Recent insights into the interactions between the baroreflex and the kidneys in hypertension

2005 ◽  
Vol 288 (4) ◽  
pp. R828-R836 ◽  
Author(s):  
Thomas E. Lohmeier ◽  
Drew A. Hildebrandt ◽  
Susan Warren ◽  
Paul J. May ◽  
J. Thomas Cunningham

Recent findings in chronically instrumented animals challenge the classic concept that baroreflexes do not play a role in the chronic regulation of arterial pressure. As alterations in renal excretory function are of paramount importance in the chronic regulation of arterial pressure, several of these recent studies have focused on the long-term interactions between the baroreflex and the kidneys during chronic perturbations in arterial pressure and body fluid volumes. An emerging body of evidence indicates that the baroreflex is chronically activated in several experimental models of hypertension, but in most cases, the duration of these studies has not exceeded 2 wk. Although these studies suggest that the baroreflex may play a compensatory role in attenuating the severity of the hypertension, possibly even in primary hypertension with uncertain causes of sympathetic activation, there has been only limited assessment of the quantitative importance of this interaction in the regulation of arterial pressure. In experimental models of secondary hypertension, baroreflex suppression of renal sympathetic nerve activity is sustained and chronically promotes sodium excretion. This raises the possibility that the renal nerves may be the critical efferent link for baroreceptor-induced suppression of central sympathetic output through which long-term compensatory reductions in arterial pressure are produced. This contention is supported by strong theoretical evidence but must be corroborated by experimental studies. Finally, although it is now clear that pressure-induced increases in baroreflex activity persist for longer periods of time than previously suggested, studies using new tools and novel approaches and extending beyond 2 wk of hypertension are needed to elucidate the true role of the baroreflex in the pathogenesis of clinical hypertension.

2012 ◽  
Vol 113 (10) ◽  
pp. 1652-1658 ◽  
Author(s):  
Thomas E. Lohmeier ◽  
Radu Iliescu

Device-based therapy for resistant hypertension by electrical activation of the carotid baroreflex is currently undergoing active clinical investigation, and initial findings from clinical trials have been published. The purpose of this mini-review is to summarize the experimental studies that have provided a conceptual understanding of the mechanisms that account for the long-term lowering of arterial pressure with baroreflex activation. The well established mechanisms mediating the role of the baroreflex in short-term regulation of arterial pressure by rapid changes in peripheral resistance and cardiac function are often extended to long-term pressure control, and the more sluggish actions of the baroreflex on renal excretory function are often not taken into consideration. However, because clinical, experimental, and theoretical evidence indicates that the kidneys play a dominant role in long-term control of arterial pressure, this review focuses on the mechanisms that link baroreflex-mediated reductions in central sympathetic outflow with increases in renal excretory function that lead to sustained reductions in arterial pressure.


1975 ◽  
Vol 97 (3) ◽  
pp. 259-265
Author(s):  
K. Sagawa

This paper reviews Guyton’s model which is large not only in the number of its components but also in the time scale that it spans. The evolution of this model is explained in three stages. Guyton started with a drastically simplified model of the entire cardiovascular system as a closed hydraulic loop. It accounted for short-term regulations of cardiac output with a special emphasis on the role of blood volume and the vascular capacity. Guyton’s research objective was then directed toward the analysis of longterm regulation of arterial pressure. Two slowly acting mechanisms were considered as particularly important: (1) the marked increase or decrease of urinary output with only slight increase or decrease in arterial pressure (the renal function curve in the Guytonian model) and (2) long-term vascular autoregulation which includes changes in the extent of vascularization as well as constriction or dilation of existing vessels to match the blood flow with the oxygen demand in tissues. This second-stage model explained the transient dynamics and steady equilibrium of renal hypertension. The current version of Guyton’s model incorporates a variety of additional endocrine and neural mechanisms which parametrically control the renal function curve. With the enormous growth, the identification (or estimation) capability of the model is bound to degrade while its use for multiple parameter sensitivity tests expands. The modeller’s group has attempted to minimize the hazards by frequent checks of model predictions with experimental studies. This interactive effort, plus their concern over these long-term regulatory mechanisms, make the Guytonian model a unique venture in modern cardiovascular physiology.


1981 ◽  
Vol 241 (6) ◽  
pp. H883-H890 ◽  
Author(s):  
O. U. Lopes ◽  
V. Pontieri ◽  
M. Rocha e Silva ◽  
I. T. Velasco

Infusions of hyperosmotic NaCl (2,400 mosmol/l; 4 ml/kg) were given to dogs in severe hemorrhagic hypotension by intravenous injection (72 expts) or intra-aortic injection (25 expts). In 46 experiments intravenous infusions were given during bilateral blockage of the cervical vagal trunks (local anesthesia or cooling). Intravenous infusions (without vagal blockade) restore arterial pressure, cardiac output, and acid-base equilibrium to normal and cause mesenteric flow to overshoot prehemorrhage levels by 50%. These effects are stable, and indefinite survival was observed in every case. Intra-aortic infusions of hyperosmotic NaCl produce only a transient recovery of arterial pressure and cardiac output but no long-term survival. Intravenous infusions with vagal blockage produce only a transient recovery of cardiac output, with non long-term survival. Measurement of pulmonary artery blood osmolarity during and after the infusions shows that a different pattern is observed in each of these three groups and strongly indicates that the first passage of hyperosmotic blood through the pulmonary circulation at a time when vagal conduction is unimpaired is essential for the production of the full hemodynamic-metabolic response, which is needed for indefinite survival.


