Biology circulation sanguine Medecine - Autoregulation in Hypertension Caused by Aortic Coarctation

« Autoregulation in Hypertension Caused by Aortic Coarctation ● Hypertension caused by aortic coarctation results in high pressure in the arms (40%-60% above normal) and normal pressure in the legs ● Autoregulation develops so completely that local blood flow control mechanisms compensate for the differences in pressure ● Local blood flow is controlled by local autoregulatory mechanisms almost exactly in accord with the needs of the tissue and not in accord with the level of the pressure Hypertension in Preeclampsia (Toxemia of Pregnancy) ● Preeclampsia, also called toxemia of pregnancy, affects 5% to 10% of expectant mothers and is characterized by hypertension that usually subsides after delivery ● Ischemia of the placenta and subsequent release of toxic factors are believed to play a role in causing hypertension in preeclampsia ● Endothelial dysfunction decreases release of nitric oxide and other vasodilator substances, causing vasoconstriction and hypertension ● Thickening of the kidney glomerular membranes reduces the glomerular fluid filtration rate and increases the arterial pressure level required to cause normal formation of urine Neurogenic Hypertension ● Acute neurogenic hypertension can be caused by strong stimulation of the sympathetic nervous system ● Excessive stimulation of the sympathetic system leads to peripheral vasoconstriction and acute hypertension ● Cutting the nerves leading from the baroreceptors or destroying the tractus solitarius in each side of the medulla oblongata causes hypertension by removing the normal inhibitory effect on the vasomotor center ● The response of the vasomotor center to the absent baroreceptor signal fades away within about 2 days, returning the pressure to nearly normal Central resetting of the baroreceptor pressure control mechanism ● Neurogenic hypertension caused by sectioning the baroreceptor nerves is mainly an acute type of hypertension, not a chronic type Role of the sympathetic nervous system in chronic hypertension ● Activation of the sympathetic nervous system leads to activation of the renal sympathetic nerves, impairs renal pressure natriuresis, and causes chronic hypertension ● Excess weight gain and obesity often lead to activation of the sympathetic nervous system Genetic causes of hypertension ● Spontaneous hereditary hypertension has been observed in several strains of animals ● In the Okamoto spontaneously hypertensive rat, there is evidence that in early development of the hypertension, the sympathetic nervous system is considerably more active than in normal rats ● In humans, several different gene mutations have been identified that can cause hypertension, called monogenic hypertension ● Monogenic hypertension is rare, and all the known forms together account for less than 1% of cases of human hypertension Primary (Essential) Hypertension ● About 90% to 95% of all people who have hypertension are said to have primary hypertension ● Excess weight gain and a sedentary lifestyle appear to play a major role in causing primary hypertension ● Most patients with hypertension are overweight ● Clinical studies have shown the value of weight loss for reducing blood pressure in most patients with hypertension Characteristics of primary hypertension caused by excess weight gain and obesity ● Cardiac output is increased in part because of the additional blood flow required for the extra adipose tissue ● Blood flow in the heart, kidneys, gastrointestinal tract, and skeletal muscle is increased Hypertension and Obesity ● Hypertension is increased in overweight patients due to increased metabolic rate and growth of organs and tissues in response to their increased metabolic demands ● Total peripheral vascular resistance may be increased if hypertension is sustained for many months and years Sympathetic Nerve Activity in Obese Patients ● Sympathetic nerve activity, especially in the kidneys, is increased in overweight patients ● The causes of increased sympathetic activity in obese persons are not fully understood, but studies have suggested that hormones such as leptin that are released from fat cells may directly stimulate multiple regions of the hypothalamus, which in turn have an excitatory influence on the vasomotor centers of the brain medulla ● There is also evidence for reduced sensitivity of arterial baroreceptors in buffering increases in arterial pressure, as well as activation of chemoreceptors in obese persons, especially in those who also have obstructive sleep apnea Increased Angiotensin II and Aldosterone Levels in Obese Patients ● Angiotensin II and aldosterone levels are increased in many obese patients ● This increase may be caused partly by increased sympathetic nerve stimulation, which increases renin release by the kidneys and therefore formation of angiotensin II, which in turn stimulates the adrenal gland to secrete aldosterone Impaired Renal Pressure Natriuresis Mechanism in Obesity Hypertension ● The renal-pressure natriuresis mechanism is impaired in obesity hypertension, and the kidneys will not excrete adequate amounts of salt and water unless the arterial pressure is high or kidney function is somehow improved ● Impaired renal pressure natriuresis in obesity hypertension is caused mainly by increased renal tubular reabsorption of salt and water due to increased sympathetic nerve activity and increased levels of angiotensin II and aldosterone Graphic Analysis of Arterial Pressure Control in Essential Hypertension ● The curves of Figure 19-15 are called sodium-loading renal function curves because the arterial pressure in each case is increased very slowly, over many days or weeks, by gradually increasing the level of sodium intake ● Two types of curves can be recorded in patients with essential hypertension: (1) salt-insensitive hypertension and (2) salt-sensitive hypertension ● Note in both cases that the curves are shifted to the right, to a higher pressure level Note: The above summary is based on the provided text, which is discussing the relationship between obesity and hypertension, and the possible factors that contribute to the development of hypertension in obese patients.

