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The extent of vasoconstriction may be slight or severe depending on the substance or circumstance. Many vasoconstrictors also cause pupil dilation. Medications that cause vasoconstriction include: antihistamines, decongestants, and stimulants. Severe vasoconstriction may result in symptoms of intermittent claudication. [1]
Some causes of orthostatic hypotension include neurodegenerative disorders, low blood volume (e.g. caused by dehydration, bleeding, or the use of diuretics), drugs that cause vasodilation, other types of drugs (notably, narcotics and marijuana), discontinuation of vasoconstrictors, prolonged bed rest (immobility), significant recent weight loss ...
Each drug has a benefit-risk profile and balancing the risk of no treatment with the competing potential risks of various therapies should be considered. [49] For people over the age of 65 years old, the balance between the benefits of pain-relief medications such as NSAIDS and the potential for adverse effects has not been well determined. [50]
Renin concentration in blood plasma tends to be higher in younger people with hypertension when vasoconstriction may be the main reason for high blood pressure. Conversely, renin is lower in older people or in people of African American or African Caribbean ethnicity when salt retention may contribute more to elevated blood pressure. [21]
Since β 2 adrenergic receptors can cause vascular smooth muscle dilation, beta blockers may cause some vasoconstriction. However, this effect tends to be small because the activity of β 2 receptors is overshadowed by the more dominant vasoconstricting α 1 receptors.
OSA is prevalent in older adults and should be considered in cases of resistant hypertension, hypertension refractory to appropriate aggressive medical therapy. [3] OSA remains an under-diagnosed cause of secondary hypertension, likely due to the fact that many of the risk factors associated with OSA such as obesity , advanced age, and ...
Like other β adrenergic agonists, they cause smooth muscle relaxation. β 2 adrenergic agonists' effects on smooth muscle cause dilation of bronchial passages, vasodilation in muscle and liver, relaxation of uterine muscle, and release of insulin. They are primarily used to treat asthma and other pulmonary disorders.
However, high-dose therapy is linked to excessive coronary, splanchnic vasoconstriction, and hypercoagulation. [6] Excessive vasoconstriction can cause cardiac output reduction or even fatal heart complication particularly in those with weak myocardial function. [6] [4] [28] [29]