Current
Hypertension Reviews
ISSN: 1573-4021
Current Hypertension Reviews
Volume 2, Number 2, May 2006
Contents
Arterial Stiffness: A Potential Therapeutic Target
to Reduce Cardiovascular Mortality Pp. 97-102
Anabelle Opazo Saez, Anna Mitchell, Thomas Philipp
and Jens Nürnberger
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New Generation Calcium Channel Blockers in Hypertensive
Treatment Pp. 103-111
Yuri Ozawa, Koichi Hayashi and Hiroyuki Kobori
[Abstract] [Purchase
Issue/Articles]
Aldosterone and the Pathogenesis of Hypertension
Pp. 113-122
Moffat J. Nyirenda, Roger R. Brown and Paul L. Padfield
[Abstract] [Purchase
Issue/Articles]
A Newly Found Gasotransmitter, Hydrogen Sulfide, in
the Pathogenesis of Hypertension and Other Cardiovascular
Diseases Pp. 123-126
Junbao Du, Chunyu Zhang, Hui Yan and Chaoshu
Tang
[Abstract] [Purchase
Issue/Articles]
Job Stress and Blood Pressure: A Critical Appraisal
of Reported Studies Pp. 127-138
Samuel J. Mann
[Abstract] [Purchase
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Coronary Artery Disease and End-Stage Renal Disease
– A Clinical Perspective Pp. 139-145
José Jayme Galvão de Lima and Luís
Henrique W. Gowdak
[Abstract] [Purchase
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Atherogenesis in White Coat Hypertension Pp.
147-150
Yesari Karter
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Intratubular Renin-Angiotensin System in Hypertension
Pp. 151-157
Yuki Suzaki, Minolfa C. Prieto-Carrasquero and Hiroyuki
Kobori
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Plasma Glucose Concentrations and Cardiac Hypertrophy
in Essential Hypertension Pp. 159-166
Pablo Stiefel, José Villar and Javier
Navarro-Antolín
[Abstract] [Purchase
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Hypertension in Children with Cystic Kidney Diseases
Pp. 167-177
Tomás? Seeman
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Issue/Articles]
Abstracts
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Arterial Stiffness: A Potential Therapeutic Target
to Reduce Cardiovascular Mortality
Anabelle Opazo Saez, Anna Mitchell, Thomas Philipp
and Jens Nürnberger
Stiffening of the arterial wall is one major mechanism responsible
for morbidity and mortality in cardiovascular disease including
hypertension and coronary heart disease. Various physiological
and pathophysiological parameters influence arterial stiffening
including age, gender, blood pressure, nutrition, smoking,
and diseases such as hypertension, diabetes, renal failure,
and hypercholesterolemia. Thus, assessing arterial stiffness
has become a widely used tool to investigate the function
of large arteries in epidemiological and clinical studies.
Traditionally, arterial stiffness has been assessed by pulse
wave velocity, a non-invasive parameter which has been shown
to predict cardiovascular mortality. In addition, pulse wave
analysis has been increasingly used to determine augmentation
index, a parameter that describes the effect of pulse wave
reflection on the central aortic pressure configuration. For
many years arterial stiffness had been thought to be relatively
unaffected by drugs. However, recent studies suggest that
arterial stiffness can be pharmacologically modulated. Hence,
improving arterial stiffness may be a potential therapeutic
target to reduce cardiovascular mortality. This review attempts
to summarize the current tools used to assess arterial stiffness
and the drugs that modify large artery stiffness in-vivo.
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New Generation Calcium Channel Blockers in Hypertensive
Treatment
Yuri Ozawa, Koichi Hayashi and Hiroyuki Kobori
During a couple of decades, a number of antihypertensive
drugs have been developed, and the choice of hypertension
treatment has been expanded. Among antihypertensive drugs,
calcium channel blockers, which inhibit L-type voltage-gated
calcium channels, are potent vasodilators, and have been used
as a first- or second-line drug. Dihydropyridine-class calcium
channel blockers are categorized into three generations according
to the length of activity, and long-acting calcium channel
blockers cause less activation of sympathetic nervous system,
and are reported to offer beneficial action compared with
short-action agents. Furthermore, novel types of calcium channel
blockers have been developed that possess the blocking action
on other calcium channel subtypes (T- and N-type), and exert
agent-specific action apart from their class effects, such
as the effects on heart rate and renin/aldosterone release.
