Sympathetic Activity, Vascular Capacitance, and Long-Term Regulation of Arterial Pressure

Fink, Gregory D.

doi:10.1161/hypertensionaha.108.119990

Cited by 74 publications

(82 citation statements)

References 78 publications

(82 reference statements)

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“…Furthermore, our studies highlight the fact that neurogenic mechanisms underlying some forms of hypertension may not be limited to effects on the kidneys alone. Our results in fact indicate that changes in sympathetic control of splanchnic vascular resistance and capacitance dominate the neurogenic component of ANG II-salt hypertension (8). Whether the splanchnic vascular bed is an important sympathetic target in other salt-sensitive forms of hypertension is yet to be determined.…”

Section: Discussionmentioning

confidence: 64%

“…This appears to contribute to the hypertension by increasing splanchnic vascular resistance and reducing splanchnic vascular capacitance, and through their expected overall impact on total peripheral resistance and effective circulating blood volume. These combined effects would elevate AP by effectively translocating blood from the highly compliant venous compartment to the less compliant arterial compartment as suggested in a recent review (8).…”

Section: Discussionmentioning

confidence: 95%

“…These findings suggest that the increase in MCFP during ANG II-salt hypertension is secondary to sympathetically mediated venoconstriction in the splanchnic vascular bed, causing a reduction in splanchnic vascular capacitance. Based on these findings, it has been proposed that the neurogenic reduction in splanchnic vascular capacitance contributes to higher levels of ANG II-induced hypertension in high-salt rats by redistributing blood volume from the venous to the arterial circulation (8).…”

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confidence: 99%

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Time-dependent changes in autonomic control of splanchnic vascular resistance and heart rate in ANG II-salt hypertension

Kuroki

Guzmán

Fink

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Kuroki MT, Guzman PA, Fink GD, Osborn JW. Time-dependent changes in autonomic control of splanchnic vascular resistance and heart rate in ANG II-salt hypertension. Am J Physiol Heart Circ Physiol 302: H763-H769, 2012. First published November 23, 2011 doi:10.1152/ajpheart.00930.2011.-Previous studies suggest that ANG II-induced hypertension in rats fed a high-salt (HS) diet (ANG II-salt hypertension) has a neurogenic component dependent on an enhanced sympathetic tone to the splanchnic veins and independent from changes in sympathetic nerve activity to the kidney or hind limb. The purpose of this study was to extend these findings and test whether altered autonomic control of splanchnic resistance arteries and the heart also contributes to the neurogenic component. Mean arterial pressure (MAP), heart rate (HR), superior mesenteric artery blood flow, and mesenteric vascular resistance (MVR) were measured during 4 control days, 14 days of ANG II delivered subcutaneously (150 ng · kg Ϫ1 · min Ϫ1 ), and 4 days of recovery in conscious rats fed a HS (2% NaCl) or low-salt (LS; 0.1% NaCl) diet. Autonomic effects on MAP, HR, and MVR were assessed by acute ganglionic blockade with hexamethonium (20 mg/kg iv) on day 3 of control, days 1,3,5,7,10, and 13 of ANG II, and day 4 of recovery. MVR increased during ANG II infusion in HS and LS rats but remained elevated only in HS rats. Additionally, the MVR response to hexamethonium was enhanced on days 10 and 13 of ANG II selectively in HS rats. Compared with LS rats, HR in HS rats was higher during the 2nd wk of ANG II, and its response to hexamethonium was greater on days 7, 10, and 13 of ANG II. These results suggest that ANG II-salt hypertension is associated with delayed changes in autonomic control of splanchnic resistance arteries and the heart. salt-sensitive hypertension; differential regulation of sympathetic outflow; splanchnic nerve activity; ganglionic blockade; hemodynamic measurement in conscious rats; angiotensin II UNDER CERTAIN CONDITIONS, hypertension resulting from systemic administration of angiotensin II (ANG II-induced hypertension) is exacerbated by activation of the sympathetic nervous system (SNS). Our group and others have shown that salt intake is one such condition (19,21). In rats fed a relatively high salt diet (2% NaCl), the level of blood pressure achieved in ANG II-induced hypertension is significantly higher than in rats fed a normal salt diet (0.4% NaCl); this is associated with an increase in whole body norepinephrine (NE) spillover (14) and enhanced mean arterial pressure (MAP) responses to ganglionic blockade (13,15). In contrast, these measures of whole body sympathetic tone in rats fed a normal salt diet remain near control levels.Despite increased "whole body" sympathetic tone in ANG II-salt (i.e., those fed a high-salt diet) hypertensive rats, we recently reported that sympathetic nerve activity (SNA) to the kidney and hind limb were reduced or unchanged, respectively (28). Suppression of renal SNA has also been directly measured duri...

