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Vasoconstricting drugs

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. [Pg.102]

Nephrotoxicity is caused by drugs that principally affect the renal hemodynamics of the patient depended on vasodilator prostaglandin biosynthesis or angiotensin converting enzyme (ACE) mediated vasoconstriction drugs causing nephrotoxicity include NSAIDs (fenprofen), ACE inhibitors (captopril, and cyclosporin). [Pg.400]

Two imidazolines, priscol (211) and privine, are valuable vasodilating and vasoconstricting drugs, while there are also a number of antagonists to histamine, such as antisine, methiamide and cimethidine, which are also imidazolines. [Pg.498]

Figure 6-4. Autonomic and hormonal control of cardiovascular function. Note that two feedback loops are present the autonomic nervous system loop and the hormonal loop. Each major loop has several components. Thus, the sympathetic nervous system directly influences four major variables peripheral vascular resistance, heart rate, contractile force, and venous tone. The parasympathetic nervous system directly influences heart rate. In addition, angiotensin II directly increases peripheral vascular resistance (not shown), and the sympathetic nervous system directly increases renin secretion (not shown). Because these control mechanisms have evolved to maintain normal blood pressure, the net feedback effect of each loop is negative feedback tends to compensate for the change in arterial blood pressure that evoked the response. Thus, decreased blood pressure due to blood loss would be compensated by increased sympathetic outflow and renin release. Conversely, elevated pressure due to the administration of a vasoconstricting drug would cause reduced sympathetic outflow and renin release and increased parasympathetic (vagal) outflow. Figure 6-4. Autonomic and hormonal control of cardiovascular function. Note that two feedback loops are present the autonomic nervous system loop and the hormonal loop. Each major loop has several components. Thus, the sympathetic nervous system directly influences four major variables peripheral vascular resistance, heart rate, contractile force, and venous tone. The parasympathetic nervous system directly influences heart rate. In addition, angiotensin II directly increases peripheral vascular resistance (not shown), and the sympathetic nervous system directly increases renin secretion (not shown). Because these control mechanisms have evolved to maintain normal blood pressure, the net feedback effect of each loop is negative feedback tends to compensate for the change in arterial blood pressure that evoked the response. Thus, decreased blood pressure due to blood loss would be compensated by increased sympathetic outflow and renin release. Conversely, elevated pressure due to the administration of a vasoconstricting drug would cause reduced sympathetic outflow and renin release and increased parasympathetic (vagal) outflow.
There are several ways to stop gastrointestinal bleeding by catheter intervention infusion of vasoconstrictive drugs (vasopressin), embolization and intentional induction of vasospasm. [Pg.56]

Lion of action. The largest use of this drug, however, depends on its vasoconstricting action phenylephrine is used extensively as a nasal decongestant due to its ability to constrict the blood vessels in mucous tissue on local application. In one published... [Pg.63]

The adrenergic drugs are useful in improving hemodynamic status by improving myocardial contractility and increasing heart rate, which results in increased cardiac output. Peripheral resistance is increased by vasoconstriction. In cardiogenic shock or advanced shock associated with low cardiac output, die adrener-... [Pg.204]

Methylergonovine is contraindicated in patients with a known hypersensitivity to the drug, hypertension, and preeclampsia and should not be used to induce labor (Pregnancy Category C). Methylergonovine is used cautiously in patients with renal or hepatic impairment. When methylergonovine is administered concurrently with vasopressors or to patients who are heavy cigarette smokers, excessive vasoconstriction may occur. [Pg.561]

The relevance of PCP receptors is supported by reports that the ability of PCP-like drugs to produce PCP-like stimulus in drug discrimination paradigms (Shannon 1981 Holtzman 1980 Brad and Balster 1981), produce vasoconstriction (Altura et al. 1983) and produce ataxia (Vincent et al. 1979 Vignon et al. 1982 Vaupel et al. 1984) correlates well with their ability to bind to PCP receptors. [Pg.94]

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... [Pg.369]

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... [Pg.370]

These animal studies should indicate to the pharmacist that blood flow can, under certain circumstances, be an important patient variable that may affect the absorption of drugs. Patients in heart failure would generally be expected to have a decreased cardiac output and, therefore, a decreased splanchnic blood flow. This could lead to a decreased rate of absorption for drugs when the blood flow rates in Eq. (7) become rate-limiting. In addition, redistribution of cardiac output during cardiac failure may lead to splanchnic vasoconstriction in patients [57], Other disease states and physical activity can also decrease blood flow to the GIT [2 4], Thus, the pharmacist must be aware of the possible effect of blood flow rate, especially alterations in the rate, on the availability of drugs. [Pg.123]

Hypertension (blood pressure >140/90 mmHg) may be caused by an elevation in cardiac output or excessive vasoconstriction. Diuretics are used in these patients to reduce cardiac output. Assume that the hearts of these individuals are operating on the ascending portion of the cardiac function curve. As the plasma volume is reduced in response to treatment with diuretic drugs, venous return and preload are reduced, as are ventricular filling and stroke volume, and cardiac output, thus bringing blood pressure back within the normal range. [Pg.188]

Angiotensin II causes vasoconstriction by direct stimulation of ATj receptors on the vascular smooth muscle. It also enhances release of the neurotransmitter norepinephrine from the sympathetic nerve fibers present in the blood vessels. The vasopressor effects of Ag II may be inhibited pharmacologically in order to decrease TPR and treat hypertension. An important class of orally active drugs is the ACE inhibitors, including captopril and enalopril, which prevent formation of Ag II. More recently, angiotensin receptor antagonists have been developed that act at the vascular smooth muscle. These drugs, which include losartin and valsartan, are also orally active. [Pg.209]

Platelets play a role in each of the mechanisms of normal hemostasis vasoconstriction, formation of the platelet plug, and blood coagulation. However, they are also involved in pathological processes that lead to atherosclerosis and thrombosis (formation of a blood clot within the vascular system). Antiplatelet drugs interfere with platelet function and are used to prevent the development of atherosclerosis and formation of arterial thrombi. [Pg.234]


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