Subpressor angiotensin II infusions do not stimulate sympathetic activity in humans

Goldsmith, Steven R.; Hasking, Gregory J.

doi:10.1152/ajpheart.1990.258.1.h179

Cited by 10 publications

(5 citation statements)

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“…However, ANG II infusion alone had no effect on the basal output of NE from the heart (22). In human subjects, IV infusion of subpressor (15) and pressor (16) doses of ANG II does not result in increased NE spillover in plasma. In the present study, we found that infusion of pharmacological doses of ANG II into the arterial blood supply of right atrial neurons caused a threefold increase in ISF NE without spillover of NE into the coronary sinus.…”

Section: Discussionmentioning

confidence: 95%

Angiotensin II modulates catecholamine release into interstitial fluid of canine myocardium in vivo

Farrell

Wei

Tallaj

et al. 2001

American Journal of Physiology-Heart and Circulatory Physiology

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This study tested the hypothesis that exogenous infusion of angiotensin II (ANG II) leads to the release of catecholamines [norepinephrine (NE) and epinephrine (EPI)] into the cardiac interstitial fluid (ISF) space of dogs with adrenals intact (AI) (n = 7) and with adrenals clamped (AC) (n = 5). LV ISF samples were collected at 3-min intervals during administration of ANG II (100 microM ANG II at 1 ml/min for 10 min) to right atrial neurons via their local arterial blood supply and during electrical stimulation of the stellate ganglia of open-chest anesthetized dogs. In AI dogs, ANG II caused ISF NE to increase fivefold (P < 0.05) without a significant increase in coronary sinus (CS) NE. Electrical stimulation (5 ms, 4 Hz, 8-14 V, and 10 min) of the stellate ganglia caused a similar increase in ISF NE (P < 0.05), accompanied by a sevenfold increase in CS NE (P < 0.05). ISF EPI increased greater than sixfold during ANG II infusion (P < 0.05) and during stellate stimulation. However, during ANG II infusions, aorta plasma EPI levels increased fourfold in AI dogs, whereas in AC dogs, CS NE and EPI levels were unaffected during ANG II infusions. Nevertheless, baseline ISF NE and EPI did not differ and increased to a similar extent during ANG II infusions in AI versus AC dogs. Thus exogenously administered ANG II increases the amount of NE liberated into the ISF independent of the adrenal contribution, the amount matching that induced by electrical stimulation of all cardiac sympathetic efferent neurons. In contrast, NE spillover into the CS occurred only during electrical stimulation of stellate ganglia. NE release and uptake mechanisms within the myocardium are differently affected, depending on how the final common pathway of the sympathetic efferent nervous system is modified.

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Section: Discussionmentioning

confidence: 95%

Angiotensin II modulates catecholamine release into interstitial fluid of canine myocardium in vivo

Farrell

Wei

Tallaj

et al. 2001

American Journal of Physiology-Heart and Circulatory Physiology

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“…Indeed, in contrast to animal studies (Sanderford & Bishop, 2000, 2002), some earlier studies showed that physiological elevations of arginine vasopressin did not alter cardiac or sympathetic baroreflex function, while much higher levels of vasopressin enhanced the vasomotor sympathetic response to unloading of baroreceptors in healthy humans (Ebert & Cowley, 1992; Goldsmith, 1994). It was also found that subpressor doses of angiotensin II did not affect plasma noradrenaline (norepinephrine) concentration (Goldsmith & Hasking, 1990); however, much higher doses of angiotensin II increased muscle sympathetic nerve activity (Matsukawa et al 1991). Although humoral changes were not measured in our subjects, the data suggest that their influences on vasomotor sympathetic neural control were limited.…”

Section: Discussionmentioning

confidence: 99%

Vasomotor sympathetic neural control is maintained during sustained upright posture in humans