2020 ◽  
Author(s):  
Eduardo Rossi ◽  
Frances Beckett ◽  
Costanza Bonadonna ◽  
Gholamhossein Bagheri

<p>Most volcanic ash produced during explosive volcanic eruptions sediments as aggregates of various types that typically have a greater fall velocity than the particles of which they are composed. As a result, aggregation processes are commonly known to affect the sedimentation of fine ash by considerably reducing its residence time in the atmosphere. Nonetheless, speculations also exist in the literature that aggregation does not always result in a premature sedimentation of their constitute particles but that it can also result in a delayed sedimentation (i.e. the so-called rafting effect). However, previous studies have considered rafting as a highly improbable phenomenon due to a biased representation of aggregate shapes.</p><p>Here we provide the first theoretical evidence that rafting may not only occur, but it is probably more common than previously thought, helping to elucidate often unexplained field observations. Starting from field evidence of rafted aggregates at Sakurajima Volcano (Japan), we clarify the conditions for which aggregation of volcanic ash results either in a premature or a delayed sedimentation.</p><p>Moreover, using the Lagrangian dispersion model NAME, we show the practical consequences of rafting on the final sedimentation distance of aggregates with different morphological features. As an application we chose the case study of the 2010 eruption of Eyjafjallajökull volcano (Iceland), for which rafting can increase the travel distances of ash <500 m up 3.7 times with respect to sedimentation of individual particles.</p><p>These findings have fundamental implications both for real-time forecasting and long-term hazard assessment of volcanic ash dispersal and sedimentation and for weather modelling. The constraints on rafting presented and discussed in this work will help the scientific community to clarify the often unexpected role of aggregation in creating a delayed sedimentation of coarse ash.</p>


2016 ◽  
Vol 95 (2) ◽  
pp. 103
Author(s):  
Brendha Cação ◽  
Ávaro Simões ◽  
Cícero Mendes ◽  
Heraldo P. Souza

Clinical and experimental evidences pointed to the role of immune cells and inflammatory mediators on the development of diseases in obese patients. Therefore, it is our objective to explore experimental studies that approach the relationship between the different types of inflammatory reaction inside the adipose tissue, particularly the macrophage polarization and the development of obesity complications. Further, we intend to speculate how to translate this knowledge, obtained from experimental studies, to treatments applicable to the human diseases. PubMed database was sought using the terms “obesity”, “macrophage” and “polarization”. After applying the filters “Language - English” and “Species - Animals”, we arrived to 90 references. Sixty-two were excluded for being reviews or not related to the main subject. Results in experimental models of obesity pointed a relevant correlation between the macrophage polarization to a type 1 response (M1) inside white adipose tissue and the development of insulin resistance, diabetes and other complications of obesity. Several articles report strategies to shift to a type 2 phenotype (M2), using drugs or lifestyle changes. How these findings could be translated to new human treatments is still an open question that only well designed researches could answer.


2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
H. M. Semchyshyn

There is compelling evidence that long-term intake of excessive fructose can have deleterious side effects in different experimental models. However, the role of fructosein vivoremains controversial, since acute temporary application of fructose is found to protect yeast as well as animal tissues against exogenous oxidative stress. This review suggests the involvement of reactive carbonyl and oxygen species in both the cytotoxic and defensive effects of fructose. Potential mechanisms of the generation of reactive species by fructose in the nonenzymatic reactions, their implication in the detrimental and protective effects of fructose are discussed.


Hypertension ◽  
1999 ◽  
Vol 34 (5) ◽  
pp. 1101-1105 ◽  
Author(s):  
Charlotte Wagner ◽  
Markus Hinder ◽  
Bernhard K. Krämer ◽  
Armin Kurtz

1982 ◽  
Vol 243 (2) ◽  
pp. H284-H288 ◽  
Author(s):  
R. A. Norman ◽  
D. J. Dzielak

Renal denervation has been reported to delay development of hypertension in Okamoto spontaneously hypertensive rats (SHR) but to have no effect on the final hypertensive state. However, functional reinnervation begins to occur about 1 mo after renal denervation. The arterial pressure of SHR undergoing repeated bilateral renal denervations at the age of 4, 7, 10, 13, and 16 wk was compared with that in sham-operated SHR. In addition, the effect of successive renal denervations at 4, 7, and 10 wk of age in Wistar-Kyoto (WKY) control rats was determined. Both indirect measurement of pressure by the tail-cuff technique and mean arterial pressure (MAP) measurement indicated that renal denervation prevents full expression of hypertension in SHR. MAP in 19-wk-old renal-denervation SHR averaged 159 +/- 5.1 mmHg (SE) vs. 178 +/-0 4.2 mmHg in sham-operated SHR. Renal denervation had no effect on arterial pressure of WKY rats. Renal norepinephrine content in the renal-denervated WKY rats and SHR was less than 20% of that in the sham-operated groups. Successive bilateral renal denervations every 3 wk blocks 30-40% of the expected progressive elevation of arterial pressure in aging SHR.


2016 ◽  
Author(s):  
Daniele Lana

Neurodegenerative processes alter neuronal and glial physiology and cause cognitive and mnemonic impairments. Aim of this PhD thesis is to investigate the involvement of the cholinergic system and the role of mTOR pathway in the mechanisms of memory encoding in the hippocampus and to study the pathophysiological processes at the base of the cognitive impairments in different experimental models of neurodegeneration: in particular normal brain aging, neuroinfiammation and chronic cerebral hypoperfusion. These mechanisms are studied focusing on the morpho-functional alterations in the neuron-astrocytemicroglia triad.


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