Atrial Natriuretic Peptide Attenuates the Reflex Sympathetic Responses to Lower Body Negative Pressure

Imam, Khaled; Maddens, Michael; Mohanty, Pramod K.; Sowers, James R.; Felicetta, James V.

doi:10.1097/00000441-198907000-00001

Cited by 13 publications

(3 citation statements)

References 20 publications

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“…baroreflexes; arterial pressure; hemodynamics FOR DECADES, LOW LEVELS (i.e., Յ20 mmHg) of lower body negative pressure (LBNP) have been firmly believed to be a useful tool for separating the contribution of cardiopulmonary and arterial baroreflexes to circulatory control in humans (1, 34, 56). They have been utilized "selectively" to unload cardiopulmonary baroreceptors in many studies based on the fact that steady-state mean arterial pressure and heart rate have been found unchanged (5,26,28,40,46,54), forearm blood flow and conductance decreased (38, 56), while muscle sym- …”

mentioning

confidence: 99%

Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans

Fu¹,

Shibata

Hastings³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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mentioning

confidence: 99%

Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans

Fu¹,

Shibata

Hastings³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…It is also possible that additional mechanisms, in addition to cardiac hypertrophy, were involved in the present study. Hormones, such as atrial natriuretic peptide (ANP), are known to positively influence the sensitivity of the cardiopulmonary reflex 26,27 . However, Thomas et al 14 .…”

Section: Discussionmentioning

confidence: 99%

Role of Cardiac Hypertrophy in Reducing the Sensitivity of Cardiopulmonary Reflex Control of Renal Sympathetic Nerve Actvity in Spontaneously Hypertensive Rats

Andrade

Abreu

Moysés

et al. 2008

Clin Exp Pharma Physio

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The gain of the volume-sensitive cardiopulmonary reflex (VSCR) is impaired in spontaneously hypertensive rats (SHR). Sensitivity of VSCR control of efferent renal sympathetic nerve activity (RSNA) in SHR is restored when cardiac hypertrophy and hypertension are reduced by enalapril treatment. The present study investigated which of these two parameters, cardiac hypertrophy or hypertension, has more influence on the impairment of VSCR control of RSNA in SHR. Rats (SHR or Wistar-Kyoto (WKY) rats) were treated with enalapril (10 mg/kg per day; SHRE and WKYE groups, respectively) or hydralazine (5 mg/kg per day; SHRH and WKYH groups, respectively) mixed in their food for 1 month. Control SHR and WKY rats were fed a normal diet. After the treatment regimen, the VSCR was evaluated by determining the decrease in RSNA elicited by acute isotonic saline volume expansion. Mean arterial pressure (MAP) was assessed via an intrafemural catheter and cardiac hypertrophy was determined by the left ventricular (LV) weight/bodyweight (BW) ratio. Afferent baroceptor nerve activity (BNA) was also evaluated during volume expansion to verify participation of the baroreflex. Volume expansion produced an attenuated renal sympathoinhibitory response in SHR compared with WKY rats. Enalapril treatment restored the volume expansion-induced decrease in RSNA in SHRE (-41 +/- 8%) compared with WKY rats (-44 +/- 3%). Although both enalapril and hydralazine treatment reduced MAP in SHR (P < 0.01; 126 +/- 5, 133 +/- 6 and 160 +/- 6 mmHg in SHRE, SHRH and SHR, respectively), hydralazine did not restore the sensitivity of VSCR control of RSNA in SHRH. Spontaneously hypertensive rats with established hypertension had a higher LV/BW ratio compared with WKY rats (3.22 +/- 0.14 vs 1.98 +/- 0.06 mg/g, respectively; P < 0.01). Enalapril reduced the LV/BW ratio in SHRE (2.30 +/- 0.07 mg/g; P < 0.01). Although hydralazine reduced LV hypertrophy, there was a weaker reduction in SHRH (2.68 +/- 0.04 mg/g; P < 0.05) compared with SHRE. There was no statistically significant difference among the WKY rat, WKYE and WKYH groups (P > 0.05). There was no change in afferent BNA during volume expansion in normal or hypertensive animals. Taken together, these results indicate that the impairment of VSCR control of RSNA in the SHR model of hypertension correlates better with the magnitude of cardiac hypertrophy than the level of arterial pressure.

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“…ANF lowers plasma renin activity (PRA) in supine, resting, salt-depleted volunteers and in seated healthy subjects undergoing water diuresis (Struthers et al, 1986; Anderson et a]., Cuneo et af., 1987). ANF also abolishes the PRA response to upright tilt and lower body negative pressure in man (Williams et al, 1988a;Imam et al, 1989).…”

mentioning

confidence: 99%

Comparison of the effects of ANF 99–126 and ANF 103–126 on captopril‐induced renin release in man

Lang

McMurray

Moyses³

et al. 1991

Clinical Endocrinology

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Atrial Natriuretic Peptide Attenuates the Reflex Sympathetic Responses to Lower Body Negative Pressure

Cited by 13 publications

References 20 publications

Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans

Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans

Role of Cardiac Hypertrophy in Reducing the Sensitivity of Cardiopulmonary Reflex Control of Renal Sympathetic Nerve Actvity in Spontaneously Hypertensive Rats

Comparison of the effects of ANF 99–126 and ANF 103–126 on captopril‐induced renin release in man

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