Systems analysis of arterial pressure regulation and hypertension

Guyton, Arthur C.; Tg, Coleman; Aw, Cowley; Jf, Liard; Ra, Norman; Rd, Manning

doi:10.1007/bf02584211

Cited by 110 publications

(71 citation statements)

References 22 publications

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“…16 Furthermore, Guyton and colleagues modeled the redundant and counterbalancing multiplicity of physiological and biochemical systems interacting to regulate blood pressure, long before "systems biology" came into vogue. 17,18 Although blood pressure lowering in response to mono or combination drug therapies had been shown to differ widely among individuals, 19 the first JNC report in 1977 recommended that the initial diagnostic evaluation be limited to patient history and physical examination. 20 Notwithstanding the admonition that "all patients must receive individualized therapy programs," a standardized, stepped-care approach to treatment was advocated for all patients, beginning with a thiazide diuretic.…”

Section: History Of Personalized Medicine For Hypertensionmentioning

confidence: 99%

Personalized Medicine for High Blood Pressure

2007

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Section: History Of Personalized Medicine For Hypertensionmentioning

confidence: 99%

Personalized Medicine for High Blood Pressure

2007

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“…The prevailing view on the causal relationship among salt intake, total body Na ϩ and fluid balance, and blood pressure (BP) follows the basic notion that extracellular bodily fluids are in equilibrium, [3][4][5] that the kidney controls total body Na ϩ content and thereby the extracellular volume exclusively, and that increases in extracellular volume lead to increased BP. 6,7 The underlying concept of extracellular Na ϩ , volume, and BP homeostasis controlled by the kidney relies on the idea that interstitial Na ϩ is readily equilibrated with plasma Na ϩ , can be easily mobilized into the bloodstream, and that the kidneys control interstitial Na ϩ and volume indirectly by means of blood purification.…”

mentioning

confidence: 99%

Mononuclear Phagocyte System Depletion Blocks Interstitial Tonicity-Responsive Enhancer Binding Protein/Vascular Endothelial Growth Factor C Expression and Induces Salt-Sensitive Hypertension in Rats

et al. 2010

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Abstract-We showed recently that mononuclear phagocyte system (MPS) cells provide a buffering mechanism for salt-sensitive hypertension by driving interstitial lymphangiogenesis, modulating interstitial Na ϩ clearance, and increasing endothelial NO synthase protein expression in response to very high dietary salt via a tonicity-responsive enhancer binding protein/vascular endothelial growth factor C regulatory mechanism. We now tested whether isotonic saline and deoxycorticosterone acetate (DOCA)-salt treatment leads to a similar regulatory response in Sprague-Dawley rats. Male rats were fed a low-salt diet and received tap water (low-salt diet LSD), 1.0% saline (high-salt diet HSD), or DOCAϩ1.0% saline (DOCA-HSD). To test the regulatory role of interstitial MPS cells, we further depleted MPS cells with clodronate liposomes. HSD and DOCA-HSD led to Na ϩ accumulation in the skin, MPS-driven tonicity-responsive enhancer binding protein/ vascular endothelial growth factor C-mediated hyperplasia of interstitial lymph capillaries, and increased endothelial NO synthase protein expression in skin interstitium. Clodronate liposome MPS cell depletion blocked MPS infiltration in the skin interstitium, resulting in unchanged tonicity-responsive enhance binding protein/vascular endothelial growth factor C levels and absent hyperplasia of the lymph capillary network. Moreover, no increased skin endothelial NO synthase protein expression occurred in either clodronate liposome-treated HSD or DOCA-salt rats. Thus, absence of the MPS-cell regulatory response converted a salt-resistant blood-pressure state to a salt-sensitive state in HSD rats. Furthermore, salt-sensitive hypertension in DOCA-salt rats was aggravated. We conclude that MPS cells act as onsite controllers of interstitial volume and blood pressure homeostasis, providing a local regulatory salt-sensitive tonicity-responsive enhancer binding protein/ vascular endothelial growth factor C-mediated mechanism in the skin to maintain normal blood pressure in states of interstitial Na ϩ and Cl Ϫ accumulation. Failure of this physiological extrarenal regulatory mechanism leads to a salt-sensitive blood pressure response. (Hypertension. 2010;55:755-761.)

