Do primary dysfunctions in neural control of arterial pressure contribute to hypertension?

Hypertension ◽  
1991 ◽  
Vol 18 (3_Suppl) ◽  
pp. I38-I38 ◽  
Author(s):  
C. M. Ferrario ◽  
D. B. Averill
Keyword(s):  
Arterial Pressure ◽  
Neural Control

Subregions of rostral ventral medulla control arterial pressure and regional hemodynamics

1989 ◽  
Vol 257 (3) ◽  
pp. R635-R640 ◽  
Author(s):  
B. F. Cox ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Tidal Volume ◽  
Vascular Resistance ◽  
Neural Control ◽  
Cardiovascular Response ◽  
Cardiovascular Effects ◽  
Ventrolateral Medulla ◽  
Ventral Medulla ◽  
Ventromedial Medulla ◽  
Regional Hemodynamics

The cardiovascular effects of inactivating rostral ventromedial medulla (RVMM) under conditions of normal (2.5 ml) and reduced (1.5 ml) tidal volume were studied in urethan-anesthetized rats. Bilateral microinjection of lidocaine (200 nl, 4%) reduced mean arterial pressure (MAP), renal, mesenteric, and particularly hindquarter vascular resistance. These effects were not significantly altered by reducing tidal volume. Electrical stimulation of RVMM increased MAP and regional vascular resistances, again with the hindquarter change most prominent. The integrated cardiovascular response to stimulating rostral ventrolateral medulla (RVLM) appears to require integrity of RVMM; however, the converse is not true. Overall, these studies indicate that 1) the potential for RVMM to maintain neurogenic control of arterial pressure is as great as RVLM; 2) RVMM is capable of playing a proportionally greater role in the controlling hindquarter vascular resistance; 3) the integrity of RVMM appears to be important for responses elicited from RVLM; and 4) unlike RVLM, neural control of arterial pressure is sustained by RVMM under conditions of reduced tidal volume. We conclude that RVLM and RVMM are functionally and anatomically distinct subregions of rostral ventral medulla with equivalent capacity to maintain vasomotor tone.

Spinal vasopressin mechanisms of cardiovascular regulation

1986 ◽  
Vol 251 (3) ◽  
pp. R510-R517 ◽  
Author(s):  
J. P. Porter ◽  
M. J. Brody
Keyword(s):  
Spinal Cord ◽  
Arterial Pressure ◽  
Neural Control ◽  
Intrathecal Injection ◽  
Cardiovascular Regulation ◽  
Spinal Subarachnoid Space ◽  
Vascular Beds ◽  
Vasopressinergic Neurons ◽  
Stimulation Of ◽  
Related Increase

Extrahypothalamic vasopressin-containing neurons have been implicated in the central neural control of the cardiovascular system. In the present study we investigated the possibility that vasopressinergic neurons arising from the paraventricular nucleus (PVN) and terminating in the spinal cord are involved in the regulation of vasomotor functions. Vasopressin (1-17 pmol) was injected into the spinal subarachnoid space of conscious rats instrumented with Doppler flow probes and indwelling intrathecal catheters. The peptide produced a dose-related increase in arterial pressure accompanied by vasoconstriction in the mesenteric, renal, and hindquarter vascular beds. Pretreatment, intrathecally, with 0.5 nmol of the vasopressin antagonist d(CH2)5Me(Tyr)AVP completely prevented the increase in arterial pressure expected after subsequent intrathecal injection of vasopressin. However, the changes in arterial pressure and vascular resistances produced by stimulation of the PVN were not affected by the intrathecal antagonist. Stimulation of the PVN in Brattleboro rats, which lack hypothalamic and spinal vasopressin, produced hemodynamic responses similar to those produced in Long-Evans control rats. Taken together, these data suggest that spinal vasopressin can act within the spinal cord to alter vasomotor functions; however, the hemodynamic effects evoked by stimulation of the PVN do not appear to depend on spinal vasopressinergic mechanisms.

