Effects of intravenous infusions of angiotensin II on muscle sympathetic nerve activity in humans

Matsukawa, Tetsuya; Gotoh, Eiji; Minamisawa, Kohsuke; Kihara, Minoru; Ueda, Shinichiro; Shionoiri, Hiroshi; Ishii, Masao

doi:10.1152/ajpregu.1991.261.3.r690

Cited by 75 publications

(74 citation statements)

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“…In agreement with Noll et al, 26 who found unchanged muscle sympathetic nerve activity in conjunction with reduced diastolic blood pressure after oral short-term administration of captopril to healthy subjects, we found unchanged muscle sympathetic nerve activity after intravenous administration of enalaprilat, suggesting resetting of the baroreflex control of muscle sympathetic nerve activity to lower blood pressures. This notion is further supported by the findings of Matsukawa et al, 27 who examined muscle sympathetic nerve activity in healthy subjects during equipotent infusions of Ang II and phenylephrine. They found a dose-dependent reduction of muscle sympathetic nerve activity after Ang II that was smaller than during the infusion of phenylephrine.…”

Section: Discussionsupporting

confidence: 59%

Differentiated Response of the Sympathetic Nervous System to Angiotensin-Converting Enzyme Inhibition in Hypertension

et al. 2000

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Abstract-Hypertension with renal artery stenosis is associated with both an activated renin-angiotensin system and elevated sympathetic activity. Therefore, in this condition it may be favorable to use a therapeutic modality that does not reflexly increase heart rate, renin secretion, and sympathetic nervous activity. The purpose of the present study was to assess overall, renal, and muscle sympathetic activity after short-term administration of an angiotensin-converting enzyme inhibitor (enalaprilat) and a nonspecific vasodilator (dihydralazine) to hypertensive patients with renal artery stenosis. Forty-eight patients undergoing a clinical investigation for renovascular hypertension were included in the study. An isotope dilution technique for assessing norepinephrine spillover was used to estimate overall and bilateral renal sympathetic nerve activity. In 11 patients simultaneous intraneural recordings of efferent muscle sympathetic nerve activity were performed. Thirty minutes after dihydralazine administration, mean arterial pressure fell by 15%, whereas plasma angiotensin II, muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover increased (PϽ0.05 for all). In contrast, after enalaprilat administration a fall in arterial pressure similar to that for dihydralazine was followed by decreased angiotensin II levels and unchanged muscle sympathetic nerve activity, heart rate, and total body norepinephrine spillover, whereas renal norepinephrine spillover increased by 44% (PϽ0.05). Acute blood pressure reduction by an angiotensin-converting enzyme inhibitor provokes a differentiated sympathetic response in patients with hypertension and renal artery stenosis, inasmuch that overall and muscle sympathetic reflex activation are blunted, whereas the reflex renal sympathetic response to blood pressure reduction is preserved. (Hypertension. 2000;36:543-548.)Key Words: hypertension, renovascular Ⅲ sympathetic nervous system Ⅲ renin-angiotensin system R enovascular hypertension is a condition associated with both an activated renin-angiotensin system and elevated sympathetic nerve activity. 1,2 Previous data, obtained in experimental models, indicate a positive interaction between the renin-angiotensin and the sympathetic nervous systems. 3 Therefore, in renovascular hypertension it may be favorable to use a therapeutic modality that does not reflexly further increase heart rate, renin secretion, and sympathetic nervous activity. It is well known that certain drugs used in cardiovascular medicine affect various indices of sympathetic activity. For example, sympathetic activity increases in response to nonspecific vasodilators, whereas therapy with angiotensin-converting enzyme (ACE) inhibitors has demonstrated reduced peroneal sympathetic activity. 4 Thus, it appears that vasodilators and ACE inhibitors produce different sympathetic nerve responses; the effects of the latter could be due to either a direct-acting central mechanism 5,6 or a reduction of angiotensin II (Ang II) facilitatory e...

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Section: Discussionsupporting

confidence: 59%

Differentiated Response of the Sympathetic Nervous System to Angiotensin-Converting Enzyme Inhibition in Hypertension

et al. 2000

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“…As such, it is possible that angiotensin II could increase SNS activity in a similar manner in obese humans. Muscle sympathetic nerve activity increases with angiotensin II infusion (Matsukawa et al, 1991) and decreases with angiotensin converting enzyme inhibition (Miyajima et al, 1999) in normotensive humans. Furthermore, multiple components of the renin-angiotensin system are expressed in adipose tissue and angiotensinogen, the major substrate for angiotensin II formation, is expressed to a greater extent in visceral than subcutaneous adipocytes (Engeli et al, 2000).…”