The text also includes a graphic analysis of arterial pressure control in essential hypertension, which is divided into two types: salt-insensitive and salt-sensitive hypertension. The curves of this figure are determined by gradually increasing the level of sodium intake and recording the changes in arterial pressure. Salt sensitivity of blood pressure ● Salt sensitivity of blood pressure is not an all-or-none finding, it is quantitative ● Some individuals are more salt-sensitive than others ● Salt sensitivity of blood pressure is not a fixed characteristic, it increases with age and decrease in kidney function ● Structural or functional differences in the kidneys may be the reason for the difference between salt-insensitive essential hypertension and saltsensitive hypertension Treatment of Essential Hypertension ● Current guidelines for treating hypertension recommend lifestyle modifications aimed at increasing physical activity and weight loss in most patients ● Pharmacological treatment with antihypertensive drugs must be initiated if patients are unable to lose weight ● Two general classes of drugs are used to treat hypertension: vasodilator drugs and natriuretic or diuretic drugs Vasodilator drugs ● Vasodilator drugs increase renal blood flow and glomerular filtration rate ● They cause vasodilation in many other tissues of the body, as well as in the kidneys ● Different vasodilators act in one of the following ways: (1) by inhibiting sympathetic nervous signals to the kidneys or by blocking the action of the sympathetic transmitter substance on the renal vasculature and renal tubules; (2) by directly relaxing the smooth muscle of the renal vasculature; or (3) by blocking the action of the renin-angiotensinaldosterone system on the renal vasculature or renal tubules Natriuretic or diuretic drugs ● They reduce the reabsorption of salt and water by the renal tubules ● They block active transport of sodium through the tubular wall, which prevents the reabsorption of water Summary of Integrated Multifaceted Systems for Arterial Pressure Regulation ● Arterial pressure is regulated not by a single pressure controlling system but instead by several interrelated systems, each of which performs a specific function ● The first line of defense against acute changes in arterial pressure is the nervous control system, the second line of defense is achieved mainly by kidney mechanisms for the long-term control of arterial pressure Figure 19-1 The Role of Kidneys in Long-term Control of Arterial Pressure ● The renal-blood volume pressure control mechanism, also known as the renal-body fluid pressure control mechanism, is responsible for long-term control of arterial pressure. ● It takes a few hours to show significant response and eventually develops a feedback gain for control of arterial pressure that is nearly equal to infinity. ● This mechanism can return the arterial pressure nearly all the way back to the pressure level that provides normal output of salt and water by the kidneys. ● Many factors can affect the pressure-regulating level of the renal-body fluid mechanism, including aldosterone, which plays an important role in modifying the pressure control characteristics of the renal-body fluid mechanism. ● The renin-angiotensin system interacts with the aldosterone and renal fluid mechanisms to make the blood pressure control more stable, especially in response to changes in salt intake. Hypertension Management ● Hypertension is a major cardiovascular risk factor affecting one-third of the adult population. ● It should be managed as part of a comprehensive cardiovascular risk reduction strategy, while also assessing for hypertensive end-organ damage and ruling out secondary causes. ● Treatment involves modifying lifestyle to improve diet and body weight, and making use of a.... »