Current
Hypertension Reviews
ISSN: 1573-4021
Current Hypertension Reviews
Volume 2, Number 1, February 2006
Contents
Blood Pressure and Cognitive Impairment in the Elderly
Pp. 1-9
Giuseppe Bellelli, Angelo Bianchetti and Marco Trabucchi
[Abstract] [Purchase
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Microalbuminuria In Primary Hypertension
Pp. 11-19
Roberto Pontremoli, Francesca Viazzi, Giovanna Leoncini
and Elena Ratto
[Abstract] [Purchase
Issue/Articles]
The Resurgence of Aldosterone in Hypertension and
Cardiovascular Disease Pp. 21-32
E. Marie Freel and John M.C. Connell
[Abstract] [Purchase
Issue/Articles]
Primary Hyperaldosteronism in the Hypertensive Disease
Pp. 33-40
Carlos E. Fardella, Cristian A. Carvajal and Lorena M.
Mosso
[Abstract] [Purchase
Issue/Articles]
Usefulness of Home Blood Pressure in the Diagnosis
and Control of Hypertension in Primary Care Pp. 41-46
María A. Martínez and Juan G. Puig
[Abstract] [Purchase
Issue/Articles]
PPARγ
Agonists: Beneficial Effect on Blood Pressure Beyond Glycemic
Control? Pp. 47-60
Panteleimon A. Sarafidis and Anastasios N. Lasaridis
[Abstract] [Purchase
Issue/Articles]
Transient Receptor Potential Channels, the Kidney
and Hypertension Pp. 61-67
Paolo Menè
[Abstract] [Purchase
Issue/Articles]
Ion Channel Architecture of the Renal Microcirculation
Pp. 69-81
Malcolm R. Turner and Thomas L. Pallone
[Abstract] [Purchase
Issue/Articles]
Effect of Ouabain on the Immune System Pp.
83-95
Juliana Echevarria-Lima and Vivian M. Rumjanek
[Abstract] [Purchase
Issue/Articles]
Abstracts
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Blood Pressure and Cognitive Impairment in the Elderly
Giuseppe Bellelli, Angelo Bianchetti and Marco Trabucchi
The prevalence and incidence of dementias are expected to
increase in the future. Accordingly, the identification of
causes of dementia and of possible risk factors is very important.
A large body of evidence has shown that hypertension is a
risk factor for vascular dementia. Recently, it has been demonstrated
that hypertension could affect the course of Alzheimer disease.
A strong relationship between hypertension and cognitive decline
(CD) or dementia has been reported by several observational
studies, especially in untreated subjects. The risk increases
with increasing blood pressure (BP). However, this relationship
is not linear, since BP may decrease to normal or low levels
before dementia becomes clinically manifest. There may also
be an association between BP variability in hypertensive patients
and impaired cognition. Recent studies, using the 24-hour
non-invasive monitoring, have shown that both short-term and
long-term BP variability are associated to CD. This variability
may reflect central nervous system dysregulation or occult
injury to prefrontal autonomic centers. Trials with antihypertensive
drugs focusing on CD and dementia have shown that active treatment
may be beneficial, although the optimal BP levels have not
yet defined. Future studies, comparing the different effect
of antihypertensive drugs are expected to further clarify
this topic.
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Microalbuminuria In Primary Hypertension
Roberto Pontremoli, Francesca Viazzi, Giovanna Leoncini
and Elena Ratto
Microalbuminuria, i.e., abnormal urinary excretion of albumin
detectable by sensitive, low cost, and widely available tests,
can be found in up to one third of non diabetic patients with
primary hypertension. Microalbuminuria has been shown to predict
an increased probability of suffering a cardiovascular event
or death. The pathogenetic mechanisms leading to the development
of microalbuminuria are not yet fully known: blood pressure
load and increased systemic vascular permeability, possibly
due to early endothelial damage, seem to play a major role.
Increased urinary albumin excretion has been associated with
several unfavorable metabolic and non metabolic risk factors
and sub-clinical organ damage, such as left ventricular hypertrophy
and carotid atherosclerosis. Microalbuminuria itself has recently
been recognized as a sign of hypertensive target organ damage
and since it reflects the influence of so many clinically
relevant parameters, it can rightly be considered an integrated
marker of cardiovascular risk, a unique feature among the
several available prognostic predictors for stratifying risk
in hypertensive patients. While microalbuminuria has proven
to be a forerunner of overt renal damage in the presence of
diabetes mellitus, conflicting clinical evidence makes this
hypothesis tempting at the moment, but speculative in non
diabetic hypertensives. Effective antihypertensive treatment,
especially with drugs counteracting the renin angiotensin
system, has been found to reduce urinary albumin excretion.
More recently, regression from microalbuminuria to normoalbuminuria
has been associated with an amelioration of cardiovascular
outcome, regardless of achieved blood pressure levels and
type of drug. This evidence emphasizes the usefulness of evaluating
urinary albumin excretion not only to assess cardiovascular
risk, but also to monitor the efficacy of treatment in clinical
practice.
