Baroceptor Function in Chronic Renal Hypertension

Green, J. H.; Page, Irvine H.

doi:10.1161/01.res.4.2.205

Cited by 415 publications

(163 citation statements)

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“…The efferent electroneurograms were processed and recorded as previously described. 8 " 6 The efferent signals were detected with an AC differential preamplifier (Model P-15, Grass Instrument Co., Quincy, MA) with a time constant of 3 msec. The amplified nerve spikes were displayed on an oscilloscope (Model R103N, Tektronix Inc., Beaverton, OR) for visualization and photographing (Tektronix Camera, Model C-12).…”

Section: Methodsmentioning

confidence: 99%

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Arterial baroreceptor reflex control of sympathetic nerve activity in the spontaneously hypertensive rat.

Judy¹,

Farrell²

1979

Hypertension

152

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SUMMARY The combined and individual carotid sinus and aortic baroreceptor control of sympathetic nerve activity (SNA) and mean arterial pressure (MAP) were studied by direct measurement In groups of spontaneously hypertensive rats (SHR) and normotensive Kyoto Wistar rats (WKY) of 5 to 40 weeks of age. The SHR showed a significantly greater SNA and resultant MAP increase as a function of age compared to that of the WKY rats. Both SHR and WKY rats showed a significant rise in SNA and MAP with ablation of all four major baroreceptors. The proportionate change of SNA and MAP after ablation was greater in the younger SHR than In the younger WKY groups and the change in these decreased as a function of age in the SHR. The reflex inhibition of SNA via baroreceptor stimulation also decreased as a function of age in the SHR, due to a 43% loss of aortic inhibitory function; no significant loss of carotid sinus function was found in either the SHR or WKY. The decrement in aortic function occurred after the rapid phase of blood pressure development; therefore baroreceptor dysfunction cannot be the cause of the high SNA and MAP observed in young SHR. An upward resetting of central sympathetic centers was evaluated via the baroreceptor deafferentatlon; and, it appears that the hyperactive sympathetic nervous system and resultant hypertension in the SHR is due to central resetting of sympathetic centers rather than baroreceptor dysfunction. T HE sympathetic nervous system has been shown to be hyperactive in the spontaneously hypertensive rat (SHR), and to be a significant factor in the development and maintenance of high blood pressure in this genetic model of hypertension. 16 The factors responsible for the elevated sympathetic nerve activity (SNA) in the SHR are unknown. Historically, it was hypothesized that in experimental renal hypertension a loss of carotid sinus and aortic reflex inhibitory control of SNA resulted in an increase in SNA which in turn produced the hypertensive condition. However, in such studies, the arterial baroreceptors have been shown to adapt or reset during hypertension, such that they have an increased stimulus pressure threshold, a normal firing frequency, and an extended operational range."

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Section: Methodsmentioning

confidence: 99%

“…It is interesting that centrally acting antihypertensive drugs, such as clonidine, L-dopa, and alpha-methyl dopa, effectively lower blood pressure in the SHR by suppressing SNA centrally (Judy, unpublished data). 6 These compounds presumably stimulate the central alpha adrenergic system, which lowers MAP by reducing peripheral sympathetic activity. 8 …”

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confidence: 99%

Arterial baroreceptor reflex control of sympathetic nerve activity in the spontaneously hypertensive rat.

Judy¹,

Farrell²

1979

Hypertension

152

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“…However, these changes are attenuated by the effects of baroreceptor resetting, whereby there is a shift in the function curve relating afferent baroreceptor activity to blood pressure, in the direction of the prevailing arterial pressure; estimates of the time course of baroreceptor resetting vary from minutes 6 to days or weeks. 7 Thus, as a result of resetting, the deleterious autonomic effects associated with initial doses of dihydropyridines may not persist with chronic therapy. In addition to the effects of resetting, the autonomic effects of dihydropyridine therapy may be reflected by changes in the gain or sensitivity of the baroreceptor reflex.…”

Section: Introductionmentioning

confidence: 99%

The effects of acute and chronic dihydropyridine calcium antagonist therapy on baroreflex sensitivity: a re-analysis using the sequence method

et al. 2000

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The objective of this study was to examine the effects of dihydropyridine calcium antagonist therapy on 24-h baroreflex sensitivity. Twenty-three patients with moderate essential hypertension were studied before and during acute (10 patients) and chronic (21 patients) treatment with a dihydropyridine calcium antagonist (nifedipine, nicardipine or felodipine) as monotherapy in a dose titrated to produce a fall in mean cuff pressure of at least 10%. Twenty-four hour unrestricted ambulatory intra-arterial blood pressure (IABP) and heart rate (R-R interval) were monitored. Baroreflex sensitivity (BRS) was assessed throughout the 24-h period by off-line computer analysis of spontaneous variations in IABP and R-R interval. During acute first dose treatment with a calcium antagonist there was a significant fall in blood

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“…An initial alteration in arterial baroreceptor reflex whichis a major restraining mechanism of sympathetic activities wasan attractive hypothesis of a cause of essential hypertension (1). This idea, however, was hardly supported after it became clear that secondary baroreceptor resetting occurs rapidly and regularly in hypertension (4). Further, it was demonstrated that removal of arterial baroreceptors (sinoaortic denervation) in dogs did not cause a long-lasting elevation of the average blood pressure (5).…”

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confidence: 99%

The Sympathetic Nervous System in Essential Hypertension: Pathophysiological Significance.

Takishita

2001

Intern. Med.

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Baroceptor Function in Chronic Renal Hypertension

Cited by 415 publications

References 0 publications

Arterial baroreceptor reflex control of sympathetic nerve activity in the spontaneously hypertensive rat.

Arterial baroreceptor reflex control of sympathetic nerve activity in the spontaneously hypertensive rat.

The effects of acute and chronic dihydropyridine calcium antagonist therapy on baroreflex sensitivity: a re-analysis using the sequence method

The Sympathetic Nervous System in Essential Hypertension: Pathophysiological Significance.

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