Vasoconstrictive factors

Nakai K, Matsuda N, Amano M, et al. Acellular and cellular hemoglobin solutions as vasoconstrictive factor. Artif Cells Blood Substit Immobil Biotechnol 1994 22 559. 

In order to clarify the vasoconstrictive factors, sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) was carried out in the initial phase of our study. In the patients with myoglobinuric acute renal failure, myoglobin bands were detected. However, there were no ALPE-specific bands (Fig. 62). 

Wood, P. (1958). Pulmonary hypertension with special reference to the vasoconstrictive factor. Br. Heart J. 20, 557-570. 

Dismption of the endothehal surface of blood vessels expose coUagen fibers and connective tissue. These provide surfaces that promote platelet adherence, platelet release reaction, and subsequent platelet aggregation. Substances Hberated from the platelets stimulate further platelet aggregation, eg, adenosine diphosphate maintain vasoconstriction, eg, serotonin and participate in blood coagulation, eg, platelet Factors III and IV. In addition, the release reaction modifies platelet membranes in a manner that renders phosphoHpid available for coagulation. The thrombin [9002-04-4] elaborated by the coagulation mechanism is a potent agent in the induction of the platelet release reaction. 

Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the central nervous system (CNS) is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. This results from several factors, including loss of appetite, malabsorption due to gastrointestinal edema, elevated metabolic rate, and elevated levels of proinflammatory cytokines. 

Amphotericin B-induced ARF occurs in as many as 40% to 65% of patients treated with the conventional desoxycholate formulation.30 Nephrotoxicity is due to renal arterial vasoconstriction and distal renal tubule cell damage. Risk factors include high doses, treatment for at least 7 days, preexisting kidney dysfunction, and concomitant use of other nephrotoxic drugs.31 Three lipid-based formulations of amphotericin B have been developed in an attempt to decrease the incidence of ARF amphotericin B lipid complex, amphotericin colloidal dispersion, and liposomal amphotericin B. The range of... 

Cyclosporine and tacrolimus are calcineurin inhibitors that are administered as part of immunosuppressive regimens in kidney, liver, heart, lung, and bone marrow transplant recipients. In addition, they are used in autoimmune disorders such as psoriasis and multiple sclerosis. The pathophysiologic mechanism for ARF is renal vascular vasoconstriction.41 It often occurs within the first 6 to 12 months of treatment, and can be reversible with dose reduction or drug discontinuation. Risk factors include high dose, elevated trough blood concentrations, increased age, and concomitant therapy with other nephrotoxic drugs.41 Cyclosporine and tacrolimus are extensively metabolized by... 

Hypertension, or a chronic elevation in blood pressure, is a major risk factor for coronary artery disease congestive heart failure stroke kidney failure and retinopathy. An important cause of hypertension is excessive vascular smooth muscle tone or vasoconstriction. Prazosin, an aradrenergic receptor antagonist, is very effective in management of hypertension. Because oq-receptor stimulation causes vasoconstriction, drugs that block these receptors result in vasodilation and a decrease in blood pressure. 

Other factors regulating ADH secretion include blood volume and blood pressure. A decrease in blood volume of 10% or more causes an increase in ADH secretion sufficient to cause vasoconstriction as well as antidiuresis. A decrease in mean arterial blood pressure of 5% or more also causes an increase in ADH secretion. The resulting water conservation and vasoconstriction help increase... 

Most arterioles of the peripheral circulation are strongly constricted by direct sympathetic stimulation. This widespread vasoconstriction serves two purposes. First, it contributes to the increase in MAP. Second, it is an important factor in the redirection of blood flow away from inactive tissues and toward the working muscles. 

Vascular constriction. The first mechanism to occur is vascular constriction. Immediately after a blood vessel is cut or severed, the vascular smooth muscle automatically constricts. This results in a decrease in the flow of blood through the vessel that helps to limit blood loss. The vasoconstriction is caused by several factors ... 

P2Y receptors that are found on endothelial cells elicit a Ca2+-dependent release of endothelium-dependent relaxing factor (EDRF) and vasodilation. A secondary activation of a Ca2+-sensitive phospholipase A2 increases the synthesis of endothelial prostacyclin, which limits the extent of intravascular platelet aggregation following vascular damage and platelet stimulation. The P2Y-mediated vasodilation opposes a vasoconstriction evoked by P2X receptors located on vascular smooth muscle cells. The latter elicit an endothelial-independent excitation (i.e. constriction). P2Y receptors are also found on adrenal chromaffin cells and platelets, where they modulate catecholamine release and aggregation respectively. 

