

Author(s):

Y. Ikeda ◽

T. Kawada ◽

M. Sugimachi ◽

O. Kawaguchi ◽

T. Shishido ◽

...

Keyword(s):

Arterial Pressure ◽

Mechanical Response ◽

Carotid Sinus ◽

Dynamic Pressure ◽

Open Loop ◽

Pressure Regulation ◽

Frequency Range ◽

Sinus Pressure ◽

Arterial Pressure Regulation

The baroreflex loop consists of a fast neural arc and a slow mechanical arc. We hypothesized that the neural baroreflex arc compensates the slow mechanical response and thus improves the quality of blood pressure regulation. We estimated the open-loop transfer characteristics of the neural baroreflex arc (HP), i.e., from carotid sinus pressure to sympathetic nerve activity (SNA), and that of the effective peripheral baroreflex arc (Hp), i.e., from SNA to arterial pressure, in anesthetized rabbits. The gain of Hn was constant below 0.12 +/- 0.057 Hz and increased with a slope of 6.1 +/- 0.06 dB/octave above its frequency up to 1 Hz. In contrast, the gain of Hp was constant below 0.071 +/- 0.03 Hz and decreased with a slope of -11.0 +/- 1.48 dB/octave above the frequency. These data indicate that Hn accelerates slow peripheral responses in the frequency range of 0.1-1 Hz. Although too much acceleration in the high-frequency range could result in instability of the system, numerical analysis of the closed-loop baroreflex response indicated that the neural arc optimized arterial pressure regulation in achieving both stability and quickness.

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