Support of arterial blood pressure by major pressor systems in conscious dogs

1988 ◽  
Vol 255 (3) ◽  
pp. H483-H491 ◽  
Author(s):  
P. H. Brand ◽  
P. J. Metting ◽  
S. L. Britton
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Steady State ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Autonomic Function ◽  
Autonomic Ganglia ◽  
Arterial Blood

The roles of the autonomic nervous system, vasopressin, and angiotensin II in support of blood pressure were evaluated in seven conscious, resting dogs while hydrated or dehydrated. Mean arterial blood pressure (MAP) was monitored, and the dogs were given hexamethonium to block autonomic ganglia. Thirty minutes later, they were given captopril, and after another 30 min, a vasopressin V1 antagonist, d(CH2)5TyrMeAVP, was given. The order okf administration of captopril and d(CH2)5TyrMeAVP was alternated in different experiments. Hexamethonium had no effect on steady-state MAP in either hydrated or dehydrated dogs. In hydrated dogs, the average MAP was 100 mmHg; d(CH2)5TyrMeAVP decreased MAP by approximately 12 mmHg, and captopril decreased MAP by 24 mmHg. The magnitude of the effect of these two inhibitors was independent of the order of their administration. Dehydration doubled the effect of d(CH2)5TyrMeAVP on MAP but had no effect on the response to captopril. The results suggest that 1) autonomic function is not essential for maintenance of arterial blood pressure in resting dogs; 2) during autonomic ganglionic blockade, arterial blood pressure is supported by both angiotensin II and vasopressin; and 3) dehydration increases the role of vasopressin in control of blood pressure.

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Endogenous Formation

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

Role of angiotensin and vasopressin on blood pressure of ganglionic blocked dogs

1983 ◽  
Vol 244 (1) ◽  
pp. H115-H120 ◽  
Author(s):  
P. C. Houck ◽  
M. J. Fiksen-Olsen ◽  
S. L. Britton ◽  
J. C. Romero
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Vasopressin Antagonist ◽  
Ganglionic Blockade ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
Group 2 ◽  
Group 1

This study was designed to investigate the possible role of angiotensin and vasopressin in the maintenance of arterial blood pressure during acute blockade of the autonomic nervous system. Two groups of eight dogs each were anesthetized with pentobarbital sodium, and autonomic ganglia were blocked with hexamethonium (20 mg/kg). Thirty minutes later group 1 received the vasopressin antagonist 1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine arginine vasopressin (10 micrograms/kg) followed after a 30-min interval by captopril (1 mg/kg). Group 2 received the same drugs, except the order of administration of vasopressin antagonist and captopril was reversed. Vasopressin antagonist during ganglionic blockade (group 2) produced a greater fall in blood pressure than did captopril during ganglionic blockade (group 1). These data indicate that vasopressin plays a greater pressor role than angiotensin in the acute response to ganglionic blockade. Additional studies were performed to determine if the autonomic nervous system alone can support the resting blood pressure in the anesthetized dog. Combined blockade of angiotensin and vasopressin without autonomic blockade produced a significant decrease in blood pressure, suggesting that the autonomic nervous system alone is not able to support the control blood pressure in the anesthetized dog.

Paraventricular stimulation with glutamate elicits bradycardia and pituitary responses

1989 ◽  
Vol 256 (1) ◽  
pp. R112-R119 ◽  
Author(s):  
D. N. Darlington ◽  
M. Miyamoto ◽  
L. C. Keil ◽  
M. F. Dallman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Arterial Blood Pressure ◽  
Excitatory Neurotransmitter ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
Paraventricular Nuclei ◽  
Measured Activation

The excitatory neurotransmitter, L-glutamate (0.5 M, pH 7.4), or the organic acid, acetate (0.5 M, pH 7.4), was microinjected (50 nl over 2 min) directly into the paraventricular nuclei (PVN) of pentobarbital sodium-anesthetized rats while arterial blood pressure and heart rate and plasma adrenocorticotropic hormone (ACTH), vasopressin, and oxytocin were measured. Activation of PVN neurons with L-glutamate led to increases in plasma ACTH, vasopressin, and oxytocin and a profound bradycardia (approximately 80 beats/min) with little change in arterial blood pressure. Microinjection of acetate had no effect on the above variables. The decrease in heart rate was shown to be dependent on the concentration of glutamate injected and the volume of injectate. The bradycardia was mediated through the autonomic nervous system because ganglionic blockade (pentolinium tartrate) eliminated the response; atropine and propranolol severely attenuated the bradycardia. The bradycardia was greatest when L-glutamate was microinjected into the caudal PVN. Injections into the rostral PVN or into nuclei surrounding the PVN led to small or nonsignificant decreases in heart rate. Focal electric stimulation (2-50 microA) of the PVN also led to decreases in heart rate and arterial blood pressure. These data suggest that activation of PVN neurons leads to the release of ACTH, vasopressin, and oxytocin from the pituitary and a bradycardia that is mediated by the autonomic nervous system.

