Current
Hypertension Reviews
ISSN: 1573-4021
Current Hypertension Reviews
Volume 3, Number 4, November 2007
Contents
Interactions of Biologically Active Factors and Vascular
Mediators During Hypertension in Pregnancy Pp. 231-241
Amanda K. Stennett and Raouf A. Khalil
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Vascular Arginase and Hypertension Pp. 242-249
Leif D. Nelin, Michael R. Stenger, Daniel T. Malleske
and Louis G. Chicoine
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Coffee and Caffeine Effects on Hypertension
Pp. 250-254
Anna Vittoria Mattioli
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Issue/Articles]
Physical Activity and Hypertension: Evidence of Cross-Sectional
Studies, Cohort Studies and Meta-Analysis Pp. 255-263
Noël C. Barengo, Gang Hu and Jaakko Tuomilehto
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Current Perspectives on Hypertension in Asian Indians
Pp. 264-269
H.M. Mardikar, Dhananjay Deo, N.V. Deshpande and Debabrata
Mukherjee
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Gene-Wide Approach: New Frontiers in Cardiovascular
Genetic Epidemiology Pp. 270-275
Bruna Gigante
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Renal Artery Stenosis: A Unique Disease or a Broad
Spectrum of Different Diseases? Pp. 276-283
Alessandro Zuccalà, Francesco Losinno, Francesca
Lifrieri and Pierpaolo Di Nicolò
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Genetics of Polygenic Hypertension from Animal Models
to Humans Pp. 284-297
Alan Y. Deng
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Abstracts
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Interactions of Biologically Active Factors and Vascular Mediators
During Hypertension in Pregnancy
Amanda K. Stennett and Raouf A. Khalil
Normal pregnancy is associated with changes in the cardiovascular
system, including vascular remodeling of the uterine and systemic
circulation in order to meet the metabolic demands of the
developing fetus. These cardiovascular changes are due to
alterations in the amount/activity of vascular mediators such
as nitric oxide, prostacyclin and endothelin in the endothelium;
calcium and protein kinase C in the smooth muscle; and metalloproteases
in the extracellular matrix. Hypertension in pregnancy is
a major complication, and can lead to life threatening neurovascular
disorders. It has been suggested that hypertension in pregnancy
may develop from an inadequate invasion of cytotrophoblasts
into the uterine artery, causing reduction in the uteroplacental
perfusion pressure, and resulting in placental ischemia/hypoxia.
This placental hypoxic state is thought to induce the release
of various biologically active factors such as cytokines,
reactive oxygen species, and hypoxia-inducible factors. Elevated
plasma/tissue levels of these factors during pregnancy could
cause vascular dysfunction, vasoconstriction and hypertension.
The purpose of this review is to discuss the interactions
between biologically active circulating factors and vascular
mediators, released during preeclampsia as compared to those
released in other conditions characterized by hypoxia, in
order to provide insight into the sequence of events that
leads to the development of hypertension in pregnancy.
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Vascular Arginase and Hypertension
Leif D. Nelin, Michael R. Stenger, Daniel T. Malleske
and Louis G. Chicoine
Hypertension has been associated with both decreased production
of the potent vasodilator nitric oxide (NO) and vascular remodeling.
L-arginine is the substrate for endogenous NO production by
the NO synthases (NOS). L-arginine is also the substrate for
the arginases, which metabolize L-arginine to L-ornithine
and urea. There are 2 described isoforms of arginase, arginase
I and arginase II; both isoforms are inducible and widely
expressed in the body. Recently, it has been found that arginase
I and II are expressed in vascular tissue, and that arginase
activity can be induced by many hypertensive stimuli, including
chronic inflammation and salt loading. Induction of arginase
activity results in decreased L-arginine bioavailability to
NOS and thereby may decrease the endogenous production of
NO in the vasculature. Furthermore, L-ornithine produced by
arginase can be further metabolized to polyamines and proline,
which are central to vascular smooth muscle cell proliferation
and vascular remodeling. Thus, arginase is involved in the
pathogenesis of hypertension by promoting vascular remodeling
and attenuating the endogenous production of NO. This review
will examine the regulation of arginase expression and its
role in the pathogenesis of hypertension, as well as the therapeutic
potential of arginase inhibition for treating some forms of
hypertension.
