Pathogenesis of hypertension in the sinoaortic-denervated spontaneously hypertensive rat.

Osborn, John W.

doi:10.1161/01.hyp.18.4.475

Cited by 23 publications

(15 citation statements)

References 28 publications

(31 reference statements)

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“…In this way, the long-term control of arterial pressure occurs independently of arterial baroreceptor input. Such result is in agreement with Osborn [26]. …”

Section: Discussionsupporting

confidence: 93%

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Neural set point for the control of arterial pressure: role of the nucleus tractus solitarius

2010

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BackgroundPhysiological experiments have shown that the mean arterial blood pressure (MAP) can not be regulated after chemo and cardiopulmonary receptor denervation. Neuro-physiological information suggests that the nucleus tractus solitarius (NTS) is the only structure that receives information from its rostral neural nuclei and from the cardiovascular receptors and projects to nuclei that regulate the circulatory variables.MethodsFrom a control theory perspective, to answer if the cardiovascular regulation has a set point, we should find out whether in the cardiovascular control there is something equivalent to a comparator evaluating the error signal (between the rostral projections to the NTS and the feedback inputs). The NTS would function as a comparator if: a) its lesion suppresses cardiovascular regulation; b) the negative feedback loop still responds normally to perturbations (such as mechanical or electrical) after cutting the rostral afferent fibers to the NTS; c) perturbation of rostral neural structures (RNS) to the NTS modifies the set point without changing the dynamics of the elicited response; and d) cardiovascular responses to perturbations on neural structures within the negative feedback loop compensate for much faster than perturbations on the NTS rostral structures.ResultsFrom the control theory framework, experimental evidence found currently in the literature plus experimental results from our group was put together showing that the above-mentioned conditions (to show that the NTS functions as a comparator) are satisfied.ConclusionsPhysiological experiments suggest that long-term blood pressure is regulated by the nervous system. The NTS functions as a comparator (evaluating the error signal) between its RNS and the cardiovascular receptor afferents and projects to nuclei that regulate the circulatory variables. The mean arterial pressure (MAP) is regulated by the feedback of chemo and cardiopulmonary receptors and the baroreflex would stabilize the short term pressure value to the prevailing carotid MAP. The discharge rates of rostral neural projections to the NTS would function as the set point of the closed and open loops of cardiovascular control. No doubt, then, the RNS play a functional role not only under steady-state conditions, but also in different behaviors and pathologies.

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“…In this way, the long-term control of arterial pressure occurs independently of arterial baroreceptor input. Such result is in agreement with Osborn [26]. …”

Section: Discussionsupporting

confidence: 93%

“…In all studies in which these receptors were denervated, blood pressure oscillations increased significantly while mean arterial pressure (MAP) did it only for a few days [19-26]. Even when both carotid and aortic baroreceptors and chemoreceptors were removed, MAP increased only for a short period of time [27].…”

Section: Antecedentsmentioning

confidence: 99%

Neural set point for the control of arterial pressure: role of the nucleus tractus solitarius

2010

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“…These results suggest that a normally operating arterial baroreceptor reflex is required to prevent chronic salt-induced increases in arterial pressure. This idea is not compatible with previous studies that have shown that SAD did not affect chronic regulation of arterial pressure in experimental 14 ' 15 or spontaneous 9 hypertension. The implication of these previous findings is that, although the baroreceptor reflex acutely buffers changes in blood pressure, chronic regulation of pressure is not dependent on this reflex because of the resetting properties of arterial baroreceptors.…”

Section: Figure 2 Line Plots Show Nacl-induced Changes In Sodium Andcontrasting

confidence: 96%

Salt-dependent hypertension in the sinoaortic-denervated rat.

