Current Hypertension Reviews - Volume 4, Issue 1, 2008

Hypertension and hyperlipidemia frequently co-exist in the same patients and are responsible for an increase in the extent of cardiovascular risk. The treatment of both risk factors clearly improves the individual risk profile. The possible mechanisms of interaction seem to be related with RAS activation, resulting in endothelial dysfunction and increased oxidative stress. The underlying mechanisms of the interaction between these two risk factors may reveal the development of new treatment strategies to control both factors at the same time. Available data on therapeutic approach of cardiovascular disease risk suggests the use of RAS blocking agents, calcium channel blockers and statins can be particularly appropriated for the prevention of cardiovascular risk in patients with hypertension. These classes of drugs improve endothelial function and protect the vessels wall from atherogenesis. The results of trials carried out with the combination of a statins (atorvastatin) and a calcium channel blocker (amlodipine) clearly support the important of such combination for the achievement of specific targets of treatment in patients with multiple risk factors. Although many preclinical and clinical studies offer positive effects of the combined use of statins and ARBs for patients with increased risk of cardiovascular events, there is yet need for direct evidences of their efficacy in preventing events in high risk patients.

Renal hypertrophy is an important contributor to end-stage renal disease, but little is known about its underlying physiological mechanisms, primarily because of complex etiologies, intricate gene-gene and gene-environment interactions. Kidney mass (Km) can be viewed as a proximal predictor of renal hypertrophy and, consequently, identifying the physiological mechanisms determining Km will probably facilitate our understanding of the factors causing renal hypertrophy. Genetic approaches are powerful in detecting etiological steps involved in pathways and cascades leading to Km control. Recent genetic analyses employing inbred rat models have defined 2 broad categories of genes known as quantitative trait loci (QTLs) responsible for Km. The first class controls Km independently of cardiovascular and hemodynamic phenotypes, suggesting that their underlying physiological mechanisms can be renal-specific and dissociated from those regulating cardiovascular traits. The second class of QTLs modulates Km as well as cardiovascular phenotypes, implying that these renal and cardiovascular traits may share physiological mechanisms. It is expected that some of the mechanisms discovered in animal models may be translated into humans. The strategies of gene discovery for KmQTLs consist of identifying gene candidates (e.g. gene profiling and targeted mutation screening) and in vivo functional validation (e.g. fine congenic resolution, transgenesis and gene targeting).

Pulmonary hypertension (PH) is a disorder with poor prognosis sustained by progressive elevation of pulmonary vascular resistance to blood flow. It is a serious condition for which treatments exist but there is no cure. The main determinants are vasoconstriction, pulmonary vascular remodelling, and in situ thrombosis associated with exuberant cellular proliferation and precapillary arterial bed obstruction. When unrecognized or untreated, PH has an unpredictable but worsening course that leads to cardiorespiratory decompensation. In the past ten years there have been significant improvements in both diagnostic and therapeutic strategies that have led to substantial changes in prognosis. However the number of subjects who over time become unresponsive to maximal medical treatment is still considerable so that surgical interventions are needed as last chance for survival. Lung transplantation (LTx) is a viable therapy for severe symptomatic PH. Even though survival after LTx has improved consistently, the recipients with an underlying diagnosis of PH seem to be affected by a greater 1-year mortality following LTx compared to recipients with other diagnoses. This article discusses the disease mechanisms and the pathophysiological processes involved in the development of PH. It provides some information on current and newer pharmacologic options, and it also considers the physiologic aspects of lung transplantation.

Epidemiological studies have demonstrated that changes in the lifestyle, in particular in the dietary habits, strongly contribute to the development of hypertension and other cardiovascular diseases. In the past two decades, in many western countries, type and mode of consumption of daily food intake changed accordingly to the changes in the rhythms of life. The solution of consuming fast food is obviously time-saving but it associated to the strong enhancement in the intake of calories, saturated fats, soluble carbohydrates and salt. All these nutrients are able to deteriorate the metabolic profile of the cardiovascular risk. Moreover the habitual consumption of fast food has been frequently indicated as one of the main causes of the lack of dialogue in the family, which is no-more gathered around the table to consume dinner. The alternative choice to the fast food is the slow food that promotes the recovery of the taste and quality of food, based on the traditions of the Mediterranean diet. In particular, this type of diet is rich in indigestible carbohydrates, unsaturated lipids, vegetable, proteins and potassium, which is the first physiological sodium antagonist. This diet has been proved to beneficially affect blood pressure regulation, to reduce serum lipids, blood glucose and cardiovascular risk profile. Moreover particular attempt to the size of portions is also able to prevent increase in body weight, which is one of the most important undesirable effects of the Mediterranean diet. Fans of the slow food suggest to consume the meal sitting around a carefully prepared table, enjoying talks and food, in order to antagonize the stress of the daily life in the 21st century. Aim of this paper is to show two different menu, one typical of the fast food and the second typical of the slow food philosophy, and discuss about their composition along with the effects of their macronutrients on blood pressure, body weight, serum lipids and blood glucose.