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The Resurgence of Aldosterone in
Hypertension and Cardiovascular Disease
E. Marie Freel and John M.C. Connell
Aldosterone is a key cardiovascular hormone. Recent studies
have illustrated its role in cardiac fibrosis and left ventricular
hypertrophy as well as in impaired vascular reactivity. Moreover,
many of these actions have been shown to be independent of
its known effects on blood pressure. In a clinical setting,
the benefits of aldosterone blockade in cardiovascular disease
have been adequately demonstrated in recent large, randomised
clinical trials. Aldosterone blockade was once limited by
dose-related side effects, however, the introduction of a
new, more selective, aldosterone receptor antagonist (eplerenone)
has led to an increase in its use as a therapeutic strategy
in cardiovascular disease.
The role of aldosterone in hypertension has also been recently
re-evaluated. As a result more widespread screening of hypertensive
subjects using the aldosterone to renin ratio (ARR), the prevalence
of Primary Aldosteronism (PA) is now estimated, albeit controversially,
to be at least 10%. It is now accepted that screening for
PA should be more widespread and not limited to those with
hypokalaemia. Moreover, whilst there remains debate over the
exact labelling of individuals with hypertension and raised
ARR it is clear that such subjects have aldosterone levels
inappropriate for the prevailing renin (‘aldosterone-associated
hypertension’). It is important that such individuals
are identified since they can be offered more targeted treatment
with selective aldosterone blockade or even surgery to control
or normalise blood pressure.
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Primary Hyperaldosteronism in the Hypertensive Disease
Carlos E. Fardella, Cristian A. Carvajal and Lorena M.
Mosso
Primary aldosteronism (PA) is one of the potentially curable
forms of hypertension. The hypertension is secondary to aldosterone
action in the kidney, reabsorbing sodium and water that increases
the intravascular volume and blood pressure. PA was previously
believed to account for less than 1% of hypertensive patients
when hypokalemia is used as screening method. However, recent
studies using the plasma aldosterone to renin activity ratio
(ARR) as screening test have demonstrated a high prevalence
of PA in hypertensive populations. This prevalence vary depending
on the severity of hypertensive disease being higher in stages
2 (8.55%) and 3 (13.5%) of the disease. Only a small proportion
of PA patients (between 9 and 37%) are hypokalemic. The diagnosis
of PA is advocated to confirm the autonomy of aldosterone
secretion from the renin-angiotensin system and to differentiate
the clinical subtypes of the disease. The most common subtypes
of PA are idiopathic aldosteronism and aldosterone-producing
adenoma. Other causes are glucocorticoid-remediable aldosteronism,
unilateral or primary adrenal hyperplasia and adrenal carcinoma.
This article reviews the new data about prevalence, diagnosis
criteria and describes the clinical, biochemical and genetic
characteristics of the different subtypes of the disease.
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Usefulness of Home Blood Pressure
in the Diagnosis and Control of Hypertension in Primary Care
María A. Martínez and Juan G. Puig
Self- measurement of blood pressure (BP) at home has gained
increasing importance for the diagnostic and therapeutic evaluation
of hypertensive patients. In comparison with clinic BP, self-measurement
of BP with automated devices has several advantages: (1) higher
reproducibility; (2) elimination of the “white coat
effect” and observer bias; and (3) improvement of both
compliance and BP control. Furthermore, there is evidence
that home BP better correlates with target-organ damage and
prognosis and provides a more accurate evaluation of treatment
effect. On the other hand, it has great potential advantages
of lower equipment and staff cost compared with ambulatory
BP. These features of home BP have led various medical organizations
to recognize its clinical usefulness in the diagnosis of white
coat hypertension and in evaluating response to antihypertensive
medication, particularly in the primary care setting. We aim
here to present a critical review of the uses, strengths and
weaknesses of the technique of home BP monitoring for the
assessment of hypertension in the clinical practice.
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PPARγ
Agonists: Beneficial Effect on Blood Pressure Beyond Glycemic
Control?
Panteleimon A. Sarafidis and Anastasios N. Lasaridis
The Metabolic or Insulin Resistance Syndrome is a cluster
of cardiovascular risk factors, such as type 2 diabetes mellitus,
hypertension, central obesity, dyslipidaemia, and other disorders,
which have been proposed to be secondary to insulin resistance.
