Reduced baroreflex changes in muscle sympathetic nerve activity during blood pressure elevation in essential hypertension

Matsukawa, Tetsuya; Gotoh, Eiji; Hasegawa, Osamu; Shionoiri, Hiroshi; Tochikubo, Osamu; Ishii, Masao

doi:10.1097/00004872-199106000-00009

Cited by 62 publications

(40 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…5,20,21 Given these uncertainties, it is reasonable to argue that an impaired baroreceptor restraint of sympathetic nerve traffic might be one mechanism of the sympathetic overactivity present in essential hypertension. We assessed spontaneous arterial baroreflex control of MSNA in our normotensive and hypertensive subjects, finding that the gain of the MSNA arterial baroreflex was similar in the two groups.…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

“…Among others, possible mechanisms include increased sympathetic nerve firing rates, 1,2 altered neuronal norepinephrine (NE) reuptake, 3,4 diminished arterial baroreflex buffering of sympathetic nerve traffic, 5 and facilitation of NE release by neurohumoral factors such as angiotensin II. 6 These possibilities, however, have not yet been conclusively tested for in humans.…”

mentioning

confidence: 99%

“…8 Whether diminished arterial baroreflex control of sympathetic nerve traffic may contribute to sympathetic overactivity was also assessed. 5 Given the accumulating evidence for a tissue renin-angiotensin system in humans, 9 which potentially interacts with the sympathetic nervous system by facilitating norepinephrine release, 6 we also tested the hypothesis that local angiotensin II levels in the heart may contribute to sympathetic activation. We thought that in the assessment of these possibilities, combining various measurements in the same subjects would provide the most direct test of their potential mechanistic role in essential hypertension.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Sympathetic Augmentation in Hypertension

et al. 2004

View full text Add to dashboard Cite

Abstract-There is growing evidence that essential hypertension is commonly neurogenic and is initiated and sustained by sympathetic nervous system overactivity. Potential mechanisms include increased central sympathetic outflow, altered norepinephrine (NE) neuronal reuptake, diminished arterial baroreflex dampening of sympathetic nerve traffic, and sympathetic neuromodulation by angiotensin II. To address this issue, we used microneurography and radiotracer dilution methodology to measure regional sympathetic activity in 22 hypertensive patients and 11 normotensive control subjects. The NE transport inhibitor desipramine was infused to directly assess the potential role of impaired neuronal NE reuptake. To evaluate possible angiotensin sympathetic neuromodulation, the relation of arterial and coronary sinus plasma concentrations of angiotensin II to sympathetic activity was investigated. Hypertensive patients displayed increased muscle sympathetic nerve activity and elevated total systemic, cardiac, and renal NE spillover. Cardiac neuronal NE reuptake was decreased in hypertensive subjects. In response to desipramine, both the reduction of fractional transcardiac 3[H]NE extraction and the increase in cardiac NE spillover were less pronounced in hypertensive patients. DNA sequencing analysis of the NE transporter gene revealed no mutations that could account for reduced transporter activity. Arterial baroreflex control of sympathetic nerve traffic was not diminished in hypertensive subjects. Angiotensin II plasma concentrations were similar in both groups and were not related to indexes of sympathetic activation. Increased rates of sympathetic nerve firing and reduced neuronal NE reuptake both contribute to sympathetic activation in hypertension, whereas a role for dampened arterial baroreflex restraint on sympathetic nerve traffic and a peripheral neuromodulating influence of angiotensin II appear to be excluded. Key Words: hypertension, essential Ⅲ catecholamines Ⅲ sympathetic nervous system Ⅲ norepinephrine Ⅲ angiotensin II A lthough there is growing evidence that essential hypertension is commonly neurogenic 1,2 and is initiated and sustained by overactivity of the sympathetic nervous system, the precise causal mechanisms leading to sympathetic augmentation in hypertensive subjects are still poorly understood. Among others, possible mechanisms include increased sympathetic nerve firing rates, 1,2 altered neuronal norepinephrine (NE) reuptake, 3,4 diminished arterial baroreflex buffering of sympathetic nerve traffic, 5 and facilitation of NE release by neurohumoral factors such as angiotensin II. 6 These possibilities, however, have not yet been conclusively tested for in humans.To further address some of these issues, we combined microneurography, to measure sympathetic nerve firing rates, with relevant radiotracer methodology to comprehensively study systemic and regional kinetics of NE and its intraneuronal and extraneuronal metabolites. To directly assess whether decreased neuronal NE reuptake contributes ...

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Sympathetic Augmentation in Hypertension

et al. 2004

View full text Add to dashboard Cite

show abstract

“…Elevated levels of sympathetic nervous activity may contribute to the development and/or maintenance of hypertension by a number of interacting mechanisms related to effects on the heart, vessels and kidneys ( Figure 1). Sympathetic over-activity has been most clearly demonstrated in early hypertension [4][5][6][7][8][9][10] but increased muscle sympathetic nerve activity is also present in older patients with established hypertension. 11,12 Excess sympathetic drive is also likely to play an important role in hypertension associated with obesity and the insulin resistance syndrome.…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide and hypertension: not just an endothelium derived relaxing factor!

Chowdhary

Townend

2001

J Hum Hypertens

View full text Add to dashboard Cite

The importance of endothelial nitric oxide (NO) generation in sustaining a tonic systemic vasodilatation is well established. Inhibiting NO production produces hypertension in animals and in humans and not surprisingly there has been considerable interest in establishing whether deficiencies of endothelial NO pathway activity are implicated in the aetiology of essential hypertension. The results of these investigations have been inconsistent with some suggestion that observed deficiencies of both basal and stimulated endothelial NO generation in hypertensive subjects may be an effect rather than the cause of raised arterial pressure. It is increasingly recognised that neuronal production of NO also influences cardiovascular homeostasis through its action as a neuromodulator within the autonomic nervous system. Overall NO has been shown to have sym-

show abstract

Effects of Exercise on Blood Pressure and Autonomic Function and Other Hemodynamic Regulatory Factors

White

Fernhall

2015

Molecular and Translational Medicine

View full text Add to dashboard Cite

Reduced baroreflex changes in muscle sympathetic nerve activity during blood pressure elevation in essential hypertension

Cited by 62 publications

References 0 publications

Sympathetic Augmentation in Hypertension

Sympathetic Augmentation in Hypertension

Nitric oxide and hypertension: not just an endothelium derived relaxing factor!

Effects of Exercise on Blood Pressure and Autonomic Function and Other Hemodynamic Regulatory Factors

Contact Info

Product

Resources

About