Osborn

Provo

1992

Hypertension

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To determine the extent to which baroreceptor function is a determinant of salt-dependent hypertension, we studied the cardiovascular and renal responses to increasing dietary sodium chloride in sinoaorticdenervated (n=9) and sham-denervated (n=9) Sprague-Dawley rats. Rats were instrumented with an arterial catheter for measurement of arterial pressure and were individually housed for daily measurements of water intake, sodium intake, urinary output, and urinary sodium excretion. Arterial pressure was monitored daily over a 30-minute period by computer. After 3 days of control measurements (0.4% sodium chloride diet), dietary sodium chloride was increased to 8.0% for 21 days, followed by a 3-day recovery period (0.4% sodium chloride). Ingestion of an 8.0% sodium chloride diet resulted in a 20-to 25-fold increase in sodium intake and a fivefold increase in water intake in both groups. In sinoaortic-denervated rats, arterial pressure increased approximately 10 mm Hg on days 5-10, 20 mm Hg on days 11-18, and 30 mm Hg on days 19-21 of 8.0% sodium chloride. Arterial pressure returned to control levels within the first 24 hours of the recovery period. Elevated sodium intake had no significant effect on arterial pressure in the sham-denervated group. Finally, there were no significant differences between groups in urine output or urinary sodium excretion at any time during the study. We conclude that a primary impairment in the afferent limb of the arterial baroreceptor reflex results in salt-dependent hypertension in the Sprague-Dawley rat. (Hypertension 1992; 19:658-662) KEY WORDS • baroreceptors • sodium-dependent hypertension • sympathetic nervous system D espite the established relation between dietary sodium and hypertension, the mechanisms whereby increased salt intake chronically elevates arterial pressure are not well understood. One hypothesis is that some forms of salt-sensitive hypertension result from impairment of cardiovascular sympathetic reflexes. This hypothesis is consistent with reports of attenuated arterial baroreceptor 1 -3 and cardiopulmonary 4 -5 reflexes in the Dahl salt-sensitive (DS) rat compared with Dahl salt-resistant (DR) controls.However, two arguments can be made against this hypothesis. First, DS rats have attenuated pressurenatriuretic responses before developing hypertension, 6 which may explain their predisposition to salt-induced elevations of arterial pressure. Second, the conclusion that impaired reflex control of the circulation leads to salt-sensitive hypertension infers that, under normal conditions, hypertension is prevented by baroreceptor reflexes. This is not compatible with the idea that baroreceptors adapt to chronic changes in pressure and are therefore unable to chronically regulate arterial pressure. 7The present study was conducted to directly test the hypothesis that a primary dysfunction of the arterial baroreceptor reflex results in salt-sensitive hypertension. We examined the effect of increased dietary intake of sodium chloride (NaCl) on arterial pressure in ...

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“…1 Dynamic characteristics of the arterial baroreflex are also preserved in SHR. 16,17 While sino-aortic baroreceptor denervation does not affect the development of hypertension in SHR, 26 it is likely that the carotid sinus baroreflex preserved the ability to reduce AP to within a normal pressure range. The present study results might provide a rationale for the use of a carotid baroreceptor stimulator as an alternative therapy for drug-resistant hypertension.…”

Section: Baroreflex Total-loop Characteristics In Wky and Shrmentioning

confidence: 99%

Predominant Role of Neural Arc in Sympathetic Baroreflex Resetting of Spontaneously Hypertensive Rats

Sata

Kawada

Shimizu

et al. 2015

Circ J

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592SATA Y et al. Circulation JournalOfficial Journal of the Japanese Circulation Society http://www. j-circ.or.jp classified as a short-term blood pressure control system, 8 carotid baroreflex activation therapy has succeeded in reducing blood pressure in patients with resistant hypertension for more than 1 year, 9 suggesting a potential role of the arterial baroreflex in the long-term regulation of blood pressure. 10 Considering the multifactorial and complex nature of hypertension, further research is needed to understand how sympathetic nerve activity (SNA) and AP are determined in hypertension. The arterial baroreflex system constitutes a key link between the autonomic nervous system and the cardiovascular system. The reflex arc of baroreflex can be divided into 2 principal arcs: the neural arc from pressure input to SNA, and the peripheral arc from SNA to AP. 11,12 Under normal physiological conditions, because the arterial baroreflex operates as a closedloop feedback control system, it is difficult to separately quantify neural and peripheral arc characteristics.The behavior of a system might be described by dynamic and static characteristics. The dynamic characteristics determine he arterial baroreflex control of arterial pressure (AP) is known to reset to a higher input pressure range in hypertension. 1 To cope with the resetting, carotid baroreflex activation is proposed as a potential treatment of drugresistant hypertension. 2,3 Involvement of both neural and cardiovascular factors has been proposed in the pathophysiology of hypertension. Previous studies have demonstrated that sympathetic outflow from the central nervous system is increased in spontaneously hypertensive rats (SHR). 4,5 Peripheral factors such as cardiac hypertrophy and increased vascular resistance are also considered responsible for high AP in SHR. 6 Abnormality in vascular function is also reported in hypertensive patients. 7 Editorial p 510Device-based neuromodulation therapy has increasingly drawn scientific interest. While the arterial baroreflex has been Background: There is ongoing controversy over whether neural or peripheral factors are the predominant cause of hypertension. The closed-loop negative feedback operation of the arterial baroreflex hampers understanding of how arterial pressure (AP) is determined through the interaction between neural and peripheral factors.

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Pathogenesis of hypertension in the sinoaortic-denervated spontaneously hypertensive rat.

Cited by 23 publications

References 28 publications

Neural set point for the control of arterial pressure: role of the nucleus tractus solitarius

Neural set point for the control of arterial pressure: role of the nucleus tractus solitarius

Salt-dependent hypertension in the sinoaortic-denervated rat.

Predominant Role of Neural Arc in Sympathetic Baroreflex Resetting of Spontaneously Hypertensive Rats

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