A number of possible mechanisms linking insulin resistance
and compensatory hyperinsulinemia with hypertension have been
described, such as renal sodium reabsorption enhancement,
sympathetic nervous system activation, or blunted insulin-mediated
vasodilatation due to endothelial dysfunction. PPARγ
agonists or thiazolidine-diones (TZDs) are a class of oral
antihyperglycemic agents that act through improvement of insulin
sensitivity. Apart from their action on glycemic control,
in several studies TZDs have been also reported to exert beneficial
effects on other parameters of the metabolic syndrome. This
review summarizes the literature data on the effect of troglitazone,
pioglitazone and rosiglitazone on blood pressure (BP), which
derive from animal and human studies that were either specifically
designed to determine the effect of TZDs on BP or just examined
BP levels among other parameters. In addition, it presents
in vitro and in vivo evidence about various
TZDs actions on the cardiovascular system that could positively
influence BP, representing therefore possible mechanisms of
this BP amelioration.
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Transient Receptor Potential Channels, the Kidney
and Hypertension
Paolo Menè
Smooth muscle cells as well as non-excitable cells express
multiple cationic channels with variable selectivity for Ca2+,
K+, Na+. Several of these channels are
sensors of Ca2+ store depletion, G-protein-coupled
receptor activation, membrane stretch, intracellular pH, oxidative
stress, phospholipid signals and other factors. A novel family
of such channels is represented by highly conserved heterotetramer
homologues of Drosophila TRP (transient receptor
potential). Direct evidence exists for roles of TRPC1, TRPC4/5,
TRPC6, TRPV, TRPP in store-operated Ca2+- gating
in various tissues, including epithelial cell Ca2+
transport, thus controlling renal and intestinal homeostasis
of divalent cations. Mice deficient in TRPV5 display phenotypic
defects amongst which hypercalciuria and impaired bone mineral
density. Polycystin 2 (PC2), encoded by the PKD2 gene, is
an epithelial transmembrane protein whose mutation is associated
to autosomal dominant polycystic kidney disease (ADPKD). PC2
behaves as a TRP-type Ca2+-permeable nonselective
cation channel located on the cilia of tubular epithelial
cells. Recent studies indicate that a PC1-PC2 channel complex
is an obligatory novel signaling pathway implicated in the
transduction of environmental signals into cellular events.
TRP-related ion channels may also play a role in the pathogenesis
of arterial hypertension through direct effects on vascular
smooth muscle contraction, renal perfusion/hemodynamics, and
the total body balance of divalent cations.
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Ion Channel Architecture of the Renal Microcirculation
Malcolm R. Turner and Thomas L. Pallone
Vascular contraction is modulated, in part, by the cytoplasmic
Ca2+ concentration in smooth muscle cells (SMCs).
Ca2+ influx through voltage gated Ca2+
channels (VGCC) is governed by membrane potential. In turn,
membrane potential is determined by the relative conductance
of the membrane to various ions. Increase in Cl-
conductance depolarizes SMCs to activate VGCC. K+
channel activation or inhibition can favor hyperpolarization
or depolarization, respectively, to modulate VGCC activity.
The importance of the kidney in the determination of extracellular
volume and blood pressure has motivated study of renal SMC
channel architecture. VGCC mediated Ca2+ entry
has been consistently found in the preglomerular microcirculation.
In contrast, the route of Ca2+ entry in the postglomerular
microcirculation varies with cortical location. Juxtamedullary
efferent arterioles and descending vasa recta express VGCC
while superficial efferent arterioles may not. The subtypes
of K+ channel that govern membrane potential also
varies along the renal microvascular circuit. Exploration
of rodent models have tended to confirm an increase in VGCC
activity in hypertension. Alterations in K+ channels
and gap junction - connexin proteins also occur but are subtype
specific. This review summarizes current knowledge of renal
SMC channel architecture and its alteration in hypertension.
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Effect of Ouabain on the Immune System
Juliana Echevarria-Lima and Vivian M. Rumjanek
Immune dysfunction has been reported in patients with hypertension
and in spontaneously hypertensive rats. Increased circulating
levels of ouabain were observed in experimental models and
in human hypertension. Despite the correlation between immunologic
depression and hypertension, the mechanisms involved are unclear.
This review examines evidences of immune dysfunction in hypertension
and presents observations suggesting that ouabain is capable
of inducing lymphocyte changes related to some of the immune
disturbances observed. Defects in thymocytes, mature lymphocyte
subsets, lymphocyte proliferation, cytokines balance and increased
immunoglobulin production, were reported in animal models
and/or hypertensive patients. Ouabain potentiates the effects
of glucocorticoids on thymocytes, inducing plasma membrane
depolarization, loss of mitochondrial membrane potential,
changes in CD69 levels, increased intracellular calcium and
apoptosis of thymocyte subsets. The activation of mature lymphocytes
is inhibited by ouabain following different stimuli and these
cells display changes in c-myc, CD69 and CD25 levels, plasma
membrane polarization and mitochondrial membrane potential.
These cells underwent apoptosis, suggesting an exacerbation
of the process of activation induced cell death. Levels of
cytokines such as IL-1, IL-2, IL-6, TNF, and GM-CSF are modified
by ouabain. Some of the ouabain effects may result from a
mechanism different from the traditional inhibition of the
Na+/K+ ATPase.
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