Cardiovascular system vasoconstriction

The majority of endogenous prostaglandins tend to exert undesirable effects on the cardiovascular system. These compounds as a rule tend to cause vasoconstriction and promote platelet aggrega-... 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

Hypertension Hypertensive patients should use these products only with medical advice, as they may experience a change in blood pressure because of the added vasoconstriction. Studies suggest pseudoephedrine is the drug of choice. Sustained-action preparations may affect the cardiovascular system to a lesser degree. 

The most serious toxic effects of cocaine involve changes in the cardiovascular system. These include cardiac arrhythmias, myocardial ischaemia and infarction, and cerebrovascular spasm, all of which can be largely explained by the facilitation of the action of catecholamines on the cardiovascular system. Another explanation of the cardiotoxicity of cocaine lies in the direct vasoconstrictive properties of its major metabolite, norcocaine. It seems likely... 

On the cardiovascular system the effects are those of sympathetic autonomic stimulation. There is vasoconstriction in the skin and vasodilatation in... 

Reduction of portal pressure. Vasopressin (anti-duiretic hormone, see p. 711), in addition to its action on the renal collecting ducts (through receptors), constricts smooth muscle (Vj receptors) in the cardiovascular system (hence its name), and particularly in splanchnic blood vessels, so reducing blood flow in the portal venous system. Unfortunately, coronary vasoconstriction can also occur, and treatment has to be withdrawn from 20% of patients because of myocardial ischaemia. Glyceryl trinitrate (transdermally, sublingually, or intravenously) reduces the cardiac risk and, advantageously, further reduces portal venous resistance and pressure. 

Histamine is an endogenous substance that activates histamine H2, and H3 receptors, and its principal pharmacologic effects involve exocrine glands, extravascular smooth muscles, and the cardiovascular system. H, receptor stimulation increases inositol-1,4,5-triphosphate, which increases intracellular calcium, resulting in vasoconstriction. Activation of H2 receptors increases intracellular cAMP, which mediates gastric acid secretions and cardiovascular effects. H3 receptor stimulation may be involved in feedback inhibition of histamine synthesis and release. 

Oral decongestants should also be avoided by patients taking beta-blockers, as sympathomimetics stimulate both the alpha-adrenoceptors of the cardiovascular system to produce vasoconstriction and the beta-adrenoceptors to produce vasodilatation and stimulation of the heart. The overall effect is a slight increase in both blood pressure and heart rate. If the beta-receptors are blocked, unopposed alpha-adrenoceptor-mediated vasoconstriction can lead to a rise in blood pressure. 

Peripheral Pharmacological Actions of Nicotine. Nicotine effects on the cardiovascular system include tachycardia and peripheral vasoconstriction, which leads to elevated blood pressure. Because the cardiovascular effects are mainly caused by elevated levels of catecholamines and cortisol, tolerance to these effects does not occur. Other pharmacological actions of nicotine include increased gastrointestinal motility caused by parasympathetic ganglionic stimulation and skeletal muscle contraction caused by the effect on nicotinic receptors in the neuromuscular junction (184). 

The peptidoleukotrienes play a major role in the pathophysiological sequelae of anaphylaxis by exerting profound effects on smooth muscle tone. Peptidoleukotrienes contract respiratory, vascular, and intestinal smooth muscle. Furthermore, peptidoleukotrienes have potent effects on the cardiovascular system including coronary vasoconstriction, reduced heart rate, arteriolar constriction, venule dila-... 

Cardiovascular System is affected by the release of catecholamines from sympathetic nerve endings resulting in vasoconstriction, tachycardia and elevated blood pressure. 

Ergot alkaloids have complex and diverse actions. For example, the marked effects of ergotamine on the cardiovascular system are due to vasoconstriction, depression of vasomotor centers, and peripheral adrenergic blockade. 

The predominant actions of phenylephrine are on the cardiovascular system. Parenteral administration causes a rise in systolic and diastolic pressures due to peripheral vasoconstriction. Accompanying the pressor response to phenylephrine is a marked reflex bradycardia that can be blocked by atropine after atropine, large doses of the peripheral resistance is considerably increased. Circulation time is slightly prolonged, and venous pressure is slightly increased venous constriction is not marked. Most vascular beds are constricted renal, splanchnic, cutaneous, and limb blood flows are reduced, but coronary blood flow is increased. Pulmonary vessels are constricted, and pulmonary arterial pressure is raised. 

