There are several potential mechanisms that could lead to chronically elevated blood pressure and essential hypertension. Abnormalities in the body's reflex mechanisms for regulating blood pressure, including the baroreceptor reflex and stimulation of certain areas of the central nervous system, may disrupt homeostasis. Additionally, issues with the kidney's ability to regulate sodium excretion and blood volume, as well as problems with local tissue autoregulation of blood flow, could result in increased peripheral vascular resistance and higher blood pressure over time. Dysfunction of the vascular endothelium and imbalance of vasoactive substances it produces, such as decreased nitric oxide or excess angiotensin II or endothelin, may also contribute to essential hypertension. Factors like high sodium intake, low
There are several potential mechanisms that could lead to chronically elevated blood pressure and essential hypertension. Abnormalities in the body's reflex mechanisms for regulating blood pressure, including the baroreceptor reflex and stimulation of certain areas of the central nervous system, may disrupt homeostasis. Additionally, issues with the kidney's ability to regulate sodium excretion and blood volume, as well as problems with local tissue autoregulation of blood flow, could result in increased peripheral vascular resistance and higher blood pressure over time. Dysfunction of the vascular endothelium and imbalance of vasoactive substances it produces, such as decreased nitric oxide or excess angiotensin II or endothelin, may also contribute to essential hypertension. Factors like high sodium intake, low
There are several potential mechanisms that could lead to chronically elevated blood pressure and essential hypertension. Abnormalities in the body's reflex mechanisms for regulating blood pressure, including the baroreceptor reflex and stimulation of certain areas of the central nervous system, may disrupt homeostasis. Additionally, issues with the kidney's ability to regulate sodium excretion and blood volume, as well as problems with local tissue autoregulation of blood flow, could result in increased peripheral vascular resistance and higher blood pressure over time. Dysfunction of the vascular endothelium and imbalance of vasoactive substances it produces, such as decreased nitric oxide or excess angiotensin II or endothelin, may also contribute to essential hypertension. Factors like high sodium intake, low
There are several potential mechanisms that could lead to chronically elevated blood pressure and essential hypertension. Abnormalities in the body's reflex mechanisms for regulating blood pressure, including the baroreceptor reflex and stimulation of certain areas of the central nervous system, may disrupt homeostasis. Additionally, issues with the kidney's ability to regulate sodium excretion and blood volume, as well as problems with local tissue autoregulation of blood flow, could result in increased peripheral vascular resistance and higher blood pressure over time. Dysfunction of the vascular endothelium and imbalance of vasoactive substances it produces, such as decreased nitric oxide or excess angiotensin II or endothelin, may also contribute to essential hypertension. Factors like high sodium intake, low
Download as DOC, PDF, TXT or read online from Scribd
Download as doc, pdf, or txt
You are on page 1of 2
These baroreceptor reflex mechanisms may be blunted in the elderly
and in those with diabetes.
Stimulation of certain areas within the central nervous system (e.g., nucleus tractus solitarius, vagal nuclei, vasomotor center, and the area postrema) can either increase or decrease BP. For example, 2-adrenergic stimulation within the central nervous system decreases BP through an inhibitory effect on the vasomotor center.However, angiotensin II increases sympathetic outflow from the vasomotor center, which increases BP. The purpose of these neuronal mechanisms is to regulate BP and maintain homeostasis. Pathologic disturbances in any of the four major components (autonomic nerve fibers, adrenergic receptors, baroreceptors, or central nervous system) conceivably could lead to chronically elevated BP. These systems are physiologically interrelated. A defect in one component may alter normal function in another, and such cumulative abnormalities then may explain the development of essential hypertension.
PERIPHERAL AUTOREGULATORY COMPONENTS
Abnormalities in renal or tissue autoregulatory systems could cause
hypertension. It is possible that a renal defect in sodium excretion may develop first, which can then cause resetting of tissue autoregulatory processes, resulting in a higher arterial BP. The kidney usually maintains normal BP through a volumepressure adaptive mechanism. When BP drops, the kidneys respond by increasing retention of sodium and water. These changes lead to plasma volume expansion, which increases BP. Conversely, when BP rises above normal, renal sodium and water excretion are increased to reduce plasma volume and cardiac output. This ultimately will maintain homeostatic BP conditions. Local autoregulatory processes maintain adequate tissue oxygenation. When tissue oxygen demand is normal to low, the local arteriolar bed remains relatively vasoconstricted. However, increases in metabolic demand trigger arteriolar vasodilation that lowers peripheral vascular resistance and increases blood flow and oxygen delivery through autoregulation. Intrinsic defects in these renal adaptive mechanisms could lead to plasma volume expansion and increased blood flow to peripheral tissues, even when BP is normal. Local tissue autoregulatory processes that vasoconstrict then would be activated to offset the increased blood flow. This effect would result in increased peripheral vascular resistance and, if sustained, also would result in thickening of the arteriolar walls. This pathophysiologic component is plausible because increased total peripheral vascular resistance is a common underlying finding in patients with essential hypertension.
VASCULAR ENDOTHELIAL MECHANISMS
Vascular endothelium and smooth muscle play important roles in regulating
blood vessel tone and BP. These regulating functions are mediated through vasoactive substances that are synthesized by endothelial cells. It has been postulated that a deficiency in the local synthesis of vasodilating substances (e.g., prostacyclin and bradykinin) or excess vasoconstricting substances (e.g., angiotensin II and endothelin I) contribute to essential hypertension, atherosclerosis, and other diseases. Nitric oxide is produced in the endothelium, relaxes the vascular epithelium, and is a very potent vasodilator. The nitric oxide system is an important regulator of arterial BP. Hypertensive patients may have an intrinsic deficiency in nitric oxide release, resulting in inadequate vasodilation. Although the exact role of nitric oxide in hypertension is unclear, it may be a pharmacologic target in the future.
ELECTROLYTES AND OTHER CHEMICALS
Epidemiologic and clinical data have associated excess sodium intake
with hypertension. Population-based studies indicate that high-salt diets are associated with a high prevalence of stroke and hypertension. Conversely, low-salt diets are associated with a low prevalence of hypertension. Clinical studies have shown consistently that dietary sodium restriction lowers BP in many (but not all) patients with elevated BP. The exact mechanisms by which excess sodium leads to hypertension are not known. However, they may be linked to increased circulating natriuretic hormone, which would inhibit intracellular sodium transport, causing increased vascular reactivity and increased BP. Altered calcium homeostasis also may play an important role in the pathogenesis of hypertension. A lack of dietary calcium hypothetically can disturb the balance between intracellular and extracellular calcium, resulting in an increased intracellular calcium concentration. This imbalance can alter vascular smooth muscle function by increasing peripheral vascular resistance. Some studies have shown that dietary calcium supplementation results in a modest BP reduction in hypertensive patients. The role of potassium fluctuations is also inadequately understood. Potassium depletion may increase peripheral vascular resistance, but the clinical significance of small serum potassium concentration changes is unclear. Furthermore, data demonstrating reduced cardiovascular risk with dietary potassium supplementation are very limited. This issue requires further investigation before potassium supplementation can be endorsed. Hyperuricemia has been associated with an increased risk of cardiovascular events in hypertensive patients but remains controversial because of inconsistent data. Uric acid has no physiologic function and is considered a biologicwaste product. Therefore, there is no rational explanation describing why uric acid would cause cardiovascular harm. However, elevated uric acid may be viewed
1 Critical Care Nursing Clinics of North America Volume 17 Issue 4 2005 (Doi 10.1016/j.ccell.2005.07.005) Massé, Linda Antonacci, Marie - Low Cardiac Output Syndrome - Identification and Management