Blood pressure normalization in carotid barodenervated rats: role of cardiac output

1993 ◽  
Vol 71 (10-11) ◽  
pp. 783-790 ◽  
Author(s):  
Mahmoud M. El-Mas ◽  
Robert G. Carroll ◽  
Abdel A. Abdel-Rahman

This study evaluated the role of sympathetic nervous system (SNS) activity, peripheral hemodynamic changes, and pressure diuresis in blood pressure (BP) normalization in carotid barodenervated rats. The acute and short-term effects of carotid barodenervation or sham operation on blood pressure, heart rate, cardiac output, stroke volume, total peripheral resistance, and plasma catecholamine levels were determined. Changes in plasma volume, urine output, and water and food intakes were also measured. Surgical denervation of the carotid baroreceptors resulted in rapid rises in blood pressure and heart rate in anesthetized rats. These changes were associated with significant increases in plasma catecholamine levels and total peripheral resistance whereas the cardiac index and stroke volume remained unchanged. After recovery from the anesthesia, the blood pressure of carotid barodenervated rats was still significantly higher than that of sham-operated rats at 3 and 24 h after denervation and returned to sham-operated levels by 48 h. Plasma catecholamine levels and total peripheral resistance were higher in carotid barodenervated than in sham-operated rats on the 2 days following surgery. On the other hand, cardiac index (32 ± 1 vs. 40 ± 2 mL∙min−1∙100 g−1 body mass) and stroke volume (205 ± 13 vs. 283 ± 4 μL/beat) were significantly lower on day 2 in carotid barodenervated than in sham-operated rats, which suggests a compensatory role for carotid output in blood pressure normalization after carotid barodenervaton. Both carotid barodenervation and sham operation caused a reduction in water and food intakes but the responses were greater in carotid barodenervated rats. Urine output was drastically reduced for at least 3 days after denervation and so were body masses and water and food intakes. A pressure diuresis that occurred only on the first day after carotid barodenervation when the blood pressure was still elevated may have contributed to blood pressure normalization. Plasma volumes measured 1 and 5 days after carotid barodenervation or sham operation were similar. These findings suggest that blood pressure normalization in carotid-barodenervated rats cannot be accounted for by restoration of the sympathetic nervous system activity to normal levels but rather to a transient pressure diuresis and a reduction in cardiac output which act to offset increases in sympathetic nervous system activity and total peripheral resistance.Key words: carotid barodenervation, blood pressure, sympathetic nervous system, cardiac output, total peripheral resistance, pressure diuresis.

1985 ◽  
Vol 248 (1) ◽  
pp. E95-E100 ◽  
Author(s):  
D. Baum ◽  
J. B. Halter ◽  
G. J. Taborsky ◽  
D. Porte

The effects of intravenous pentobarbital were studied in dogs. Plasma pentobarbital concentrations were inversely related to epinephrine and norepinephrine concentrations. Plasma catecholamines appeared fully suppressed at pentobarbital levels greater than 25-30 micrograms/ml. Furthermore, pentobarbital levels were negatively related to rectal temperature, heart rate, and mean blood pressure. The methods of pentobarbital administration influenced plasma pentobarbital as well as epinephrine and norepinephrine levels, temperature, heart rate, and blood pressure. These observations suggest the possibility that pentobarbital inhibits the sympathetic nervous system, which in turn may affect temperature, heart rate, and blood pressure. Because pentobarbital anesthesia affects plasma catecholamine concentrations, the regimen used in animal models requires consideration when interpreting data potentially influenced by the sympathetic nervous system.


1994 ◽  
Vol 266 (2) ◽  
pp. H435-H439 ◽  
Author(s):  
B. Kennedy ◽  
D. Shannahoff-Khalsa ◽  
M. G. Ziegler

Plasma levels of norepinephrine (NE) vary rhythmically in humans and animals with an ultradian (shorter than 1 day) periodicity. We repeatedly measured plasma NE levels, blood pressure, cardiac output, and total peripheral resistance in nine normal resting subjects over 5 h. Plasma NE correlated with total peripheral resistance (Z = 0.322, P < 0.0002) and inversely with cardiac output (Z = -0.276, P < 0.0002) for the nine subjects overall. The correlations were strongest in subjects with the most spontaneous variability in total peripheral resistance. These findings suggest that spontaneous oscillations in plasma NE levels reflect alterations in sympathetic nervous activity to resistance blood vessels. The negative correlation between cardiac output and plasma NE levels may result from the very minor cardiac NE spillover into plasma and the inverse relationship between cardiac output and total peripheral resistance.


2021 ◽  
Vol 26 (6) ◽  
pp. 612-619
Author(s):  
V. A. Tsyrlin ◽  
N. V. Kuzmenko ◽  
M. G. Pliss

The review presents data on regular and irregular waves of blood pressure (BP) recorded during its invasive (intra-arterial) and non-invasive registration. Regular pulse waves, Traube-Hering waves (second-order waves) and Mayer waves (third-order waves) are described. The characteristic of circadian and ultradian super slow waves is given. The role of the sympathetic nervous system in the origin of regular waves of BP and their relationship with the magnitude of the baroreceptor reflex are shown. Attention is drawn to the role of changes in the minute volume of blood circulation and peripheral resistance to blood flow in the occurrence of fluctuations in BP. We also review the methods and features of BP registration, which enable identification and analysis of irregular high-frequency fluctuations in BP, the relationship of these fluctuations with the magnitude of the baroreceptor reflex and the activity of the sympathetic nervous system. The data on the amplitude of high-frequency irregular fluctuations in BP in animals with simulated hypertension are presented. The review draws attention to the possibility of recording regular fluctuations in BP during its constant non-invasive registration.