Comparison of the effects of Althesin, chloralose-urethane, urethane, and pentobarbital on mammalian physiologic responses

1984 ◽  
Vol 62 (6) ◽  
pp. 654-657 ◽  
Author(s):  
Melvin Ching
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Body Temperature ◽  
Arterial Pressure ◽  
Neural Control ◽  
Core Body Temperature ◽  
Tail Flick ◽  
Tail Flick Test ◽  
Duration Of Action ◽  
Core Body

Physiological responses to anesthetic doses of four chemically dissimilar agents, namely, Althesin, urethane, chloralose-urethane, and pentobarbital sodium were compared in rats. The tail-flick test revealed Althesin had greater antinociceptive potency than urethane, chloralose-urethane, and pentobarbital, but its duration of action was shorter than that of chloralose-urethane. Althesin produced minimal or no suppression of core body temperature and mean arterial pressure, and only moderate reduction of mean pulse pressure. The heart rate and respiratory rate of Althesin-treated rats were slower than those of chloralose-urethane and urethane-treated counterparts, respectively, but were not significantly decreased from normal controls. It is concluded that Althesin is a suitable anesthetic for short-term surgery and for studies of body temperature, heart rate, and mean arterial pressure. Because release of gonadotropin-releasing hormone into hypophysial portal blood can be observed under Althesin but is suppressed or blocked by chloralose-urethane, urethane, and pentobarbital, Althesin is the anesthetic of choice in studies concerned with the neural control of ovulatory hormone release.

Altered Dynamics of the Circadian Relationship between Systemic Arterial Pressure and Cardiac Sympathetic Drive Early on in Mild Hypertension

1994 ◽  
Vol 86 (2) ◽  
pp. 209-215 ◽  
Author(s):  
S. Guzzetti ◽  
S. Dassi ◽  
M. Balsamà ◽  
G. B. Ponti ◽  
M. Pagani ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Neural Control ◽  
Mild Hypertension ◽  
Clinical Laboratory ◽  
Spectral Component ◽  
Low Frequency ◽  
Frequency Component ◽  
Regulatory Mechanisms ◽  
Non Invasive ◽  
Normotensive Subjects

1. This study was designed to test the hypothesis that simultaneous non-invasive assessment of the circadian variations in both intermittent arterial pressure and the continuous 24 h changes of spectral markers of cardiac neural control could provide new information on cardiovascular regulatory mechanisms, in hypertensive patients and normotensive subjects. To test this hypothesis we studied 18 subjects with mild hypertension and 11 normotensive subjects in whom we recorded simultaneously non-invasive intermittent arterial pressure and Holter electrocardiogram for 24 h. We also studied the same subjects during resting and standing conditions in the clinical laboratory. 2. The normalized power of the low-frequency (∼0.1 Hz) spectral component of R-R interval variability, considered mainly a marker of sympathetic drive to the sino-atrial node, was, at rest, significantly higher in the hypertensive than in the normotensive subjects, as already reported. Moreover, the values of the low-frequency component at rest recorded in the clinical laboratory were significantly correlated with those obtained from ambulatory recording during night rest. The decrease in the values of arterial pressure during the night-time was accompanied by a reduction in the power of the low-frequency component only in the case of normotensive subjects. Accordingly, the slope of the regression of the low-frequency component as a function of systolic arterial pressure during ambulatory recordings was steep in normotensive subjects and flat in hypertensive subjects. 3. The computer analysis of Holter recordings combined with ambulatory arterial pressure monitoring seems to provide a new method with which to quantify the early changes in cardiovascular regulatory mechanisms that could help to identify individuals at higher risk.

scholarly journals The neural control of arterial pressure by non‐catecholaminergic RVLM

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Ben Holloway ◽  
Chikara Abe ◽  
Daniel Stornetta ◽  
Ruth Stornetta ◽  
Patrice Guyenet
Keyword(s):  
Arterial Pressure ◽  
Neural Control

scholarly journals Investigating feedforward neural regulation of circulation from analysis of spontaneous arterial pressure and heart rate fluctuations in conscious rats

2009 ◽  
Vol 296 (1) ◽  
pp. H202-H210 ◽  
Author(s):  
Jacopo M. Legramante ◽  
Sergio Sacco ◽  
Gianfranco Raimondi ◽  
Vito N. Di Lecce ◽  
Marco Pallante ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Opposite Direction ◽  
Neural Control ◽  
Physiological Role ◽  
Pulse Interval ◽  
Adrenergic Blockade ◽  
Receptor Blockade ◽  
Sympathetic Blockade ◽  
Conscious Rats ◽  
Autonomic Blockade

