Blood vessel contraction

Many studies have shown that ginseng has a protective effect on the development of atherosclerosis that may lead to myocardial infarction and other cardiovascular diseases. The preventive effects on cardiovascular diseases of ginseng include its potential antihypertensive and antiatherosclerotic effects. Ginsenosides are likely to be responsible for some of these effects as they have been shown to have inhibitory effects on platelet aggregation and to suppress thrombin formation as well as an effect on blood vessel contraction. 

Hi-receptors mainly mediate the constriction of large and relaxation of small blood vessels, contractions of the bronchial, intestinal and uterine smooth muscle and contractions of vascular endothelial cells with the result of an increased capillary permeability. The lymphatic flow is augmented by Hi-receptor stimulation. H2-receptor stimulation induce a dilatation of pulmonary arteries, a positive inotropic and chronotropic effect on the heart and an increased glandular secretion, especially in the mucosa of the stomach. 

PCP can cause extremely high blood pressure combined with blood vessel contractions. This can increase the risk of stroke. One study suggests that chronic PCP use leads to brain damage, evidenced by memory gaps, disorientation, visual disturbances, and difficulty with speech, which might be due to mini-strokes caused by the effects of PCP. 

Beta-blockers relieve stress on the heart by slowing the heart beat and reducing blood vessel contraction in the heart, brain, and throughout the body. Generally, these drugs are used to treat abnormal heart rhythms, chest pain, high blood pressure, and certain types of tremors (familial or hereditary essential tremors). 

Vascular spasm. In which the blood vessels contract as a result of neurological reflexes and local myogenic (muscle) spasm. The degree of constriction is directly proportional to the degree of trauma. The spasm may last up to 30 minutes. 

In the body nitrates are converted to nitrites, which can oxidize hemoglobin to methemoglobin and lead to cyanosis. They also cause unconsciousness, dizziness, fatigue, shortness of breath, nausea, and vomiting. The skin is warm and sweaty and later becomes cold due to vasodilation. It causes coronary blood vessel contraction, bradycardia, atrial fibrillation, cardiac ischemia, headache, convulsions, and diarrhea. 

In various rat blood vessels, there is a direct correlation between expression of the ttiA AR subtype and the importance of extracellular Ca " in muscle contraction [40]. In rabbit aorta, similar results were found for the o,A-AR-extracellular Ca dependence [41]. In the same study, a parallel correlation was observed for Oib-ARs coupling to PLC and mobilization of intracellular Ca stores. These observations led to the hypotheses that oia-ARs couple to Cz influx while uig-ARs couple to phosphatidyl inositol (4,5) bisphosphate (PI) hydrolysis and release of intracellular Ca stores to trigger blood vessel contraction. 

For the peripheral activity, the blood pressure increase that is caused by blood vessel contraction, Eq. 55 was observed, whereas for the central nervous system-mediated activity, the blood pressure decrease, Eq. (56), resulted [60,88] ... 

For the same class of compounds Timmermans determined log Papp values (n-octanol/buffer, pH = 7.4), binding affinities to oti adrenoceptors, ICsoOti (displacement of the oti antagonist prazosin), binding affinities to a2 adrenoceptors, IC5(,a2 (displacement of the 2 agonist clonidine), antihypertensive activities (mediated by a central mechanism) in anesthetized normotensive rats (ED2s%, i v. application), and hypertensive activities (mediated by peripheral a stimulation which, in the absence of central nervous system regulation, causes blood vessel contraction) in... 

Treatment of adverse events benzodiazepines (IV), addition of vasoconstrictors that cause blood vessel contraction that may reduce vascular absorption, and IV fluid hydration prior to neuraxial blockade should all be considered. 

Physiological responses to prostaglandins encompass a variety of effects Some prostaglandins relax bronchial muscle others contract it Some stimulate uterine con tractions and have been used to induce therapeutic abortions PGEj dilates blood vessels and lowers blood pressure it inhibits the aggregation of platelets and offers promise as a drug to reduce the formation of blood clots... 

In general, activation of alpha-1 adrenergic receptors causes a contraction of smooth muscle and of blood vessels, pilomotor muscles, dilator pupillae, vas deferens, nictitating membrane, splenic capsule, and sphincters of the intestine and urinary bladder and of the bile duct. An exception is the relaxation of the smooth muscle of the intestine. Prazosin [19216-56-9] indoramin [26844-12-2] and WB-4101 are relatively selective antagonists of these receptors. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

The human histamine Hi-receptor is a 487 amino acid protein that is widely distributed within the body. Histamine potently stimulates smooth muscle contraction via Hi-receptors in blood vessels, airways and in the gastrointestinal tract. In vascular endothelial cells, Hi-receptor activation increases vascular permeability and the synthesis and release of prostacyclin, plateletactivating factor, Von Willebrand factor and nitric oxide thus causing inflammation and the characteristic wheal response observed in the skin. Circulating histamine in the bloodstream (from, e.g. exposure to antigens or allergens) can, via the Hi-receptor, release sufficient nitric oxide from endothelial cells to cause a profound vasodilatation and drop in blood pressure (septic and anaphylactic shock). Activation of... 

Vasoconstriction of peripheral blood vessels Regulates release of neurotransmitters decreases tone, motility, and secretions of gastrointestinal tract Increased heart rate, increased force of myocardial contraction... 

Blood vessels have elastic walls that expand or contract due to changes in pressure or the passage of corpuscles. How should Equations (14.11) and (14.12) be modified to reflect this behavior ... 

As noted in Table 49-3, slow cycling of the crossbridges permits slow prolonged contraction of smooth muscle (eg, in viscera and blood vessels) with less utilization of ATP compared with striated muscle. The ability of smooth muscle to maintain force at reduced velocities of contraction is referred to as the latch state this is an important feamre of smooth muscle, and its precise molecular bases are under smdy. 

Purely electrical models of the heart are only a start. Combined electromechanical finite-element models of the heart take into account the close relationship that exists between the electrical and mechanical properties of individual heart cells. The mechanical operation of the heart is also influenced by the fluid-structure interactions between the blood and the blood vessels, heart walls, and valves. All of these interactions would need to be included in a complete description of heart contraction. 

Although skeletal muscle comprises the bulk of muscle tissue in the body, smooth muscle is far more important in terms of homeostasis. Most smooth muscle is found in the walls of tubes and hollow organs. Contraction and relaxation of the smooth muscle in these tissues regulates the movement of substances within them. For example, contraction of the smooth muscle in the wall of a blood vessel narrows the diameter of the vessel and leads to a decrease in the flow of blood through it. Contraction of the smooth muscle in the wall of the stomach exerts pressure on its contents and pushes these substances forward into the small intestine. Smooth muscle functions at a subconscious level and is involuntary. It is innervated by the autonomic nervous system, which regulates its activity. 

Finally, an increase in volume or pressure within a tube or hollow organ causes stretch or distortion of the smooth muscle in the organ wall. This may cause activation of stretch-activated Ca++ channels. The subsequent influx of calcium initiates contraction of the smooth muscle. This process is referred to as myogenic contraction and is common in blood vessels. 

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