1980 ◽  
Vol 52 (4) ◽  
pp. 473-481 ◽  
Author(s):  
Wise Young ◽  
Vincent DeCrescito ◽  
John J. Tomasula ◽  
Victor Ho

✓ Spinal cord injury consistently evokes a transient 3- to 4-minute rise in systemic pressure, followed by prolonged hypotension. Because the role of the sympathetic nervous system in these blood pressure changes is not clear, the pressure responses were studied using systematic ablation of the peripheral sympathetic nervous system. In total, 24 cats were subjected to bilateral thoracic sympathectomy, adrenalectomy, splanchnicectomy, combinations of the preceding, sham operation, or no treatment. Either 3 or 24 hours after the ablations, the blood pressure responses were evoked by 400 gm-cm contusions of the thoracic cord. Although neither thoracic sympathectomy nor adrenalectomy alone abolished the hypertensive phase, the combination of the two procedures did. This suggests that both the thoracic sympathetic ganglia and the adrenal glands participate in the pressor response. Thoracic sympathectomy affected primarily the early part, whereas adrenalectomy diminished the later part of the hypertensive response. This correlates with the function of the former being neurally and the latter being humorally mediated. None of the sympathetic lesions consistently affected the hypotensive phase. Spinal contusion injury produces widespread sympathetic activation, mediating the hypertensive changes.


2007 ◽  
Vol 113 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Niels P. Riksen ◽  
Marlies Bosselaar ◽  
Stephan J.L. Bakker ◽  
Robert J. Heine ◽  
Gerard A. Rongen ◽  
...  

Plasma NEFA (non-esterified fatty acid) concentrations are elevated in patients with obesity. In the present study we first aimed to provide an integral haemodynamic profile of elevated plasma NEFAs by the simultaneous assessment of blood pressure, pulse wave velocity, FBF (forearm blood flow) and sympathetic nervous system activity during acute elevation of NEFAs. Secondly, we hypothesized that NEFA-induced vasodilation is mediated by adenosine receptor stimulation. In a randomized cross-over trial in healthy subjects, Intralipid® was infused for 2 h to elevate plasma NEFAs. Glycerol was administered as the Control infusion. We assessed blood pressure, pulse wave velocity, FBF (using venous occlusion plethysmography) and sympathetic nervous system activity by measurement of noradrenaline and adrenaline. During the last 15 min of Intralipid®/Control infusion, the adenosine receptor antagonist caffeine (90 μg·min−1·dl−1) was administered into the brachial artery of the non-dominant arm. Compared with Control infusion, Intralipid® increased pulse wave velocity, SBP (systolic blood pressure) and pulse pressure, as well as FBF (from 1.8±0.2 to 2.7±0.6 and from 2.3±0.2 to 2.7±0.6 ml·min−1·dl−1 for Intralipid® compared with Control infusion; P<0.05, n=9). Although in a positive control study caffeine attenuated adenosine-induced forearm vasodilation (P<0.01, n=6), caffeine had no effect on Intralipid®-induced vasodilation (P=0.5). In conclusion, elevation of plasma NEFA levels increased pulse wave velocity, SBP and pulse pressure. FBF was also increased, either by baroreflex-mediated inhibition of the sympathetic nervous system or by a direct vasodilating effect of NEFAs. As the adenosine receptor antagonist caffeine could not antagonize the vasodilator response, this response is not mediated by adenosine receptor stimulation.


Hypertension ◽  
2018 ◽  
Vol 72 (5) ◽  
pp. 1103-1108 ◽  
Author(s):  
Chloe Park ◽  
Abigail Fraser ◽  
Laura D. Howe ◽  
Siana Jones ◽  
George Davey Smith ◽  
...  

1988 ◽  
Vol 254 (4) ◽  
pp. H811-H815 ◽  
Author(s):  
D. G. Parkes ◽  
J. P. Coghlan ◽  
J. G. McDougall ◽  
B. A. Scoggins

The hemodynamic and metabolic effects of long-term (5 day) infusion of human atrial natriuretic factor (ANF) were examined in conscious chronically instrumented sheep. Infusion of ANF at 20 micrograms/h, a rate below the threshold for an acute natriuretic effect, decreased blood pressure by 9 +/- 1 mmHg on day 5, associated with a fall in calculated total peripheral resistance. On day 1, ANF reduced cardiac output, stroke volume, and blood volume, effects that were associated with an increase in heart rate and calculated total peripheral resistance and a small decrease in blood pressure. On days 4 and 5 there was a small increase in urine volume and sodium excretion. On day 5 an increase in water intake and body weight was observed. No change was seen in plasma concentrations of renin, arginine vasopressin, glucose, adrenocorticotropic hormone, or protein. This study suggests that the short-term hypotensive effect of ANF results from a reduction in cardiac output associated with a fall in both stroke volume and effective blood volume. However, after 5 days of infusion, ANF lowers blood pressure via a reduction in total peripheral resistance.


Hypertension ◽  
1999 ◽  
Vol 34 (1) ◽  
pp. 102-106 ◽  
Author(s):  
Mario J. Carvalho ◽  
Anton H. van den Meiracker ◽  
Frans Boomsma ◽  
Joao Freitas ◽  
Arie J. Man in ‘t Veld ◽  
...  

1992 ◽  
Vol 262 (6) ◽  
pp. E763-E778 ◽  
Author(s):  
I. A. Reid

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.


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