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Section: Discussionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

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Time-dependent changes in autonomic control of splanchnic vascular resistance and heart rate in ANG II-salt hypertension

Kuroki

Guzmán

Fink

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…1,2 In particular, it has been proposed that attenuated venous elasticity and capacity affect blood volume redistribution in such a manner that blood volume moves from peripheral veins into small arteries 3 or centrally, 2,4 contributing to chronic increases in arterial blood pressure (BP). Supporting this conceptual scheme, previous studies found reduced venous distensibility and blood holding capacity in animals 5,6 and humans [7][8][9] with hypertension.…”

Section: Introductionmentioning

confidence: 99%

“…It was hypothesized that calf venous compliance and capacitance responses to lower body negative pressure (LBNP) would be impaired in subjects with HBP compared with agematched NT controls. Previous studies suggested that the contribution of the venous system to hypertension may be instrumental at the beginning of the hypertensive process; 1,6,9 thus, we studied non-medicated subjects with prehypertension and stage-1 hypertension.…”

Section: Introductionmentioning

confidence: 99%

Limb venous compliance responses to lower body negative pressure in humans with high blood pressure

et al. 2011

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This study tested the hypothesis that limb venous responses to baroreceptor unloading are altered in individuals with high blood pressure (HBP) compared with normotensive (NT) controls. Calf venous compliance was assessed in 20 subjects with prehypertension and stage-1 hypertension (mean arterial pressure, MAP: 104 ± 1 mm Hg) and 13 NT controls (MAP: 86 ± 2 mm Hg) at baseline and during lower body negative pressure (LBNP), using venous occlusion plethysmography. Baroreflex sensitivity (BRS) was measured using the sequence technique and total peripheral resistance (TPR) was estimated from finger plethysmography. Baseline venous compliance was not different between groups, but the HBP group had lower baseline lnBRS (2.22±0.14 vs 2.7±0.18 ms mm Hg À1) and greater baseline TPR (3828 ± 138 vs 3250 ± 111 dyn sec À1 cm À5 m 2 , Po0.05). Calf venous compliance was reduced in response to LBNP only in the NT group (Po0.05). The HBP group had a greater increase in TPR (DTPR) compared with the NT group ( þ 1649 ± 335 vs þ 718 ± 196 dyn sec À1 cm À5 m 2 , Po0.05). In conclusion, the early stages of hypertension are characterized by an attenuated venoconstrictor response to baroreceptor unloading, which may compensate for an exaggerated vasoconstrictor response and protect against further increases in blood pressure.

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Physical (in)activity‐dependent structural plasticity in bulbospinal catecholaminergic neurons of rat rostral ventrolateral medulla

Mischel

Llewellyn‐Smith

Mueller

2013

J of Comparative Neurology

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Increased activity of the sympathetic nervous system is thought to play a role in the development and progression of cardiovascular disease. Recent work has shown that physical inactivity versus activity alters neuronal structure in brain regions associated with cardiovascular regulation. Our physiological studies suggest that neurons in the rostral ventrolateral medulla (RVLM) are more responsive to excitation in sedentary versus physically active animals. We hypothesized that enhanced functional responses in the RVLM may be due, in part, to changes in the structure of RVLM neurons that control sympathetic activity. We used retrograde tracing and immunohistochemistry for tyrosine hydroxylase (TH) to identify bulbospinal catecholaminergic (C1) neurons in sedentary and active rats after chronic voluntary wheel-running exercise. We then digitally reconstructed their cell bodies and dendrites at different rostrocaudal levels. The dendritic arbors of spinally-projecting TH neurons from sedentary rats were more branched than those of physically active rats (p<0.05). In sedentary rats, dendritic branching was greater in more rostral versus more caudal bulbospinal C1 neurons whereas, in physically active rats, dendritic branching was consistent throughout the RVLM. In contrast, cell body size and the number of primary dendrites did not differ between active and inactive animals. We suggest that these structural changes provide an anatomical underpinning for the functional differences observed in our in vivo studies. These inactivity-related structural and functional changes enhance the overall sensitivity of RVLM neurons to excitatory stimuli and may contribute to an increased risk of cardiovascular disease in sedentary individuals.

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Sympathetic Activity, Vascular Capacitance, and Long-Term Regulation of Arterial Pressure

Cited by 74 publications

References 78 publications

Time-dependent changes in autonomic control of splanchnic vascular resistance and heart rate in ANG II-salt hypertension

Time-dependent changes in autonomic control of splanchnic vascular resistance and heart rate in ANG II-salt hypertension

Limb venous compliance responses to lower body negative pressure in humans with high blood pressure

Physical (in)activity‐dependent structural plasticity in bulbospinal catecholaminergic neurons of rat rostral ventrolateral medulla

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