alogues such as iloprost, or prostaglandin E1 analogues such as alprostanil, mimic the actions of relaxant mediators. Ca2+ antagonists reduce depolarizing inward Ca2+ currents, while K+-channel activators promote outward (hyperpolarizing) K+ currents. Organic nitrovasodilators give rise to NO, an endogenous activator of guanylate cyclase. Individual vasodilators. Nitrates (p. 120) Ca2+-antagonists (p. 122). "1antagonists (p. 90), ACE-inhibitors, AT1antagonists (p. 124); and sodium nitroprusside (p. 120) are discussed elsewhere.
Twenty years ago in the twenty-first edition of the
Principles and Practice of Medicine, the authors
described what was then the practice for the pharmacologic
therapy of patients with heart failure,
which included digoxin and a diuretic . In addition,
the authors noted that recent studies had
supported the potential use of vasodilators in the
treatment of this population of patients.
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: " Alterations in vasodilator-stimulated phosphoprotein (VASP) phosphorylation: associations with asthmatic phenotype, airway inflammation and β2-agonist use...
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Renal hypoperfusion and impaired endothelium-dependent vasodilation in an animal model of VILI: the role of the peroxynitrite-PARP pathway...
Hypertension and coronary heart disease (CHD) are of great importance. Hypertension affects above 20% of the total population of the USA with its major impact on those over age 50. CHD is the cause of death in 30% of males and 22% of females in England and Wales. Management requires attention to detail, both clinical and pharmacological. The way drugs act in these diseases is outlined and the drugs are described according to class.
Inhibitors of the RAA System
lasting effect than does captopril. Indications are hypertension and cardiac failure. Lowering of an elevated blood pressure is predominantly brought about by diminished production of angiotensin II. Impaired degradation of kinins that exert vasodilating actions may contribute to the effect. In heart failure, cardiac output rises again because ventricular afterload diminishes due to a fall in peripheral resistance.
Arterial CO2 tension is a powerful modulator of cerebral vascular calibre, CBF and ICP (12-15.)
While the mechanisms are incompletely understood, CO2 relaxes pial arterioles by
interactions between the endothelium, vascular smooth muscle, pericytes, adjacent neurons
and glial cells. Studies supported that cerebral vessels are sensitive to changes in
extracellular pH, rather than a direct response to CO2 or bicarbonate. In the limits of
physiological PaCO2, 20-60 mmHg, the relationship between PaCO2 and CBF is linear.
The lung has a unique vascular structure and function; it has low pressure, low
resistance circulation with a highly compliant system which accommodates the same
amount of flow as the systemic circulation. In addition, pulmonary and systemic
vasculatures have divergent responses to various stimuli. For example, pulmonary
arteries constrict in the setting of hypoxia, while systemic circulation dilates. This is
due to distinctive developmental characteristics, anatomic and histological structure,
as well as physiological properties.
NO is a gaseous molecule, synthesized by NO synthase
(NOS), an enzyme that catalyses the oxidation of L-arginine
to NO and L-citrulline. At least two types of NOS can be
reported, constitutive NOS (cNOS) and inducible NOS (iNOS)
. cNOS is produced by many cells in the upper and lower
respiratory system, such as parasympathetic vasodilator
nerves, endothelial cells and ciliated mucosa cells
Metabolic acidosis can occur because of an increase in endogenous acid production (such as lactate and ketoacids), loss of bicarbonate (as in diarrhea), or accumulation of endogenous acids (as in renal failure). Metabolic acidosis has profound effects on the respiratory, cardiac, and nervous systems. The fall in blood pH is accompanied by a characteristic increase in ventilation, especially the tidal volume (Kussmaul respiration). Intrinsic cardiac contractility may be depressed, but inotropic function can be normal because of catecholamine release.
Estrogen receptors and serotonin receptors coexist in cells
in a wide variety of tissues, and this critical review of the
literature suggests that many of E2's effects may be medi-
ated by changes in the actions of serotonin (5HT). Serot-
onin is usually considered to be a neurotransmitter, but
surprisingly, only 1% of serotonin in the human body is
found in the CNS .
Palladin is an actin-associated protein that has been suggested to play crit-ical roles in establishing cell morphology and maintaining cytoskeletal
organization in a wide variety of cell types. Palladin has been shown previ-ously to bind directly to three different actin-binding proteins vasodilator-stimulated phosphoprotein (VASP), a-actinin and ezrin, suggesting that it
functions as an organizing unit that recruits actin-regulatory proteins to
specific subcellular sites.
Cytosolic phospholipase A2-a(cPLA2-a) is a calcium-activated enzyme that
plays an important role in agonist-induced arachidonic acid release. In
endothelial cells, free arachidonic acid can be converted subsequently into
prostacyclin, a potent vasodilator and inhibitor of platelet activation,
through the action of cyclooxygenase (COX) enzymes. Here we study the
relocation of cPLA2
-a in human EA.hy.926 endothelial cells following
stimulation with the calcium-mobilizing agonist, A23187.
Chapter 19 - The cardiovascular system: Blood vessels (part a). When you finish this chapter, you should: Describe the three layers that typically form the wall of a blood vessel, and state the function of each; define vasoconstriction and vasodilation; compare and contrast the structure and function of the three types of arteries;...