CARDIOVASCULAR SYSTEM In the supine patient, therapeutic doses of morphine-like opioids have no major effect on blood pressure or cardiac rate and rhythm. Such doses do produce peripheral vasodilation, reduced peripheral resistance, and an inhibition of baroreceptor reflexes. Therefore, when supine patients assume the upright position, orthostatic hypotension and fainting may occur. The peripheral arteriolar and venous dilation produced by morphine involves several mechanisms. Morphine and some other opioids provoke release of histamine, which sometimes plays a large role in the hypotension. However, vasodilation usually is only partially blocked by Hj antagonists, but it is effectively reversed by naloxone. Morphine also blunts the reflex vasoconstriction caused by increased Pco (see Chapter 15). 

HUMAN HEALTH RISKS Acute Risks eczematous dermatitis convulsions CNS depression rise in blood pressure peripheral vasoconstriction respiratory failure Chronic Risks skin sensitization effects on liver, kidneys, CNS, cardiovascular system and red blood cells. 

Adrenaline (epinephrine) stimulates alpha- and beta-receptors of the cardiovascular system, the former results in vasoconstriction (mainly alphaj) and the latter in both vasodilatation (mainly beta2) and stimulation of the heart (mainly betaj). The net result is usually a modest increase in heart rate and a small rise in blood pressure. However, if the heta-reeeptors are blocked by a non-selective beta blocker, such as propranolol or nadolol (see Table 22.1 , (p.833) for a list), the unopposed alpha vasoeonstrietion causes a marked rise in blood pressure, followed by reflex bradyeardia. Cardioselective beta blockers such as atenolol and metoprolol, whieh are more selective for betaj receptors, do not prevent the vasodilator aetion of adrenaline at beta2 receptors to the same extent, and therefore the effect of any interaction is relatively small. Consequently, adrenaline has been used to assess the degree of beta blockade produced by propranolol and other beta blockers.Phenylephrine is largely an alpha stimulator, therefore beta blockers should have a minimal effect on its action. 

AVP is synthesized in the fetal hypothalamus. In addition to its role in altering gene expression (e.g., POMC), plasma AVP levels also increase in response to fetal hypoxia-ischemia (30,70,71). The release of AVP is not mediated by peripheral chemoreceptor mechanisms and therefore is unlikely to contribute to the rapid cardiovascular changes at the onset of hypoxia (see above) (30). Exogenously administered AVP produces hypertension, peripheral vasoconstriction, and bradycardia (71-73), although the contribution of hypoxia-stimulated increases in AVP to the redistribution of fetal CVO is uncertain (74,75). Endothehal VI receptors mediate an AVP vasodUatory effect, which means that the net effect of AVP on the cardiovascular system is likely to reflect an integrated picture of vasoconstriction from a number of vascular beds, modulated by endothelium-dependent vasodUatory mechanisms (76). 

Cardiovascular problems—Alcohol affects the cardiovascular system by (1) causing vasodilatation of the peripheral vessels, producing flushing, heat loss, and a sense of warmth and (2) promoting vasoconstriction of the central blood vessels, producing resistance to the flow of blood, and increasing the work load on the heart. 

As to be expected from a peptide that has been highly conserved during evolution, NPY has many effects, e.g. in the central and peripheral nervous system, in the cardiovascular, metabolic and reproductive system. Central effects include a potent stimulation of food intake and appetite control [2], anxiolytic effects, anti-seizure activity and various forms of neuroendocrine modulation. In the central and peripheral nervous system NPY receptors (mostly Y2 subtype) mediate prejunctional inhibition of neurotransmitter release. In the periphery NPY is a potent direct vasoconstrictor, and it potentiates vasoconstriction by other agents (mostly via Yi receptors) despite reductions of renal blood flow, NPY enhances diuresis and natriuresis. NPY can inhibit pancreatic insulin release and inhibit lipolysis in adipocytes. It also can regulate gut motility and gastrointestinal and renal epithelial secretion. 

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

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