These additional benefits conferred by T/N-type calcium channel
blockade are anticipated to provide organ protective actions
in the treatment of hypertension, in addition to the blood
pressure-lowering effect of L-type calcium channel blockade.
In conclusion, novel calcium channel blockers with sustained
activity and T/N-type calcium channel blocking action could
provide more beneficial effects than classical blockers, and
may expand the clinical utility of these agents.
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Aldosterone and the Pathogenesis
of Hypertension
Moffat J. Nyirenda, Roger R. Brown and Paul L. Padfield
Hypertension remains a major public health problem, affecting
up to 20% of the adult population in Western societies. Despite
progress in treatment, the rates of blood pressure control
remain suboptimal. Hypertension is a heterogeneous disorder,
and in the majority of cases, with so-called "essential"
hypertension, no clear single identifiable cause is found.
Syndromes of excessive mineralocorticoid production or activity
are among the important causes of secondary hypertension.
Aldosterone is the principal mineralocorticoid in humans,
and primary aldosterone excess, when associated with an aldosterone
secreting adenoma (Conn’s tumor), is amenable to surgical
cure. Classically, patient with Conn’s tumor present
with spontaneous hypokalemia and have a relative excess of
aldosterone production with suppression of plasma levels of
renin (a proxy for angiotensin II, the major trophic substance
regulating aldosterone secretion). This combination of a high
aldosterone and a low renin is however more commonly associated
with 'nodular hyperplasia' of the adrenal glands, a condition
not improved by surgery and variably responsive to the effects
of mineralocorticoid antagonists such as spironolactone. Although
primary aldosteronism was previously considered to be rare,
recent studies have reported prevalence rates of up to 20%
among hypertensive patients. This reflects the increasing
use of the plasma aldosterone concentration to renin activity
ratio (ARR), rather than spontaneous hypokalemia, as a screening
tool for aldosteronism. Many patients with high ARR have normokalemia
and, although renin activity is low, the level of aldosterone
is usually within the normal range. This group of patients
may thus include those who were previously classified as having
low-renin essential hypertension. Recent data suggest that
disturbances in aldosterone metabolism and regulation may
not be uncommon in patients with essential hypertension. Thus,
relatively high serum aldosterone levels within the reference
range in normotensive individuals are associated with a substantially
increased risk of developing hypertension, highlighting the
potential role for aldosterone in the etiology of essential
hypertension. The present review addresses the physiology
of aldosterone action and its role in the pathogenesis of
hypertension.
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A Newly Found Gasotransmitter, Hydrogen Sulfide, in
the Pathogenesis of Hypertension and Other Cardiovascular
Diseases
Junbao Du, Chunyu Zhang, Hui Yan and Chaoshu
Tang
In the 1980’s, nitric oxide (NO) and carbon monoxide
(CO) were determined to be gaseous messenger molecules which
is capable of relaxing vessels and interfering with vascular
structure remodeling. However there are many mechanisms that
have not been clear about the regulation of human functions
under both physiological and pathophysiological conditions.
Hydrogen sulfide (H2S)
is a newly found gasotrasmitter that was demonstrated to play
similar role as that of NO and CO in many organs and tissues,
especially in the cardiovascular system. In this review, firstly,
we described the production of H2S
in the body, and the functions of H2S
in the cardiovascular system, especially in the vascular relaxing
and vascular remodeling. Secondly, we further discussed the
role of H2S
in hypertension, hypoxic pulmonary hypertension, shock and
ischemic hear disease. Finally, the interaction between H2S
and the other two gasotransmitters, NO and CO, was also discussed.
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Job Stress and Blood Pressure: A
Critical Appraisal of Reported Studies
Samuel J. Mann
Stress clearly causes transient elevation of blood pressure,
but its relationship to persisting elevation remains unclear.
Job stress in particular is believed by many to contribute
to persisting blood pressure elevation, but results of studies,
which have never been comprehensively reviewed, have varied
widely. The purpose of this review is to examine the results
of such studies, and, based on those results, to challenge
the prevailing belief that job stress is a significant contributor
to the development of hypertension.