Nonadrenergic noncholinergic autonomic mediation of pressor response to feeding in lambs

1993 ◽  
Vol 265 (3) ◽  
pp. R530-R536 ◽  
Author(s):  
S. A. Jones ◽  
B. L. Langille ◽  
S. Frise ◽  
S. L. Adamson
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Adrenergic Blockade ◽  
Arterial Blood ◽  
Plasma Angiotensin ◽  
Muscarinic Cholinergic ◽  
Alpha Beta

We examined factors mediating a 70% increase in arterial blood pressure that occurs during feeding in newborn lambs. We report that the increase in blood pressure during feeding was significantly reduced (to approximately 50%) and delayed in onset by combined alpha- and beta-adrenergic blockade. Plasma angiotensin and vasopressin levels did not increase significantly during feeding, nor was the pressor response to feeding attenuated while using captopril to block the production of angiotensin II. Adrenalectomy or muscarinic cholinergic blockade with atropine was also unsuccessful in attenuating the pressor response to feeding. We demonstrated that the component of the pressor response to feeding that was insensitive to alpha, beta, and muscarinic blockade was mediated by the autonomic nervous system because it was completely eliminated by ganglionic blockade with hexamethonium. Thus nonadrenergic noncholinergic autonomic mechanisms mediate approximately half the pressor response to feeding in lambs.

Changes of Plasma and Cerebrospinal Fluid Noradrenaline during Frusemide Administration and Acute Renal Artery Constriction in Dogs

1982 ◽  
Vol 63 (s8) ◽  
pp. 343s-345s ◽  
Author(s):  
Yoshiaki Masuyama ◽  
Yuji Ueno ◽  
Mikio Arita ◽  
Hidetoshi Suruda ◽  
Osamu Mohara
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Renal Artery ◽  
Arterial Blood Pressure ◽  
Plasma Noradrenaline ◽  
Direct Role ◽  
Arterial Blood ◽  
Renal Artery Constriction

1. The effects of circulating angiotensin II on cerebrospinal fluid and plasma noradrenaline during frusemide administration and acute renal artery constriction were studied in dogs. 2. The administration of frusemide produced significant increases in cerebrospinal fluid and plasma noradrenaline. Intravertebral artery infusion of [Sar1, Ala8]angiotensin II (saralasin) significantly suppressed the frusemide-induced increases in cerebrospinal and plasma noradrenaline and resulted in a fall in arterial blood pressure. 3. Acute renal artery constriction produced the marked elevation of plasma noradrenaline and arterial blood pressure, although no significant increase was found in cerebrospinal fluid noradrenaline. Though intravertebral artery infusion of saralasin did not affect cerebrospinal fluid and plasma noradrenaline, intravenous infusion of saralasin reduced the increases in arterial blood pressure and plasma noradrenaline induced by acute renal artery constriction. 4. Plasma volume was significantly reduced by frusemide administration, but unchanged by acute renal artery constriction. 5. Therefore it is suggested that circulating angiotensin II may contribute to the regulation of blood pressure at least partially by acting on the central nervous system in the sodium- and volume-depleted states. However, the renin-angiotensin system appears to play a rather direct role in the mechanism of hypertension induced by renal artery constriction, not through the action of angiotensin II on the central sympathetic nervous system.

Autonomic nervous system and blood pressure regulation in RGS2-deficient mice

2005 ◽  
Vol 288 (5) ◽  
pp. R1134-R1142 ◽  
Author(s):  
Volkmar Gross ◽  
Jens Tank ◽  
Michael Obst ◽  
Ralph Plehm ◽  
Kendall J. Blumer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Environmental Stress ◽  
G Protein ◽  
Arterial Blood Pressure ◽  
Stress Sensitivity ◽  
Pressure Regulation ◽  
Arterial Blood ◽  
Deficient Mice

Regulator of G protein signaling (RGS2) deletion in mice prolongs signaling by G protein-coupled vasoconstrictor receptors and increases blood pressure. However, the exact mechanism of the increase in blood pressure is unknown. To address this question we tested autonomic nervous system function and blood pressure regulation in RGS2-deficient mice (RGS2 −/−). We measured arterial blood pressure and heart rate (HR) with telemetry, computed time and frequency-domain measures for blood pressure and HR variability (HRV) as well as baroreflex sensitivity [BRS-low frequency (LF)], and assessed environmental stress sensitivity. Mean arterial blood pressure (MAP) was ∼10 mmHg higher in RGS2 −/− compared with RGS2 +/+ mice, while HR was not different between the groups, indicating a resetting of the baroreceptor reflex. Atropine increased MAP more in RGS2 −/− than in RGS2 +/+ mice while HR responses were not different. Urinary norepinephrine excretion was higher in RGS2 −/− than in RGS2 +/+ mice. The blood pressure decrease following prazosin was more pronounced in RGS2 −/− mice than in RGS2 +/+ mice. The LF and high-frequency (HF) power of HRV were reduced in RGS2 −/− compared with controls while BRS-LF and SBP-LF were not different. Atropine and atropine + metoprolol markedly reduced the HRV parameters in the time (RMSSD) and frequency domain (LF, HF, LF/HF) in both strains. Environmental stress sensitivity was increased in RGS2 −/− mice compared with controls. We conclude that the increase in blood pressure in RGS2 −/− mice is not solely explained by peripheral vascular mechanisms. A central nervous system mechanism might be implicated by an increased sympathetic tone. This state of affairs could lead to a baroreceptor-HR reflex resetting, while BRS remains unimpaired.

Assessment of Autonomic Nervous System Via Dynamic Pupillometry in Different Circadian Arterial Blood Pressure Patterns

2018 ◽  
Vol 121 (8) ◽  
pp. e98-e99
Author(s):  
Sercan Okutucu ◽  
Mustafa Civelekler ◽  
Hakan Aksoy ◽  
Begum Yetis Sayin ◽  
Cengiz Sabanoglu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Arterial Blood Pressure ◽  
Autonomic Nervous ◽  
Arterial Blood ◽  
Blood Pressure Patterns
Sign in / Sign up

Export Citation Format

Share Document