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“…To this extent, Guyton et al proposed that extracellular fluid volume is maintained by the kidneys via renal excretion of sodium and water depending on dietary intake. [5][6][7] The kidney in response to increased renal perfusion pressures alters sodium and water excretion to maintain fluid homeostasis, whereby increased pressure translates to increased sodium and water excretion which is now termed as "pressure natriuresis". In normotensive individuals, renal pressure natriuresis is capable of handling transient variations of intravascular volumes triggered by increased heart rate or increased peripheral vascular resistance.…”

mentioning

confidence: 99%

“…However, it is postulated that with consistent increases in pressures, the kidney shifts to a new higher-than-normal equilibrium point for salt and water excretion resulting in higher blood pressures. [4][5][6][7] Several renal transplantation studies [8][9][10][11][12] have revealed that HTN follows the kidneys; the first study demonstrated that transplantation of kidneys from hypertensive rats to normotensive rats resulted in HTN in the normal mice and similarly transplanting kidneys from normotensive rats to hypertensive rats resulted in abrogation of blood pressures in the hypertensive rats, revealing that the kidney might play an integral role in the development of HTN.…”

mentioning

confidence: 99%

Renal sympathetic denervation increases renal blood volume per cardiac cycle: a serial magnetic resonance imaging study in resistant hypertension

Delacroix¹,

Chokka²,

Nelson³

et al. 2017

IJNRD

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Aim: Preclinical studies have demonstrated improvements in renal blood flow after renal sympathetic denervation (RSDN); however, such effects are yet to be confirmed in patients with resistant hypertension. Herein, we assessed the effects of RSDN on renal artery blood flow and diameter at multiple time points post-RSDN. Methods and results: Patients (n=11) with systolic blood pressures ≥160 mmHg despite taking three or more antihypertensive medications at maximum tolerated dose were recruited into this single-center, prospective, non-blinded study. Magnetic resonance imaging indices included renal blood flow and renal artery diameters at baseline, 1 month and 6 months. In addition to significant decreases in blood pressures (p<0.0001), total volume of blood flow per cardiac cycle increased by 20% from 6.9±2 mL at baseline to 8.4±2 mL (p=0.003) at 1 month and to 8.0±2 mL (p=0.04) 6 months post-procedure, with no changes in the renal blood flow. There was a significant decrease in renal artery diameters from 7±2 mm at baseline to 6±1 mm (p=0.03) at 1 month post-procedure. This decrease was associated with increases in maximum velocity of blood flow from 73±20 cm/s at baseline to 78±19 cm/s at 1 month post-procedure. Notably, both parameters reverted to 7±2 mm and 72±18 cm/s, respectively, 6 months after procedure. Conclusion: RSDN improves renal physiology as evidenced by significant improvements in total volume of blood flow per cardiac cycle. Additionally, for the first time, we identified a transient decrease in renal artery diameters immediately after procedure potentially caused by edema and inflammation that reverted to baseline values 6 months post-procedure.

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Systems analysis of arterial pressure regulation and hypertension

Cited by 110 publications

References 22 publications

Personalized Medicine for High Blood Pressure

Personalized Medicine for High Blood Pressure

Mononuclear Phagocyte System Depletion Blocks Interstitial Tonicity-Responsive Enhancer Binding Protein/Vascular Endothelial Growth Factor C Expression and Induces Salt-Sensitive Hypertension in Rats

Renal sympathetic denervation increases renal blood volume per cardiac cycle: a serial magnetic resonance imaging study in resistant hypertension

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