A partially or completely occlusive clot forms on top of the raptured plaque. Exposure of collagen and tissue factor induce platelet adhesion and activation, which promote release of adenosine diphosphate and thromboxane A2 from platelets. These produce vasoconstriction and potentiate platelet activation. A change in the conformation of the glycoprotein (GP) Ilb/IIIa surface receptors of platelets occurs that cross-links platelets to each... 

Regardless of the etiology, fall in blood pressure (BP) is compensated by an increase in sympathetic outflow, activation of the renin-angiotensin system, and other humoral factors that stimulate peripheral vasoconstriction. Compensatory vasoconstriction redistributes blood away from the skin, skeletal muscles, kidneys, and GI tract toward vital organs (e.g., heart, brain) in an attempt to maintain oxygenation, nutrition, and organ function. 

In addition to its pump function, the heart is also a secretory organ. Cardiac cells produce two small peptides, the natriuretic factors, which oppose the vasoconstrictive actions of noradrenaline (norepinephrine) from the sympathetic nervous system and of the peptide angiotensin II. By causing vasodilation and natriuresis (increased excretion of sodium in the urine), atrial natriuretic peptide (ANP) secreted from the atria and B-type natriuretic peptide (BNP) secreted by both atria and probably more significantly, from the ventricles, reduce blood pressure. The stimulus to secretion of natriuretic peptides is wall stretch of the chambers of the heart, indicating volume and pressure overload of the vascular system. A third member of the natriuretic peptide family, CNP, is secreted by endothelial cells. 

Figure 19.17 The biochemistiy and physiology responsible for penile erection. Sexual activity itself begins with a state of arousal that leads to erection. Arousal results in part from stimulation of the sense organs. The hypothalamus coordinates the sensations and activates the autonomic nervous system. Sensory nerves from the skin of the penis and other erogenous zones stimulate the parasympathetic system. This activates nitric oxide synthase and the resultant nitric oxide, via cyclic GMP, causes vasodilation of the arterioles. This increases blood flow through the corpora cavernosa which then expands producing an erection. Pheromones secreted by the female can stimulate the odour detecting system in the nasal cavity of the male (Chapter 12 and see above). Stress, however, activates the sympathetic system releases cyclic AMP which can result in vasoconstriction of the arterioles. Other factors that can interfere with an erection are physical fatigue and alcohol.

An early consequence of overexposure to PGDN is vasodilation of the cerebral vessels, which is the major factor in the development of headache. With more severe exposure, relaxation of the vascular smooth muscle can result in a fall in blood pressure followed by a compensatory vasoconstriction. 

One important mechanism of serotonin elimination is the (re-) uptake, e.g. by platelets. Furthermore, serotonin is metabolized by monoaminox-idase to 5-hydroxyindoleacetaldehyde and, subsequently, by an aldehyde dehydrogenase to 5-hydroxyindolacetic acid. The vascular effects of serotonin are complex. The direct interaction with vascular smooth muscle induces a vasoconstriction, whereas the stimulation of 5-HT-receptors on the endothelium induces the release of vasorelaxant factors with a dilatation as a result. An intravenous application of serotonin increases the pressure in the pulmonary circulation. A continuous infusion results... 

Vascular endothelium also plays an important role in maintaining vascular tone. The endothelium can modulate both vasodilation and vasoconstriction through its ability to locally synthesize and release vasodilators such as nitric oxide, endothehum-derived hyperpolarizing factor, and PGI2, and vasoconstrictors such as endothehn, which in turn directly affect vascular smooth muscle activity. Stimulation of az-adrenoceptors located on the endothelial cells in certain vascular beds (such as the coronary artery) results in the release of nitric oxide and vasodilation. 

Total coronary blood flow is reduced by the (3-blockers. This effect may be due in part to the unopposed a-receptor-mediated vasoconstriction that follows (3-receptor blockade in the coronary arteries. Additional contributing factors to the decrease in coronary blood flow are the negative chronotropic and inotropic effects produced by the (3-blockers these actions result in a decrease in the amount of blood available for the coronary system. The decrease in mean blood pressure may also contribute to the reduced coronary blood flow. 

Both drugs are partial agonists at a-adrenergic receptors and at some serotonin and dopamine receptors they also can inhibit the release of endotheUal-derived relaxation factor. They may induce arterial vasoconstriction and have minor actions on the central nervous system. Their a-adrenergic blocking activity is relatively weak compared with those of other ergot alkaloids. 

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