Differential Effects of Captopril and Nitrates on Muscle Sympathetic Nerve Activity in Volunteers

Noll, Georg; Wenzel, René R.; Marchi, Stefano de; Shaw, Sidney; Lüscher, Thomas F.

doi:10.1161/01.cir.95.9.2286

Cited by 54 publications

(29 citation statements)

References 51 publications

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“…25 Hence, arterial baroreceptors may have been activated by methoxamine, although arterial pressure and filling pressure of the left heart were similar to baseline values. 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.…”

Section: Discussionsupporting

confidence: 93%

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: 93%

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

et al. 2000

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“…3,4,7 One study reported no increase in MSNA in hypertensive patients, 18 but the population included subjects of advanced age being treated with antihypertensive medications, which could affect baseline MSNA levels. 20 Another important observation of the present study is that acute hyperoxia-normalized sympathetic activity in hypertensive patients reaching the values observed in control subjects. This fact seems to confirm the hypothesis that tonic chemoreflex drive may be responsible, at least in part, for sympathetic overactivity in hypertension.…”

Section: Discussionsupporting

confidence: 67%

Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension

et al. 2011

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Carotid chemoreceptors provoke an increase in muscle sympathetic nerve activation (MSNA) in response to hypoxia; they are also tonically active during normoxic breathing. The contribution of peripheral chemoreceptors to sympathetic activation in hypertension is incompletely understood. The aim of our study was to investigate the effect of chemoreceptor deactivation on sympathetic activity in untreated patients with hypertension. A total of 12 untreated hypertensive males and 11 male controls participated in this randomized, crossover, placebo-controlled study. MSNA, systolic blood pressure(BP), diastolic BP, heart rate (HR), electrocardiogram, hemoglobin oxygen saturation (Sat%) and respiratory movements were measured during repeated 10-min periods of respiration with 100% oxygen or 21% oxygen in a blinded fashion. Compared with controls, hypertensives had higher resting MSNA (38±10 vs. 29±0.9 burst per min, Po0.05), systolic BP (150±12 vs. 124±10 mm Hg, Po 0.001) and diastolic BP (92 ± 10 vs. 77 ± 9 mm Hg, Po0.005). Breathing 100% oxygen caused significant decrease in MSNA in hypertensive patients (38 ± 10 vs. 26 ± 8 burst per min and 100 ± 0 vs. 90 ± 10 arbitrary units, Po0.05) and no change in controls (29±9 vs. 27±7 burst per min and 100±0 vs. 96±11 arbitrary units). BP, respiratory frequency and end tidal CO 2 did not change during chemoreceptor deactivation with hyperoxia. HR decreased and Sat% increased in both the study groups. These results confirm the role of tonic chemoreceptor drive in the development of sympathetic overactivity in hypertension.

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“…The fact that baseline BP was decreased and MSNA augmented is unlikely to affect the stress response, because isosorbide dinitrate, a vasodilator that induced similar changes in these parameters, has been shown not to alter sympathetic and BP responses to mental stress. 27 Ghrelin may possibly affect stress response through a central effect. Peripheral or intraperitoneal administration of ghrelin induces c-fos expression in the paraventricular nucleus of rats, 28 an area involved in a neural network mediating the autonomic, neuroendocrine, and skeletal-motor responses of fear and anxiety, 29 which may be a prime area for mediating the effects of ghrelin on the cardiovascular response to stress.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin Modulates Sympathetic Nervous System Activity and Stress Response in Lean and Overweight Men

Lambert

Ika-Sari

et al. 2011

Hypertension

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Abstract-Ghrelin is a growth hormone-releasing peptide secreted by the stomach with potent effects on appetite.Experimental and clinical studies indicate that ghrelin also influences cardiovascular regulation and metabolic function and mediates behavioral responses to stress. We investigated the effects of ghrelin on blood pressure (BP), sympathetic nervous system activity, and mental stress responses in lean (nϭ13) and overweight or obese (nϭ13) individuals. Subjects received an intravenous infusion of human ghrelin (5 pmol/kg per minute for 1 hour) and saline in a randomized fashion. Ghrelin decreased systolic (Ϫ6 and Ϫ11 mm Hg) and diastolic BP (Ϫ8 mm Hg for both), increased muscle sympathetic nervous system activity (18Ϯ2 to 28Ϯ3 bursts per min, PϽ0.05 and from 21Ϯ2 to 32Ϯ3 bursts per min, PϽ0.001) in lean and overweight or obese subjects, respectively, without a significant change in heart rate, calf blood flow, or vascular resistance. Ghrelin induced a rise in plasma glucose concentration in lean individuals (PϽ0.05) and increased cortisol levels in both groups (PϽ0.05). Stress induced a significant change in mean BP (ϩ22 and ϩ27 mm Hg), heart rate (ϩ36 and ϩ29 bpm), and muscle sympathetic nervous system activity (ϩ6.1Ϯ1.6 and ϩ6.8Ϯ2.7 bursts per min) during saline infusion in lean and overweight or obese subjects, respectively. During ghrelin infusion, the changes in BP and muscle sympathetic nerve activity in response to stress were significantly reduced in both groups (PϽ0.05). In conclusion, ghrelin exerts unique effects in that it reduces BP and increases muscle sympathetic nervous system activity and blunts cardiovascular responses to mental stress. These responses may represent a combination of peripheral (baroreflex-mediated) and central effects of ghrelin. (Hypertension. 2011;58:43-50.)

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Differential Effects of Captopril and Nitrates on Muscle Sympathetic Nerve Activity in Volunteers

Cited by 54 publications

References 51 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

Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension

Ghrelin Modulates Sympathetic Nervous System Activity and Stress Response in Lean and Overweight Men

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