Forty-eight studies have examined the relationship between
job stress and casual blood pressure. 20 reported a positive
association, although only 10 reported an association with
systolic pressure for the entire cohort. Twenty-six studies
have examined the relationship between job stress and ambulatory
blood pressure. Seventeen of the 26 studies reported a positive
association, although a positive association with systolic
pressure in the entire cohort was seen in only 10 of the 26
studies. A qualitative review of positive findings revealed
important concerns in the findings in many of the studies
that reported an association, as detailed in the text and
tables.
In conclusion, results of studies of the relationship between
job stress and blood pressure are highly inconsistent. In
addition, major weaknesses in the findings of most studies
that did report an association challenge the strength of the
evidence they provide. Thus after decades of research, the
evidence for a relationship between job stress and blood pressure
is weak. Further, this review brings attention to the misleading
but common practices of focusing on a single positive correlation
or on a correlation limited to a single subgroup, while downplaying
or frankly ignoring prominent negative findings, misleadingly
perpetuating hypotheses that are likely to be untrue.
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Coronary Artery Disease and End-Stage Renal Disease
– A Clinical Perspective
José Jayme Galvão de Lima and Luís
Henrique W. Gowdak
Patients with end-stage renal disease (ESRD) have ≥
3 times greater incidence and prevalence of coronary artery
disease (CAD) than the general population. All dialysis patients
must be considered at high risk for CAD, thus, managed accordingly.
Classic CAD symptoms are often misleading in these patients,
thus, are not helpful diagnostically. Conversely, age (≥
50 years), diabetes or overt clinical cardiovascular disease
(CVD) are associated with a > 40% prevalence of critical
CAD and increased incidence of CV events. In this subgroup,
coronary angiography should be considered the first and best
diagnostic approach. Noninvasive investigation (cardiac scintigraphy/stress
echocardiography), which provides adequate specificity but
poor sensitivity, may be useful in younger individuals without
associated comorbidities and in following-up patients without
significant stenosis by angiography. The role of new noninvasive
testing awaits more extensive evaluation. As prospective randomized
trials have not examined the best treatment for dialysis patients
with CAD, it remains undefined. Coronary artery bypass grafting
appears superior to coronary angioplasty or stenting. No large
study has compared medical treatment with coronary intervention,
and few observations exist concerning the impact of modern
cardioprotective therapy on outcomes. Based on studies in
the general population, routine administration of at least
few cardioprotective drugs (aspirin, β-blockers,
RAS inhibitors, statins) to all dialysis patients seems prudent.
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Atherogenesis in White Coat Hypertension
Yesari Karter
Sustained Hypertension (HT) causes atherosclerotic changes
and is one of the main risk factor of coronary artery disease.
It is not clear if White Coat Hypertension (WCH) also causes
atherosclerosis as it is associated with other target organ
changes similar to those with sustained SHT. It is well established
that in sustained HT the process of endothelial damage and
angiogenesis are abnormal. The relationship of oxidative stress
and nitric oxide (NO) is well known.The low level of NO in
WCH may be the result of enhanced oxidative stress. Increased
oxidative stress is probably the leading cause of endothelial
dysfunction. In consecutive studies, we investigated arterial
compliance and analyzed the molecules produced by endothelial
cells by biochemical methods to determine endothelial dysfunction.
Increasing of oxidative products (oxidative modification of
low-density lipoprotein –oxLDL- and malondialdehyde
–MDA-) showed the enhanced oxidative stress while the
low levels of antioxidants (paraoxonase -PON1-) denoted the
decrease in antioxidant activity.
The decrease in endothelium dependent flow mediated dilatation
and elevated plasma levels of the endogenous (NO) synthase
inhibitor asymmetric dimethyl arginine (ADMA), increases in
endothelin (ET-1), homocysteine and vascular endothelial growth
factor (VEGF) may contribute to endothelial dysfunction and
abnormal angiogenesis in WCH. The data and our current findings
were discussed to assess the increased cardiovascular risk
in WCH conferred by endothelial dysfunction and high oxidative
stress. As the elevated oxidative stres is a strong risk factor
for coronary artery disease WCH might not be considered as
an innocent trait.