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Coffee and Caffeine Effects on Hypertension
Anna Vittoria Mattioli
In recent years, some epidemiological studies reported that
coffee consumption was associated with increased in serum
cholesterol and blood pressure and subsequently increased
cardiovascular risk.
Coffee is one of the most popular beverages consumed in a
large amount in Western Countries. Coffee beverages contain
several hundred different substances, but its effects of coffee
on cardiovascular system have been mainly related to caffeine.
Caffeine is present in a number of dietary sources consumed
worldwide i.e. tea, coffee, cocoa beverages, chocolate bars
and soft drinks. Caffeine exerts various effects on the autonomic
nervous system and on blood vessels.
It is well-known that a dietary intake and lifestyle play
an important role in hypertension. Meta-analyses of randomized
control trials that examined the effects of coffee and caffeine
intake on blood pressure presented conflicting results. Shortterm
administration of caffeine in non-coffee drinkers increases
blood pressure, plasma renin activity, and catecholamines.
Heavy coffee drinkers seem to have negative effects mainly
due to the activation of sympathetic system, i.e. rise in
blood pressure, increase of risk of develop coronary artery
disease. On contrary a moderate consumption shows no detrimental
effects on cardiovascular system. In addition habitual coffee
drinkers have less sympathetic response. Recent studies underling
the antioxidants properties of coffee due to different compounds.
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Physical Activity and Hypertension: Evidence of Cross-Sectional
Studies, Cohort Studies and Meta-Analysis
Noël C. Barengo, Gang Hu and Jaakko Tuomilehto
Physical activity is a cost-effective way to decrease blood
pressure since it possesses potential for having a major public
health impact. Prospective studies, have demonstrated that
moderate-to-vigorous intensity physical activity at baseline
seem to be associated with a lower incidence of hypertension
among white men regardless of body mass index. The data among
women are controversial. Further, there is not enough evidence
at this moment to conclude that high commuting or occupational
physical activity would be associated with a reduced risk
for incident hypertension. Intervention studies however, have
demonstrated that increased physical activity reduces systolic
and diastolic blood-pressure in hypertensive and normotensive
individuals independently from weight loss. In light of the
evidence from these studies, physical activity should be practiced
at a moderate intensity level (min. 40% of VO2 max) three
times per week and for session times of at least 30 minutes
in order to reduce systolic and diastolic blood pressure.
Thus, physical activity should be considered as an important
measure for the prevention and treatment of hypertension.
Physical activity is a cost-effective way to decrease blood
pressure since it possesses potential for having a major public
health impact.
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Current Perspectives on Hypertension in Asian Indians
H.M. Mardikar, Dhananjay Deo, N.V. Deshpande and Debabrata
Mukherjee
Background: Asian Indians account
for one-fifth of all cardiovascular deaths worldwide. It is
well known that hypertension is a major risk factor for cardiovascular
mortality and morbidity, but there has been no national survey
for estimating the prevalence of hypertension in the Indian
population. Hypertension in this ethnic group is less well
studied than hypertension in blacks or Caucasians.
Methods: We searched PubMed and
MEDLINE using the words “Asian Indians” “hypertension”
“blood pressure” “epidemiology” “prevalence”
“prevention” “treatment” as search
items and went through the major Indian journals to gather
sufficient data regarding hypertension in Asian Indians. Most
of the data was acquired from studies conducted in India,
as there are only limited studies on Indians who have settled
overseas.
Results: High prevalence of hypertension
was found in the urban Indian population as compared to the
rural Indian population, while there was inconsistent data
on migrant Indians. The modern Indian diet and lifestyle may
be responsible for the urban - rural differences. Large proportion
of Indian population is unaware of their condition and significant
proportion of them is pre-hypertensive. No specific treatment
guidelines for this ethnic group are available.
Conclusion: The escalating incidence
of hypertension among Asian Indians in urban India is alarming.
This will likely add to the already existing cardiovascular
disease burden in this ethnic group and it is imperative to
conduct additional epidemiological and clinical studies to
assess the prevalence, pathogenesis, and optimal pharmacotherapy
of hypertension in Asian Indians. Aggressive screening and
treatment regimen should be adopted considering the risk of
untreated and sub-optimally treated hypertension and specific
guidelines for treatment of hypertension in Asian Indians
appears warranted.
