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Clonidine may also cause bradycardia, theoretically by increasing signaling through the vagus nerve. When given intravenously, clonidine can temporarily increase blood pressure by stimulating α 1 receptors in smooth muscles in blood vessels. [83] This hypertensive effect is not usual when clonidine is given orally or by the transdermal route.
Nephrotoxicity is toxicity in the kidneys. It is a poisonous effect of some substances, both toxic chemicals and medications, on kidney function. [1] There are various forms, [2] and some drugs may affect kidney function in more than one way. Nephrotoxins are substances displaying nephrotoxicity.
JNC8 does not recommend β-blockers as initial therapy for hypertension. [66] Heart failure may be worsened with nondihydropyridine calcium channel blockers, the alpha blocker doxazosin, and the alpha-2 agonists moxonidine and clonidine. On the other hand, β-blockers, diuretics, ACEis, ARBs, and aldosterone receptor antagonists have been shown ...
Clonidine was initially developed as a treatment for high blood pressure. Low doses in evenings and/or afternoons are sometimes used in conjunction with stimulants to help with sleep and because clonidine sometimes helps moderate impulsive and oppositional behavior and may reduce tics. [96] It may be more useful for comorbid Tourette syndrome.
It is weaker than clonidine in producing hypotension and sedation, has weaker pre-synaptic actions on the α 2A-adrenergic receptor than clonidine (10-fold less effective in decreasing locus coeruleus activity and norepinephrine release), and may have greater efficacy in activating post-synaptic α 2A-adrenergic receptors (as suggested by ...
Common side effects include: low blood pressure, cough, hyperkalemia, headache, dizziness, fatigue, nausea, and kidney impairment. [18] [19] The main adverse effects of ACE inhibition can be understood from their pharmacological action. The other reported adverse effects are liver problems and effects on the fetus. [19]
Accordingly, xylazine significantly increases K m and does not affect V max. [24] This likely occurs by direct interaction on an area that overlaps with the antidepressant binding site. [24] For example, xylazine and clonidine suppress uptake of iobenguane (MIBG), a norepinephrine analogue, in neuroblastoma cells. [24]
It has many different causes including obstructive sleep apnea, kidney disease, endocrine diseases, and tumors. The cause of secondary hypertension varies significantly with age. [1] It also can be a side effect of many medications.
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