Cardiovascular and neuroendocrine responses to baroreceptor denervation in baboons

1990 ◽  
Vol 258 (4) ◽  
pp. R930-R938 ◽  
Author(s):  
R. E. Shade ◽  
V. S. Bishop ◽  
J. R. Haywood ◽  
C. K. Hamm
Keyword(s):  
Blood Pressure ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.

Sex differences in central adrenoreceptor-mediated vasopressin response to hemorrhage

1991 ◽  
Vol 260 (5) ◽  
pp. E780-E786 ◽  
Author(s):  
J. D. Stone ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Sex Differences ◽  
Mean Arterial Blood Pressure ◽  
Intracerebroventricular Injection ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Blood Pressure Responses ◽  
Induced Changes

Hemorrhage-induced changes in the plasma vasopressin concentration and mean arterial blood pressure (MABP) were studied in conscious rats of both sexes with and without central alpha 1-adrenoreceptor blockade. Rats were subjected to two sequential hemorrhages (H1 and H2), each 0.8% of body weight after an intracerebroventricular injection of the alpha 1-adrenoreceptor antagonist corynanthine or of vehicle. H1 stimulated vasopressin secretion more in proestrous females than in males; there were no significant sex-related differences in responses to H2. Corynanthine pretreatment attenuated the vasopressin response to H2 in males, potentiated this response in proestrous females, but had no effect in estrous females. MABP decreased after H1 in all female groups and in corynanthine-pretreated males. After H2, all groups were hypotensive to the same extent. These data indicate that central alpha 1-adrenoreceptor-mediated pathways participate in vasopressin and blood pressure responses to hemorrhage, but their role is complex and is dependent on gender and on the phase of the estrous cycle.

Carotid arterial control of vasopressin secretion in sheep

1984 ◽  
Vol 247 (3) ◽  
pp. R589-R594 ◽  
Author(s):  
C. E. Wood ◽  
L. C. Keil ◽  
A. M. Rudolph
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Concentrations ◽  
Carotid Occlusion ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Vasopressin Secretion ◽  
Carotid Arterial

The purpose of this study was to test the role of carotid arterial mechanoreceptors in the control of vasopressin secretion in conscious 6- to 7-wk-old lambs. Bilateral carotid occlusion decreased lingual arterial pressure and stimulated reflex increases in heart rate and femoral arterial blood pressure but did not significantly alter plasma concentrations of vasopressin. Acute vagosympathetic blockade, produced by injection of 2% lidocaine onto the vagosympathetic trunks, did not significantly alter heart rate or blood pressure but did stimulate a slow increase in plasma vasopressin concentration, suggesting that afferent vagal fibers tonically inhibit vasopressin secretion. Bilateral carotid occlusion after vagosympathetic blockade stimulated a brisk increase in plasma vasopressin that was larger than the response to vagosympathetic blockade alone. These results suggest that vasopressin secretion in lambs is partially controlled by arterial mechanoreceptors in the carotid sinus and by extracarotid receptors with vagosympathetic afferent fibers.

Effects of chronic NO synthase inhibition in rats on renin-angiotensin system and sympathetic nervous system

1995 ◽  
Vol 268 (6) ◽  
pp. H2267-H2273 ◽  
Author(s):  
A. Zanchi ◽  
N. C. Schaad ◽  
M. C. Osterheld ◽  
E. Grouzmann ◽  
J. Nussberger ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Norepinephrine ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Sympathetic Nervous

This study was designed to assess the role of renin and of the sympathoadrenal system in the maintenance of the hypertension induced by chronic nitric oxide synthase (NOS) inhibition in rats kept on a normal (RS) or a low-sodium (LS) diet. With the administration of NG-nitro-L-arginine methyl ester (L-NAME) in drinking water (0.4 milligrams) for 6 wk, mean intra-arterial blood pressure rose to a similar extent to 201 mmHg in the RS and 184 mmHg in the LS animals. Simultaneously, plasma norepinephrine was increased to 838 and 527 pg/ml and epinephrine to 2,041 and 1,341 pg/ml in RS and LS, respectively. Plasma neuropeptide Y levels did not change. Plasma renin activity rose to 21 ng.ml-1.h-1 in RS but remained at 44 ng.ml-1.h-1 in the LS. Both losartan (10 mg/kg) and phentolamine (0.1 mg/kg) intravenous bolus injections reduced blood pressure considerably in the L-NAME hypertensive animals. Whole brain NOS activity was reduced by 84%. Hypertension induced by chronic NOS inhibition in LS as well as in RS fed rats seems to be sustained by an interaction of several mechanisms, including the activation of the sympathetic nervous system and the renin-angiotensin system.