Section: Potential Mechanisms Of Sympathetic Nervous System Activatiomentioning

confidence: 99%

Sympathetic nervous system behavior in human obesity

Davy

Orr

2009

Neuroscience & Biobehavioral Reviews

145

121

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The sympathetic nervous system (SNS) plays an essential role in the regulation of metabolic and cardiovascular homeostasis. Low SNS activity has been suggested to be a risk factor for weight gain and obesity development. In contrast, SNS activation is characteristic of a number of metabolic and cardiovascular diseases that occur more frequently in obese individuals. Until recently, the relation between obesity and SNS behavior has been controversial because previous approaches for assessing SNS activity in humans have produced inconsistent findings. Beginning in the early 1990's, many studies using state of the art neurochemical and neurophysiological techniques have provided important insight. The purpose of the present review is to provide an overview of our current understanding of the regional specific alterations in SNS behavior in human obesity. We will discuss findings from our own laboratory which implicate visceral fat as an important depot linking obesity with skeletal muscle SNS activation. The influence of weight change on SNS behavior and the potential mechanisms and consequences of region specific SNS activation in obesity will also be considered.

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“…It has been demonstrated that a high concentration of circulating Ang II is able to pass the blood-brain barrier and increase sympathetic outflow centrally. [43][44][45] However, losartan may also pass the blood-brain barrier and then bind to AT 1 receptors in the brain. 46,47 The central effects of Ang II on the sympathetic nervous system may be attenuated during chronic administration of losartan.…”

Section: Hyzaar and Absence Of Sympathetic Baroreflex Resettingmentioning

confidence: 99%

Persistent Sympathetic Activation During Chronic Antihypertensive Therapy

Zhang

Witkowski

et al. 2005

Hypertension

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Abstract-Previous studies have demonstrated that antihypertensive treatment resets baroreflex control of heart rate (HR) and increases cardiac vagal baroreflex sensitivity. However, it is uncertain whether baroreflex control of muscle sympathetic nerve activity (MSNA) also resets after treatment. We tested the hypothesis that chronic antihypertensive therapy alters baroreflex regulation of MSNA in patients with untreated moderate hypertension. Seven newly diagnosed patients with systolic blood pressure (BP) of 159Ϯ5 mm Hg (meanϮSE) and diastolic BP of 103Ϯ4 mm Hg were studied before and after 1 to 2 weeks´and 3 months (chronic) of antihypertensive treatment with losartan-hydrochlorothiazide (Hyzaar). MSNA and hemodynamics were measured supine, during a Valsalva maneuver (VM), and at 70°h ead-up tilt (HUT) for 10 minutes. Data were compared with those obtained in 7 age-matched healthy controls. We found that Hyzaar lowered mean BP acutely and chronically by 20Ϯ4 and 23Ϯ3 mm Hg (both PϽ0.01) but did not change HR. Supine MSNA increased by 43Ϯ11% and 34Ϯ11% after acute and chronic treatment (both PϽ0.01). However, MSNA responses to VM and HUT did not differ after treatment compared with before treatment, indicating unchanged reflex control. These data indicate that sympathetic neural activity was augmented substantially by antihypertensive treatment with Hyzaar, consistent with an ongoing baroreflex unloading, and did not return to baseline or "reset" after 3 months of therapy. We speculate that persistent and marked sympathetic activation by the baroreflex may be a potential mechanism for hypertension that is refractory to antihypertensive therapy and may provide a target mechanism for persistent morbidity despite adequate BP control. Key Words: baroreceptors Ⅲ autonomic nervous system Ⅲ renin-angiotensin system L owering blood pressure (BP) by antihypertensive agents decreases morbidity and mortality in patients with hypertension. 1 However, the risk of stroke, myocardial infarction, or congestive heart failure remains high in such patients, even with adequate BP control. 2 Moreover, many patients have inadequate BP control despite medical therapy often involving multiple drug regimens. 3 One potential mechanism for both of these problems may be persistent or even augmented sympathetic activation by the baroreflex.Previous studies have demonstrated that antihypertensive treatment resets the vagally mediated baroreflex control of heart rate (HR) to a lower pressure level and increases cardiac vagal baroreflex sensitivity acutely and chronically. 4 -6 However, it is uncertain whether baroreflex control of sympathetic neural activity also resets after antihypertensive therapy. Results regarding the effects of acute antihypertensive treatment on sympathetic baroreflex function are few and controversial. Enhanced, 7 attenuated, 8,9 or unchanged 10 baroreflex sensitivity has been reported. There have been fewer studies on baroreflex regulation of muscle sympathetic nerve activity (MSNA) during chronic antihypertensi...

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Effects of intravenous infusions of angiotensin II on muscle sympathetic nerve activity in humans

Cited by 75 publications

References 0 publications

Differentiated Response of the Sympathetic Nervous System to Angiotensin-Converting Enzyme Inhibition in Hypertension

Differentiated Response of the Sympathetic Nervous System to Angiotensin-Converting Enzyme Inhibition in Hypertension

Sympathetic nervous system behavior in human obesity

Persistent Sympathetic Activation During Chronic Antihypertensive Therapy

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