It has been suggested in anesthetized animals that the occurrence of sequences of consecutive beats characterized by systolic arterial pressure (SAP) and RR or pulse interval (PI) changing in the opposite direction (SAP+/RR− and SAP−/RR+, nonbaroreflex sequences) might represent the expression of neural cardiovascular regulatory mechanisms operating with feedforward characteristics. The aim of the present study was to study nonbaroreflex sequences in a more physiological experimental model, i.e., in conscious freely moving rats. We studied conscious rats before and after 1) complete autonomic blockade ( n = 12), 2) sympathetic blockade ( n = 10), 3) α ( n = 7)- and β ( n = 8)-adrenergic blockade, and 4) parasympathetic blockade ( n = 10). Nonbaroreflex sequences were defined as three or more beats in which SAP and PI of the following beat changed in the opposite direction. Complete autonomic blockade reduced the number of nonbaroreflex sequences (95.6 ± 9.0 vs. 45.2 ± 4.1, P < 0.001), as did sympathetic blockade (80.9 ± 12.6 vs. 30.9 ± 6.1, P < 0.001). The selective α-receptor blockade did not induce significant changes (80.9 ± 12.5 in baseline vs. 79.0 ± 14.7 after prazosin), whereas β-receptor blockade significantly reduced nonbaroreflex sequence occurrence (80.9 ± 12.5 in baseline vs. 48.9 ± 15.3 after propranolol). Parasympathetic blockade produced a significant increase of nonbaroreflex sequences (95.1 ± 6.9 vs. 136.0 ± 12.4, P < 0.01). These results demonstrate the physiological role of the nonbaroreflex sequences as an expression of a feedforward type of short-term cardiovascular regulation able to interact dynamically with the feedback mechanisms of baroreflex origin in the neural control of the sinus node.

Long-term control of arterial blood pressure

1992 ◽  
Vol 72 (1) ◽  
pp. 231-300 ◽  
Author(s):  
A. W. Cowley
Keyword(s):  
Nervous System ◽  
Arterial Pressure ◽  
Volume Regulation ◽  
Neural Control ◽  
Muscle Tone ◽  
Feedback Signal ◽  
Work Related ◽  
Arterial Blood ◽  
The Moment

Two concepts for the long-term regulation of arterial pressure were considered in this review, the neural control hypothesis and the volume regulation hypothesis. The role of the nervous system and fluid volume regulation are intertwined in a way that has made it difficult to experimentally evaluate their separate contributions in the long-term regulation of arterial pressure. Nevertheless, from a substantial body of work related to the neural control of cardiovascular function, it appears that the ability of the nervous system to control arterial pressure is limited to the detection and correction of rapid short-term changes of arterial pressure. A long and exhaustive search has yet yielded no new neural mechanisms beyond the classic sinoaortic baroreceptors that can detect changes of arterial pressure. The baroreceptor mechanisms are of great importance for the moment-to-moment stabilization of arterial pressure, but because they do not possess sufficient strength and because they reset in time to the prevailing level of arterial pressure, they cannot provide a sustained negative feedback signal to provide long-term regulation of arterial pressure in face of sustained stimuli. This is not to say that the nervous system cannot affect the long-term level of arterial pressure. A distinction is made here between the many factors that can influence the long-term level of pressure and those that actually serve to detect changes of pressure and serve to maintain the level of pressure within a narrow range over the period of our adult lifetime. In this sense, there is evidence that in genetically susceptible individuals, environmental stresses can influence the long-term level of arterial pressure via the central and peripheral neural autonomic pathways. It is inappropriate, however, to view the nervous system as a long-term controller of arterial pressure because there is yet no evidence that the CNS can detect changes of arterial pressure nor changes in total body sodium and water content over sustained periods whereby it could provide an adequate long-term normalization of such error signals. In contrast, evidence has grown in support of the renal pressure-diuresis volume regulation hypothesis for the long-term control of arterial pressure over the past decade. An enhanced understanding of the mechanisms of pressure diuresis-natriuresis coupled with studies exploring how changes of vascular volume can influence vascular smooth muscle tone provide a compelling basis for this hypothesis of long-term arterial pressure regulation. This overall concept is represented and summarized in Figure 12.(ABSTRACT TRUNCATED AT 400 WORDS)

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