Hypertension is a leading cause of morbidity and mortality with surveillance often based on self-reported data. A systematic review and meta-analysis was completed to determine what empirical evidence exists regarding the agreement between measured and self-reported estimates of hypertension. Four electronic databases were searched to identify observational and experimental studies on adult populations. Searching identified 144 studies that examined the relationship between self-reported and directly-measured hypertension. Studies demonstrate that the prevalence of hypertension based on self-report is underestimated and that awareness levels are low and highly variable, ranging from 0 to 97%. Meta-analysis generated overall awareness estimates of 58% at the 140/90 mmHg cut-off and 62% at the 160/95 mmHg cut-off. Awareness levels were consistently higher for females. In many of the reviewed studies, standard guidelines for blood pressure measurement were not being followed or reporting of guideline compliance was poor. Lack of awareness is an important public health issue, yet this review demonstrates that the current practice of surveillance based on awareness alone is insufficient. These data indicate the importance of directly measuring blood pressure according to standardized protocols wherever possible, and increasing population awareness both to increase the validity of self-report and to ensure early diagnosis and treatment.

It is presumed that life on Earth has evolved in the presence of natural and ubiquitous magnetic fields. It is not surprising that biological systems can respond to a wide range of static magnetic fields (SMF). It is suggested that some physiological responses seem to be mediated through the nervous system. For weak intensity SMF, the effects of geomagnetic activity on the arterial baroreflex (reflex initiated by receptors in the aortic arch that alter peripheral vasomotion) in conscious animals were investigated by measuring blood pressure and microcirculation. Baroreflex sensitivity (BRS) was assessed as an indicator of cardiac autonomic regulation on the basis of the heart rate/mean arterial blood pressure relationship during a vasodilator (sodium nitroprusside) or a vasoconstrictor (phenylephrine) treatment. This study suggests that the geomagnetic field directly modifies microcirculatory responses related to BRS. These findings may have serious implications for individuals with ischemic diseases during periods of intense geomagnetic activity or geomagnetic storms. Concerning the moderate intensity SMF effects, pharmacological procedures and experimental animals have been used to assess the sympathetic responsiveness to SMF. We have reported that continuous exposure to moderate intensity SMF for several weeks can depress or suppress the action of sympathetic agonists (norepinephrine, phenylephrine, and dobutamine) and a sympathetic antagonist (reserpine) on hemodynamics and/or blood pressure by modulating sympathetic nerve activity or BRS in animals. In contrast, in humans there is little evidence to suggest that the SMF exposure of up to 8 tesla can alter blood pressure. Thus, this review describes the SMF effects (and non-effects) on the blood pressure in animals and humans.

Post dural puncture headache and hypertension (PDPH) is a low pressure headache closely related to Cerebrospinal fluid (CSF) hygrodynamics. PDPH occurs because of a CSF leak that occurs as a consequence of a dural puncture. The leakage of CSF produces traction on the brain and the meninges and causes compensatory cerebral vasodilatation resulting in a headache. Cerebrovascular autoregulation is a gradual process which minimizes intracranial pressure changes in the presence of systemic blood changes. Cerebral autoregulation prevents the cerebral blood vessels from dilating in moderate hypertension. There is a loss of autoregulation in end stage intracranial hypertension where there are passive changes in cerebral blood flow and cerebral blood volume, when there are changes in the systolic pressure. Hypertensive encephalopathy is associated with the breakdown of the blood brain barrier and is a complication of chronic severe hypertension Since the cerebral venous system has no valves fluctuations in the systemic venous pressure will directly affect CSF pressure. There is increased drainage of CSF into the venous system secondary to increased CSF pressure in severe systemic hypertension.. It appears that CSF volume is decreased in the presence of systemic hypertension however it is still unclear if the CSF pressure in systemic hypertension is decreased as well. Clinical data on post dural puncture headaches in the presence of hypertension in humans is rare