Mechanisms involved in central cardiovascular effects of prostaglandin F2 alpha

1982 ◽  
Vol 242 (5) ◽  
pp. R545-R551 ◽  
Author(s):  
G. Feuerstein ◽  
C. J. Helke ◽  
R. L. Zerbe ◽  
D. M. Jacobowitz ◽  
I. J. Kopin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rectal Temperature ◽  
Cardiovascular Effects ◽  
Plasma Norepinephrine ◽  
Central Administration ◽  
Prostaglandin F2 Alpha ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
Bilateral Vagotomy

Prostaglandin F2 alpha (PGF2 alpha) injected into the cerebroventricular system (icv) of halothane-anesthetized rats increased the arterial blood pressure, heart rate, and rectal temperature. These effects were accompanied by a preferential increase in plasma norepinephrine concentration. Plasma levels of epinephrine, renin, and vasopressin were not changed in the PGF2 alpha-icv-treated rats. Bilateral vagotomy did not affect the PGF2 alpha-induced hypertension and tachycardia nor was there any change in the selective increase in plasma norepinephrine concentration. Hexamethonium pretreatment suppressed, in a dose-response manner, the increases in blood pressure, heart rate, and rectal temperature in response to PGF2 alpha-icv. Plasma norepinephrine and epinephrine levels were not altered by PGF2 alpha-icv in hexamethonium-treated rats, but plasma vasopressin concentration was markedly elevated in all hexamethonium-infused rats. These results suggest that selective central activation of the sympathetic nervous system underlies the profound cardiovascular and temperature responses elicited by central administration of PGF2 alpha.

Effects of Enkephalins on Arterial Blood Pressure are Reduced by Propranolol

1978 ◽  
Vol 55 (s4) ◽  
pp. 237s-241s ◽  
Author(s):  
W. Simon ◽  
K. Schaz ◽  
U. Ganten ◽  
G. Stock ◽  
K. H. Schlör ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular Effects ◽  
Pressure Control ◽  
Methionine Enkephalin ◽  
Leucine Enkephalin ◽  
Arterial Blood ◽  
Wistar Kyoto ◽  
Blood Pressure Responses ◽  
The Brain

1. The cardiovascular effects of enkephalins have been tested in normotensive Wistar—Kyoto rats. Methionine—enkephalin and leucine—enkephalin increased blood pressure and heart rate after infusion into the brain ventricles. 2. After intravenous injection, blood pressure was increased by methionine—enkephalin and leucine—enkephalin, but heart rate was increased by methionine—enkephalin only. 3. Propranolol treatment reduced the increases in blood pressure following intraventricular methionine—enkephalin and leucine—enkephalin, while only the methionine—enkephalin-induced increases in heart rate were reduced by propranolol. 4. Heart rate and blood pressure responses after intravenous administration of methionine— enkephalins and leucine—enkephalin were not affected by propranolol. 5. Since opioid peptides occur in the blood and in regions of the brain involved in blood pressure regulation, the demonstrated cardiovascular effects to intraventricular and intravenous enkephalins support a role of these peptides in central and peripheral mechanisms of blood pressure control.

Hemodynamic and renal functional changes after acute unilateral nephrectomy in the dog: role of carotid sinus baroreceptors

1982 ◽  
Vol 242 (2) ◽  
pp. F181-F189 ◽  
Author(s):  
J. C. Ayus ◽  
M. H. Humphreys
Keyword(s):  
Blood Pressure ◽  
Constant Pressure ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Systemic Circulation ◽  
Unilateral Nephrectomy ◽  
Functional Changes ◽  
Arterial Blood ◽  
Bilateral Carotid

We examined the role of the carotid sinus baroreceptors in the hemodynamic and renal functional changes initiated by acute unilateral nephrectomy (AUN). In 15 anesthetized dogs, AUN caused increases in sodium (UNaV) and potassium excretion (UKV) without significant changes in GFR, renal blood flow, or mean arterial pressure. Cardiac output (CO) was measured in five of these animals and decreased from 2.5 +/- 0.2 to 1.9 +/- 0.3 liter/min as total peripheral resistance (TPR) increased. In 11 dogs with bilateral acute surgical carotid sinus denervation, AUN failed to cause any change in renal hemodynamics, UNaV, or UKV that could be distinguished from sham-operated time controls. CO was measured in seven of these dogs and also did not change. AUN caused an immediate, transient elevation in blood pressure that returned to control levels 15 min after nephrectomy. When bilateral carotid occlusion (BCO) was carried out prior to AUN in animals with intact carotid sinus baroreceptors, AUN again caused an immediate increase in blood pressure but no changes in CO or electrolyte excretion. In separate studies, AUN increased UNaV and UKV significantly; when BCO was then carried out after AUN, cation excretion remained elevated. In seven dogs undergoing continuous perfusion of the carotid circulation bilaterally at constant pressure, AUN again failed to increase cation excretion despite a 30 mmHg rise in arterial blood pressure. These studies demonstrate that AUN fails to initiate hemodynamic or compensatory renal functional changes in dogs with bilateral carotid sinus denervation or in animals in which intact baroreceptors are shielded from the systemic circulation by BCO or perfusion at constant pressure, indicating the importance of these baroreceptors in the early changes after AUN.

scholarly journals Increased superoxide levels in ganglia and sympathoexcitation are involved in sarafotoxin 6c-induced hypertension