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Intratubular Renin-Angiotensin System in Hypertension
Yuki Suzaki, Minolfa C. Prieto-Carrasquero and Hiroyuki
Kobori
It is well recognized that the renin-angiotensin system plays
an important role in the regulation of arterial pressure and
sodium homeostasis. Recent years, many studies have shown
that local tissue angiotensin II levels are differentially
regulated and cannot be explained on the basis of circulating
concentrations. All of the components needed for angiotensin
II generation are present within the various compartments
in the kidney including the renal interstitium and the tubular
network. The cascade of the renin-angiotensin system demonstrates
three major possible sites for the pharmacological interruption
of the renin-angiotensin system: the interaction of renin
with its substrate, angiotensinogen, the angiotensin converting
enzyme, and angiotensin II type 1 receptors. This brief article
will focus on the role of the intratubular renin-angiotensin
system in the pathophysiology of hypertension and the responses
to the renin-angiotensin system blockade by renin inhibitors,
angiotensin converting enzyme inhibitors and angiotensin II
type 1 receptor blockers.
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Plasma Glucose Concentrations and Cardiac Hypertrophy
in Essential Hypertension
Pablo Stiefel, José Villar and Javier
Navarro-Antolín
Recently, increasing evidences relate left ventricular mass
(LVM) and plasma glucose concentrations in hypertensive patients.
In this respect, it has been described a positive and significant
relation between LVM and Hemoglobin A1c in essential hypertension.
Moreover, hypertensive individuals with diabetes have higher
LVM than non-diabetic hypertensive patients with similar blood
pressure. It has been also described that an improvement of
glycemic control contributes to left ventricular hypertrophy
regression in hypertensive patients with type 2 diabetes,
and that these changes occurred independently of variation
in blood pressure. Finally, we have recently published that
“glucose effectiveness” (that represents the ability
of glucose per se to effect its own disappearance
from plasma independent of dynamic changes from basal insulin)
is strongly related to left ventricular mass in subjects with
stage 1 hypertension or high-normal blood pressure. The mechanisms
by which glucose in itself can induce proliferation and hypertrophy
seem to be mainly related to the activation of protein Kinase
C pathways. However, it has been also shown that glucose increases
intracellular calcium “in vitro” and
this increase directly stimulates vascular proliferation and
hypertrophy. In the present paper we will review different
clinical studies and in vitro experiments, showing
that glucose in itself, independently of insulin, can induce
vascular proliferation,and cardiac hypertrophy.
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Hypertension in Children with Cystic Kidney Diseases
Tomás Seeman
Cystic kidney diseases are one of the most common urogenital
malformations and are responsible for a substantial morbidity
and mortality. Autosomal recessive polycystic kidney disease
(ARPKD), autosomal dominant polycystic kidney disease (ADPKD),
multicystic dysplastic kidney (MCDK) and juvenile nephronophthisis
(JNP) are the most common and most serious cystic kidney diseases.
Hypertension is the main risk factor for progression of various
nephropathies, including cystic kidney diseases. The prevalence
of hypertension varies depending on the method of BP measurement
and the type of cystic disease. Ambulatory BP monitoring (ABPM)
is a more potent tool for detection of hypertension than the
clinic BP. Hypertension is most common in children with ARPKD,
the prevalence ranges between 60 - 100% and hypertension accounts
for substantial cardiovascular morbidity and mortality in
these patients. In children with ADPKD the prevalence of hypertension
is 15 - 38% despite normal renal function and is the most
important treatable factor for progression of the disease.
Hypertension is a relative uncommon finding in children with
MCDK (0 - 20%) and is more often caused by contralateral kidney
damage than by affected multicystic kidney. Children with
JNP are usually normotensive until the late stages of renal
insufficiency.
The drugs of first choice in children with cystic kidney diseases
are ACE-inhibitors. Most children with ARPKD have severe hypertension
and require combination therapy with 2 - 4 drugs (beta-blockers,
diuretics, calcium channel blockers). Treatment of hypertension
is important not only to delay progression of the kidney disease
but also to decrease the cardiovascular morbidity and mortality.
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