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Gene-Wide Approach: New Frontiers in Cardiovascular
Genetic Epidemiology
Bruna Gigante
The potential role of genetic variations in the pathogenesis
of cardiovascular diseases is a field of continuous investigation
and the perception of the role of genes has dramatically changed
during the last 20 years. The two more commonly used experimental
designs, based on a candidate gene or a genome wide approach,
have been somehow replaced by the possibility to build haplotypes
in the context of a single gene using a so-called gene-wide
approach. Human diseases, however, are far from theoretical
and in silico speculation and the analysis of the contribution
of the individual genetic background to their pathogenesis
still needs a working hypothesis that, starting from the patho-physiology
of the disease under investigation, takes advantage of the
newly available technologies and software. In this perspective,
the gene-wide approach may represent an attractive methodology
to bridge the gap between bench and bedside. Here we review
the rationale behind this approach, the available methodologies
and the potential clinical applications.
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Renal Artery Stenosis: A Unique Disease or a Broad
Spectrum of Different Diseases?
Alessandro Zuccalà, Francesco Losinno, Francesca
Lifrieri and Pierpaolo Di Nicolò
Renal ischaemia due to renal artery stenosis (RAS) may be
the cause of end-stage renal failure in a growing number of
patients. In recent years, decisions taken on the optimal
management of patients with renal artery stenosis have sparked
controversy and debate among cardiologists, internists and
nephrologists. The main reason underlying the ongoing controversy
may be the heterogeneity of clinical entities that are normally
grouped together through the use of the umbrella term renal
artery stenosis. Actually, when thinking of renal artery
stenosis our view is still deeply shaped by Goldblatt’s
seminal study. Yet it should be remembered that in Goldblatt’s
experiment renal artery clipping occurred in the context of
a perfectly healthy vascular tree. A clinical situation that
comes close to Goldblatt’s experiment is the one in
which the stenosis mainly, if not exclusively, affects the
renal artery in relatively young subjects whose vascular tree
is not badly damaged. In clinical practice, this situation
is frequently encountered in subjects bearing fibromuscular
dysplasia (FMD), non-ostial or truncal stenosis (Tru-RAS),
and stenosis of the transplanted kidney (TRAS). Contrariwise,
ostial stenosis is more precisely a lesion of the thickened
aortic wall that encroaches upon the renal artery ostium,
rather than a lesion in the renal artery itself. Hence, the
reference paradigm ought not to be Goldblatt’s model
but rather more complex models in which the narrowing of the
renal artery is associated to other factors, such as a high
cholesterol diet, smoking or aging. The causes of renal impairment
are likely to be different in the two situations. In pure
renal artery stenosis (FMD, TruRAS, TRAS), the decrease in
GFR is mainly caused by hypoperfusion secondary to stenosis,
which is then reversible after revascularization, while in
subjects with ostial stenosis and/or in older subjects with
a badly injured aorta the pathogenesis is multifactorial,
with intrarenal atheroma, cholesterol embolism and ischaemic
damage all making a contribution. This may account for the
lack of correlation between the degree of stenosis and the
entity of renal impairment, as well as the low rate of renal
function recovery in subjects with ostial stenosis. In our
view, keeping the different entities separate enables clinicians
to take the right decision on revascularization.
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Genetics of Polygenic Hypertension from Animal Models
to Humans
Alan Y. Deng
Essential hypertension research faces daunting hurdles in
gene identification and elucidating mechanisms underlying
gene-gene interactions and genome regulations. Recent discoveries
in experimental models of polygenic hypertension have revealed
the genetic architecture and a functional hierarchy of genes
influencing BP. These findings are potentially shedding new
conceptual lights on complex genetic mechanisms controlling
essential hypertension. Seemingly ‘conflicting’
results in association studies of candidate genes with essential
hypertension may be interpreted by their inherent genetic
property of population specificity. A lack of detection of
genes demonstrating major BP effects may be attributed to
the masking and compounding effects of genetic heterogeneity,
among other factors, present among human subjects. The future
research can be greatly benefited from combining animal model
studies with human population-based analyses, i.e. translating
the discovery in experimental models into humans, and conversely,
validating human findings via animal model investigations.
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