Shook

Okazaki

et al. 2006

The Journal of Physiology

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Vasomotor sympathetic activity plays an important role in arterial pressure maintenance via the baroreflex during acute orthostasis in humans. If orthostasis is prolonged, blood pressure may be supported additionally by humoral factors with a possible reduction in sympathetic baroreflex sensitivity. We tested the hypothesis that baroreflex control of muscle sympathetic nerve activity (MSNA) decreases during prolonged upright posture. MSNA and haemodynamics were measured supine and during 45 min 60 deg upright tilt in 13 healthy individuals. Sympathetic baroreflex sensitivity was quantified using the slope of the linear correlation between MSNA and diastolic pressure during spontaneous breathing. It was further assessed as the relationship between MSNA and stroke volume, with stroke volume derived from cardiac output (C 2 H 2 rebreathing) and heart rate. Total peripheral resistance was calculated from mean arterial pressure and cardiac output. We found that MSNA increased from supine to upright (17 ± 8 (S.D.) versus 38 ± 12 bursts min −1 ; P < 0.01), and continued to increase to a smaller degree during sustained tilt (39 ± 11, 41 ± 12, 43 ± 13 and 46 ± 15 bursts min −1 after 10, 20, 30 and 45 min of tilt; between treatments P < 0.01). Sympathetic baroreflex sensitivity increased from supine to upright (−292 ± 180 versus −718 ± 362 units beat −1 mmHg −1 ; P < 0.01), but remained unchanged as tilting continued (−611 ± 342 and −521 ± 221 units beat −1 mmHg −1 after 20 and 45 min of tilt; P = 0.49). For each subject, changes in MSNA were associated with changes in stroke volume (r = 0.88 ± 0.13, P < 0.05), while total peripheral resistance was related to MSNA during 45 min upright tilt (r = 0.82 ± 0.15, P < 0.05). These results suggest that the vasoconstriction initiated by sympathetic adrenergic nerves is maintained by ongoing sympathetic activation during sustained (i.e. 45 min) orthostasis without obvious changes in vasomotor sympathetic neural control.

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“…16 There are no signs of sympathetic overactivity during angiotensin II infusion in dogs 17 or men. 18 Taken together, these findings argue against a significant role for the central nervous system in the slow pressor responses of angiotensin II.…”

Section: Discussion Slow Responses To Angiotensin IImentioning

confidence: 99%

Low-Dose Angiotensin II Increases Free Isoprostane Levels in Plasma

et al. 1999

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Abstract-Chronic intravenous infusion of subpressor doses of angiotensin II causes blood pressure to increase progressively over the course of several days. The mechanisms underlying this response, however, are poorly understood. Because high-dose angiotensin II increases oxidative stress, and some compounds that result from the increased oxidative stress (eg, isoprostanes) produce vasoconstriction and antinatriuresis, we tested the hypothesis that a subpressor dose of angiotensin II also increases oxidative stress, as measured by 8-epi-prostaglandin F 2␣ (isoprostanes), which may contribute to the slow pressor response to angiotensin II. To test this hypothesis, we infused angiotensin II (10 ng/kg per minute for 28 days via an osmotic pump) into 6 conscious normotensive female pigs (30 to 35 kg). We recorded mean arterial pressure continuously with a telemetry system and measured plasma isoprostanes before starting the angiotensin II infusion (baseline) and again after 28 days with an enzyme immunoassay. Angiotensin II infusion significantly increased mean arterial pressure from 121Ϯ4 to 153Ϯ7 mm Hg (PϽ0.05) without altering total plasma isoprostane levels (180.0Ϯ24.3 versus 147.0Ϯ29.2 pg/mL; PϭNS). However, the plasma concentrations of free isoprostanes increased significantly, from 38.3Ϯ5.8 to 54.7Ϯ10.4 pg/mL (PϽ0.05). These results suggest that subpressor doses of angiotensin II increase oxidative stress, as implied by the increased concentration of free isoprostanes, which accompany the elevation in mean arterial pressure elevation. Thus, isoprostane-induced vasoconstriction and antinatriuresis may contribute to the hypertension induced by the slow pressor responses of angiotensin II. Key Words: kidney Ⅲ oxidative stress Ⅲ prostaglandins Ⅲ lipid peroxidation T he fast pressor effect of angiotensin II, induced by an intravenous bolus injection, is characterized by a rapid elevation of blood pressure, reaching a maximal increase of blood pressure in 1 to 2 minutes. 1,2 This effect is due to an arterial vasoconstriction. However, the mechanism responsible for the progressive increase in blood pressure with long-term administration of subpressor doses of angiotensin II 3 (slow pressor response) remains undefined. 4 Several processes have been implicated in mediating this response, but none of them appears to completely account for this phenomenon. [5][6][7][8] More recently, it has been shown that angiotensin can stimulate superoxidation (O 2 ), which may quench nitric oxide (NO) with the formation of strong oxidative compounds such as peroxynitrite (ONOO Ϫ ). 9,10 Under these conditions, ONOO Ϫ could oxidize arachidonic acid, releasing isoprostanes. 11,12 Among these substances, the 8-isoprostaglandin F 2␣ is considered the most ubiquitous and reliable index of oxidative stress.Isoprostanes are not only reliable markers of oxidative stress but also possess intrinsic vasoconstrictor and antinatriuretic properties via specific receptors, 11,12 raising the possibility that they contribute to the hypertensive effe...

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Subpressor angiotensin II infusions do not stimulate sympathetic activity in humans

Cited by 10 publications

References 0 publications

Angiotensin II modulates catecholamine release into interstitial fluid of canine myocardium in vivo

Angiotensin II modulates catecholamine release into interstitial fluid of canine myocardium in vivo

Vasomotor sympathetic neural control is maintained during sustained upright posture in humans

Low-Dose Angiotensin II Increases Free Isoprostane Levels in Plasma

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