2008 ◽  
Vol 295 (5) ◽  
pp. R1546-R1554 ◽  
Author(s):  
Melissa Li ◽  
Xiaoling Dai ◽  
Stephanie Watts ◽  
David Kreulen ◽  
Gregory Fink
Keyword(s):  
Blood Pressure ◽  
Sympathetic Innervation ◽  
Sympathetic Ganglia ◽  
Plasma Norepinephrine ◽  
Sprague Dawley ◽  
Surgical Ablation ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Hypertension Development

Endothelin (ET) type B receptors (ETBR) are expressed in multiple tissues and perform different functions depending on their location. ETBR mediate endothelium-dependent vasodilation, clearance of circulating ET, and diuretic effects; all of these should produce a fall in arterial blood pressure. However, we recently showed that chronic activation of ETBR in rats with the selective agonist sarafotoxin 6c (S6c) causes sustained hypertension. We have proposed that one mechanism of this effect is constriction of capacitance vessels. The current study was performed to determine whether S6c hypertension is caused by increased generation of reactive oxygen species (ROS) and/or activation of the sympathetic nervous system. The model used was continuous 5-day infusion of S6c into male Sprague-Dawley rats. No changes in superoxide anion levels in arteries and veins were found in hypertensive S6c-treated rats. However, superoxide levels were increased in sympathetic ganglia from S6c-treated rats. In addition, superoxide levels in ganglia increased progressively the longer the animals received S6c. Treatment with the antioxidant tempol impaired S6c-induced hypertension and decreased superoxide levels in ganglia. Acute ganglion blockade lowered blood pressure more in S6c-treated rats than in vehicle-treated rats. Although plasma norepinephrine levels were not increased in S6c hypertension, surgical ablation of the celiac ganglion plexus, which provides most of the sympathetic innervation to the splanchnic organs, significantly attenuated hypertension development. The results suggest that S6c-induced hypertension is partially mediated by sympathoexcitation to the splanchnic organs driven by increased oxidative stress in prevertebral sympathetic ganglia.

Effect of chronic left ventricular failure on beta-endorphin

1992 ◽  
Vol 73 (6) ◽  
pp. 2675-2680 ◽  
Author(s):  
E. Mellow ◽  
E. Redei ◽  
K. Marzo ◽  
J. R. Wilson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Plasma Norepinephrine ◽  
Endogenous Opiates ◽  
Beta Endorphin ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
C 30

Stimulation of endogenous opiate secretion worsens circulatory dysfunction in several forms of shock, in part by inhibiting sympathetic activity. To investigate whether endogenous opiates have a similar effect in chronic heart failure (HF), we measured beta-endorphin concentrations and hemodynamic responses to naloxone infusion (2 mg/kg bolus + 2 mg.kg-1 x h-1) in six control (C) dogs and eight dogs with low-output HF produced by 3 wk of rapid ventricular pacing. The dogs with HF exhibited reduced arterial blood pressure (C, 123 +/- 4 vs. HF, 85 +/- 7 mmHg; P < 0.01) and cardiac outputs (C, 179 +/- 14 vs. HF, 76 +/- 2 ml.min-1 x kg-1; P < 0.01) and elevated plasma norepinephrine concentrations (C, 99 +/- 12 vs. HF, 996 +/- 178 pg/ml; P < 0.01) but normal beta-endorphin concentrations (C, 30 +/- 11 vs. HF, 34 +/- 12 pg/ml; P = NS). Naloxone produced similar transitory increases in blood pressure (C, 14 +/- 5 vs. HF, 26 +/- 25%) and cardiac output (C, 37 +/- 13 vs. HF, 22 +/- 15%) in both groups (both P = NS). No significant changes in norepinephrine concentration or systemic vascular resistance were observed in either group. These findings suggest that beta-endorphin secretion does not exacerbate circulatory dysfunction in chronic heart failure.

Central indomethacin enhances volume-dependent vasopressin release

1984 ◽  
Vol 247 (6) ◽  
pp. R1017-R1021
Author(s):  
D. P. Brooks ◽  
L. Share ◽  
J. T. Crofton ◽  
A. Nasjletti
Keyword(s):  
Blood Pressure ◽  
Prostaglandin E2 ◽  
Mean Arterial Blood Pressure ◽  
Inhibitory Effect ◽  
Volume Depletion ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Ventriculocisternal Perfusion ◽  
Severe Hemorrhage ◽  
Vasopressin Secretion

The effect of centrally administered indomethacin on hemorrhage-induced vasopressin release was studied in the morphine-sedated, urethan/chloralose-anesthetized dog. Ventriculocisternal perfusion of indomethacin 1) significantly reduced the amount of prostaglandin E2 in the effluent from the cisterna magna, 2) significantly enhanced the vasopressin response to volume depletion, and led to a greater fall in mean arterial blood pressure during severe hemorrhage. The results suggest that central prostaglandins may have an inhibitory effect on vasopressin secretion during volume depletion.

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